\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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Some bacteria have the remarkable capacity to fix atmospheric nitrogen to ammonia under ambient conditions, a reaction only mimicked on an industrial scale by a chemical process. This microbiological process converts atmospheric nitrogen into a plant-usable form, thus decreasing the need to use chemical fertilizers in crop production. Chapters in this volume cover different aspects of this fantastic phenomenon, including biofertilizer, organic nitrogen in agricultural systems, nitrogen fertilization for sustainable crop production, and others. 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That communication technologies in general and the media in particular are essential ingredients in the process of globalization has long been a commonly accepted assumption in the social sciences (Thompson, 1995). The deterritorialized nature of new communication technology generated early idealistic ideas about the emergence of a “global village” (McLuhan, 1964), and in response to the rapidly increasing complexity of global communication infrastructures, theories about the rise of a “network society” (Castells, 1996) followed. Satellite technology has enabled the simultaneous distribution of news across nation-state borders, and transnational[1] - media networks such as CNN have “become emblematic of a world in which place and time mean less and less” (Hjarvard, 2001: 18). Transnational news services are believed to offer new styles and formats for journalistic practices, contributing to the loosening up of national identities, and arguments about an emerging “global public sphere” have been pursued (e.g. Volkmer, 2003). Thus, the media are allegedly key elements of the compression of time and space, one of the salient features of globalization (Harvey, 1989), and are viewed as both products of and significant contributors to the fluidity of globalization (Chalaby, 2003).
However, these notions about the media’s pertinent role in globalization processes have also been fiercely challenged by quite a few media scholars, who instead emphasize the continuing stability and centrality of the nation-state paradigm. National propaganda is often present in transnational media as well, not least in CNN, as are stereotypical and negative depictions of the “others” (Hafez, 2009; Thussu, 2003). Given the existence of obstacles such as language barriers and the “digital divide,” which separates the “haves” from the “have nots” with regard not only to communication technology itself, but also to the skills necessary for using it, there are no real signs of a media network with the ability to constitute a global public sphere (Hafez, 2007). Severe scepticism concerning the notion of global media has also been expressed by scholars within the political economy tradition who claim that global media are in fact better described as Western or American media, and only contribute to maintaining Western dominance (e.g. Herman & McChesney, 1997). Some authors are critical of the very idea of globalization, of the way the concept has developed and been used in the social sciences (e.g. Calhoun, 2007; Sparks 2007a, 2007b). Thus, within the field of global media studies there is an ongoing conflict between the “globalists,” proponents of the fluidity argument, and the “sceptics,” who pursue the stability argument (Cottle 2009: 30f).
Nonetheless, these two positions – their obviously conflicting views notwithstanding – have in common one fundamental and largely taken-for-granted assumption about global media: global media are interpreted as media networks or technology whose nature is global (or at least transnational) in terms of geographic reach. I would propose, however, that having global reach is not a necessary condition of global media. From a discourse theoretical perspective, an emergent trajectory of the research field (Cottle, 2009), “global” is instead understood as a discursive feature. From this point of view it could be argued that global media cannot be reduced to transnational media networks; a global discourse might develop in any kind of media, be it local, national, or transnational, as well as in any kind of media content – local, domestic, or foreign (Berglez, 2008; Olausson, 2010). Any medium might, in fact, be labeled “global” if it provides its audiences with a global interpretative framework. Thus, the argument put forward in this chapter is that the view on global media as transnational media networks and technology needs to be supplemented with a discourse theoretical approach, which also includes national media and takes the very knowledge production of the global into consideration.
I will develop this position first by examining the arguments of the line of research that equates global media with transnational media networks, including its contradictory arguments about the ability of these networks to contribute to or be part of globalization processes. Following this, the discourse perspective will be introduced and exemplified with some empirical examples from a study on the emergence of a transnational (European) identity in national news reporting on global climate change (Olausson, 2010). The chapter ends with a discussion in which the discourse theoretical approach is put in relation to broader issues of cultural and political transformation, conclusions are drawn about the media’s relationship to globalization processes, and suggestions are made for an integral explanation of global media.
By necessity, the two perspectives on global media are outlined here with rather broad strokes and the presentation might be somewhat lacking in detail and precision. This is the price to be paid when trying to squeeze the complexity of a research field into rather rigid “boxes.” Nonetheless, this categorization will hopefully elucidate the argument that the established understanding of global media as media of transnational reach needs to be complemented with a discourse approach that also includes national media if we want to achieve an integral explanation of global media.
Cross-border communication technologies such as the internet, mobile phones, and satellites have contributed to the deterritorialization of space over the last decades, and transnational media networks and news services such as CNN, BBC World News, FoxNews, and Al-Jazeera have entered and transformed the media landscape. In a dialectic fashion, these media are believed both to constitute and to be constituted by globalization, transforming understandings of time and space (Chalaby, 2003; Thompson, 1995). Due to their deterritorialized nature, diverse audiences, and independence of any national loyalties, arguments about their ability to loosen up distinctions between domestic and foreign have been pursued:
“The cross-border coverage of transnational television networks, their multinational audience and international production operations tear apart the relationship between place and television and challenge the traditional relationship between broadcasting and the nation-state.” (Chalaby, 2003: 457)
Global broadcasting corporations not only provide people with a better understanding of global politics (Chalaby, 2003), they also offer new journalistic styles and formats able to transgress the nation-state outlook and, in a dialectic relationship with national news angles, give rise to new horizons for political identity and citizenship (Volkmer, 2003). Accordingly, transnational media have been attributed the potential to constitute a global, or at least a transnational, public sphere (Chalaby, 2003; Volkmer, 2003).
The idea that transnational media networks are able to move beyond the nation-state paradigm has, however, not escaped criticism. Hafez (2007) argues that there is not enough empirical evidence of a media system that could accurately be described as “global” in the sense of enhancing the possibilities of a global public sphere. On the contrary, the majority of empirical evidence points in the direction of reinforced stability of the nation-state paradigm. Information and news may be transnational in character, but the media in fact still are, to a considerable extent, local and national phenomena. In times of war, Western propaganda is also present in transnational media, as are polarizing perspectives of “us” and “them” and stereotypical depictions of the “other” (Hafez, 2007; Thussu, 2003):
“Today’s international exchanges of images and information, it seems, are no guarantee for global intertextuality in news, for growing awareness of ‘the other’s’ stories and perspectives, and for an increased complexity of world views in the mass media and beyond.” (Hafez, 2009: 329)
Even though CNN, as the topical case in point, under regular circumstances does contribute various “global” perspectives and viewpoints, it is extremely sensitive to American patriotism and displays bias in times of military conflicts in which the US is involved, such as the 2003 Iraq war (Hafez, 2009). Not even the communication technology most associated with cross-border communication, the internet, has according to Hafez (2007) proved to fulfil this expectation. Most people use this technology locally – to communicate with people in their nearby surroundings – not to engage in cultural interaction across nation-state borders. Furthermore the necessary technological means are far from being globally diffused; “no electricity, no internet,” as was pointed out by Sparks (2007b: 152). The nation-state paradigm is, according to this view, as powerful as ever before and has, in several respects, even gained in importance. Hafez (2007) illustratively labels this viewpoint in the field of global media studies “the myth of media globalization,” and Sparks (2007a) dismisses the entire theoretical framework of globalization arguing that current developments are better explained as part of the continuing capitalist and imperialist expansion (cf. Nohrstedt & Ottosen, 2001).
The scepticism surrounding global media is far from new. The well-established field of international communication, based on the political economy tradition, has a long history of persistently arguing that global media are in fact best described as Western (or American) media, at most of global scope (e.g. Herman & McChesney, 1997; Schiller, 1993). The central argument of these scholars is that escalating media conglomeration has led to a notable Western (American) bias both in terms of ownership and with regard to the distribution of media products. The media achieve their global characteristics as a result of purchases made by a small number of Western-, predominantly US-based multinational media giants, who distribute their products – permeated with neoliberal values and Western lifestyles – all over the globe. Even the “glocalization” that takes place when cultural products are tailored to fit a specific local market is viewed as a commercial strategy and as such nothing more than yet another sign of cultural imperialism (Sparks, 2007b). The rise of competing non-western media networks such as Al-Jazeera notwithstanding, the westernizing tendencies of global media have not been eliminated since the power of western, and particularly US-dominated media networks such as CNN, is not only restricted to their own large-scale activities; they set the agenda also for other networks (Thussu, 2003).
Thus, claims about cultural imperialism and cultural homogenization have been made, and warnings have been issued about the democratic dangers that surface when it is no longer possible to hold media institutions accountable to political regulation at the nation-state level. The prospects for democracy do not seem any brighter if we add the argument that active citizens, due to the commercial logic of global media, over time transform into pure consumers in Western-dominated markets (e.g. Herman & Chomsky, 1988; Herman & McChesney, 1997). The consequences of the ravages of seemingly global media, it is alleged, are harmful both to indigenous cultures and to democracy. In this fashion global media counteract rather than promote a global public sphere, and contribute to the maintenance and stability of Western (US) dominance.
In this research tradition, media conglomeration, concentration, and commercialization have functioned as the analytical point of departure – restricting the interest to the shape and structure of transnational media institutions – and claims about media effects have been made without much analytical attention being paid to the actual reception and use among locally situated audiences. As a counterbalance to this macro-perspective, the research field of cultural studies has instead focused on the micro-dimension of global media (e.g. Barker, 1999; Crane 2002; Tomlinson, 1999). Instead of viewing the impacts of global media as a one-way process that completely erases local cultures, scholars within this research tradition emphasize processes of cultural “creolization” (Hannerz, 1996) or “hybridization,” i.e. the creation of completely new cultural expressions in the encounter between different cultural forms:
“Most forms of culture in the world today are, to varying extents, hybrid cultures in which different values, beliefs and practices have become deeply entwined.” (Thompson, 1995: 170, emphasis in original)
The idea of the “active audience,” quite capable of negotiating and opposing media information, has been a guiding principle in cultural studies. Suggestions have even been made (though not uncontested) that the opportunities to “pick and choose” cultural forms due to the rapid development of communication technologies and the creative hybridization that follows, will most likely lead to new and improved conditions for global dialogue (Lull, 2007). Thus, cultural studies have to a considerable extent problematized the idea of the homogenizing effects of global media and questioned the cultural imperialism thesis of the international communication field.
The perspectives accounted for above are fairly well established in the research field of global media. The main arguments of international communication and of cultural studies respectively are frequently discussed in the literature (e.g. Rantanen, 2005), as are the “globalist” and the “sceptic” perspectives (e.g. Cottle, 2009). Despite their conflicting opinions when it comes to the media’s relation to globalization, the “globalists” and the “sceptics” share at least one basic viewpoint on global media, namely that the proper objects of study first and foremost are those media whose global nature is defined in terms of geographic reach. The discourse perspective that will now be discussed takes a somewhat different stance towards this assumption.
The discourse approach to global media proposed here does not direct specific attention to the geographic reach of the media, but focuses primarily on the very epistemology of the global (Berglez, 2008). As pointed out by Cottle (2009: 28) in his discussion of the principle paradigms structuring the field of global media studies, it is necessary to go beyond the paradigms of “global dominance” and “global public sphere,” since these approaches to global media fail to explain how issues such as crises of different kinds are mediated and constituted in practice and how they, through their formation in the news media, achieve their “global” characteristics:
“Global crises are principally constituted epistemologically as ‘global crises’ through the news media where most of us get to know about them and where they are visualized, narrativized, publicly defended and sometimes challenged and contested.” (Cottle, 2009: 165, emphasis in original)
Admittedly, local or national crises, such as 9/11, the 2010 flooding in Haiti, or the 2011 Egyptian revolution, need the connectivity that a cross-border communication infrastructure provides in order to become known, more or less simultaneously, to people around the globe. But, to achieve their global features – to become global crises, involving people and generating action across the world – they are entirely dependent on discursive constructions of them as such.
Extending this line of argument, when studying the production of knowledge about the global it is necessary to acknowledge national media as equally important objects of study as any media of transnational reach. As Robertson (2008) argues, the issue of media globalization is an empirical question, and the assumption of most authors that global broadcasters are, or at least should be, more inclined to produce global outlooks than national broadcasters, must be empirically demonstrated rather than axiomatically asserted. In the debate on global media, however, national media, which doubtlessly still are the media that most people turn to, are most often dismissed as not significant knowledge producers concerning the global due to their inclination to depict the world according to nation-state logic (Altmeppen, 2010; Hafez, 2007, 2009). This logic saturates much of their contents, not least in the form of what Billig (1995) terms “banal nationalism,” a national mode of reporting which makes the world orbit around the nation-state, and in terms of taken-for-granted conceptions of the world as constituted by self-governing national “islands” rather than being a complex transnational network (Berglez & Olausson, 2011). In national media the domestic and foreign worlds are, by tradition, separated, and the nation-state becomes disconnected from the rest of the world (Berglez, 2007). At best, relations between the domestic and foreign are constructed through the domestication of foreign events, i.e. by the addition of a national angle to the story from “outside” in order to make it more relevant to the national audience as it is perceived (Clausen, 2004; Gurevitch et al., 1991; Riegert, 1998).
This tendency of national media to reproduce and maintain nation-state discourse and identity must of course be acknowledged. However, the national outlook should not be viewed as totally precluding other, transnational or global outlooks on the world. As suggested by Volkmer (2003), national media are to an increasing extent influenced by transnational media style and formats. Furthermore, and even more importantly, due to the globalization of risks such as climate change, and conflicts such as transnational terrorism or the Global War on Terror (as labeled by George W. Bush), national discourse is constantly (and perhaps to an increasing extent) challenged by transnational or global discourses that strive for the hegemonic position (Laclau & Mouffe, 1985). It is thus not a question of either national or global discourse but both-and, with national and local views functioning in interaction with transnational or global outlooks (Beck, 2006).
In a similar fashion, Hjarvard (2001) suggests that the possible emergence of a global public sphere should be viewed in terms of both-and; the transnational communicative space that has come into existence through the development of transnational media should be seen as a supplement to national public spheres. The globalizing tendencies of politics, economics, and culture have put the national public sphere under constant pressure, as has the increasing connectivity with other national public spheres. This will ultimately lead to what Hjarvard labels a “global reflexivity,” since fewer and fewer topics can be dealt with without including information from “outside.” In this way, national public spheres will gradually become deterritorialized through the “increased presence of global connections within the national framework” (Hjarvard 2001: 24, emphasis added). Like Hjarvard, Cottle (2009) emphasizes the media’s ability to provide…
“…a transnational and global perspective on a problem that both migrates across and transcends national frames of reference or explanation, exposing international interconnections, contextualizing motives and exploring both the scope of the problem and its human consequences.” (Cottle 2009: 100, emphasis added)
The issue of whether or not the media are capable of displaying global or transnational connections is pivotal to the discourse approach to global media suggested here. Global discourse in the news media is, as argued by Berglez (2008), characterized by the depiction of connections – including antagonistic ones – between people, processes, events, and phenomena at the local, national, transnational, and global levels. This focus on interconnections between various geopolitical scales makes the global news style quite different from the traditional foreign news style, which primarily reports from one nation to another without displaying any connections between the two (Berglez, 2008). If a global discourse is present, the most local (in terms of geography) of all media might be labeled “global” (in terms of discourse), providing a global interpretative framework by linking national and transnational identities or positioning a local event in a global context or vice versa.
Thus, the decisive criterion of global media, from a discourse theoretical perspective, is the ability to display complex and often subtle connections between various geopolitical scales. These relations do not have to be of the “objective” or realist kind to be acknowledged as building blocks of a global discourse. More precisely, a global discourse does not have to comprise “real” relations of causality, motives, and interconnections, for instance that it is the carbon dioxide emissions of the First World that is the cause of the extreme droughts in the Third World. The connections displayed in media discourse could also be of a purely constructivist nature, i.e. be the “creations” of media logic itself. The inherent characteristics of news media, such as their preference for dramatic and emotionally charged reporting (perhaps occasionally also supplemented with the journalist’s deliberate intent to incite action among citizens) sometimes lead to the emergence of a global discourse that involves interconnections between people across vast distances.
A telling example of this kind of global discourse, building on pure constructivist connections, is the “globalization of emotions” (Cottle, 2009: 99) that the media have engaged in over the last decades in relation to human suffering caused by wars or natural disasters. As noted by Nohrstedt (2009, cf. Shaw, 1996), there has been an increasing tendency in the news media to display the “true face” of war, i.e. the casualties and human suffering it causes, something which could be viewed as an invitation to audiences around the world to unite in compassionate responses. In her seminal work on “the spectatorship of suffering” Chouliararki (2006: 24) discusses on the one hand how the various routines of the media, such as almost endless repetition, in all probability create distance between the audience and the distant sufferers, and on the other hand how the media are capable also of establishing an “imaginary ‘we’ that brings all spectators together in the act of watching.” With the purpose of exploring how distant suffering is depicted in television news, and building on Boltanski’s (1999) theories on the topic, she distinguishes between the following three different modes of representation, each of which invites the viewers to respond to the suffering observed on the television screen in a specific way: empathy, denunciation, and contemplation. Another example, which builds on the theories of Boltanski (1999), is Robertson’s (2008) exploration of the news reporting on the 2004 Asian tsunami. In searching for a global, or cosmopolitan, outlook deriving from compassion for and empathy with the sufferers, she examines five nationally-based European broadcasters and compares them with three European channels broadcasting to global audiences. Interestingly enough, the results show that a global discourse, in terms of constructions of “togetherness,” could be found on all the channels. It was far from the case that transnational broadcasters contribute more global outlooks than the national channels; in one case a transnational broadcaster even provided a less global outlook – a finding which indisputably strengthens the argument of including national media when exploring global discourse.
As Cottle (2009) points out, media research has been focused on examining how news content “positions” the audience in relation to distant suffering; there has been a lack of empirical studies that show how the “discourse of global compassion” (Höijer, 2004) in the news media actually is received and handled by the audience. Höijer (2004), however, has demonstrated that the emotionally charged portrayal of human suffering in the news tends to trigger a variety of complex responses among the audience, and her findings challenge the notion of a pronounced compassion fatigue among people in general (Moeller, 1999). Audience research has also shown that the news reporting on distant suffering has the potential to trigger transnational identification with distant sufferers, if not for more than a moment (Olausson, 2005; Olausson & Höijer, 2010). These processes of identification are characterized by the empathetic capacity for “feeling oneself in one’s fellow man” (Boltanski, 1999: 92).
The global discourse built on compassion in the news media is composed – not always but in many cases – of pure constructivist connections. There are no “real” relations between the sufferers and the spectators beyond those “created” in news discourse, which highlights the constitutive role of the media in the process of globalization. Global media are not only the products of a globalized economy and technology, or the intermediaries of pre-existing events, processes, or connections already shaped by globalization, but are to a considerable extent also contributors to the expansion of transnational identifications and connections (cf. Volkmer, 2008a).
Thus, events or processes in various parts of the world, be they natural disasters, environmental hazards or wars, take global shape not only, or even primarily, in terms of worldwide impacts or as effects of the technological reach of transnational media, but also, and most essentially in this context, in terms of their formation in the news media where people, places, and objects are linked more closely together (cf. Cottle, 2009). This discursive demonstration or “creation” of transnational connections takes place not least in national media, their inclination to apply national angles and reinforce national identity notwithstanding.
When arguing in favor of the inclusion of national media in the search for a global discourse, it is necessary to address the question of “methodological nationalism,” raised by Beck (2006). Not only the media but also social research has been criticized as being caught in a nation-state logic in ways that do not correspond to the globalizing trends of late-modern society. However, the determining cause of methodological nationalism is not the study of national media per se; this fallacy rather comes into existence when the analysis is conducted through a national lens, and this could be the case whether the object of study is national or transnational in character. Or, to put it differently, when examined through a “national prism” both national and transnational media might take on national features, just as both national and transnational media might assume global features when examined through a “transnational prism” (Cottle 2009: 168). Indeed, the nation-state logic still permeates national news media but with a discourse theoretical approach and the analytical application of a “transnational prism” it is possible to detect at least embryonic forms of transnational or global connections also in national media, a suggestion that will be empirically illustrated below.
Much research on the possible emergence of a European public sphere and a European identity has been carried out over the last years. Volkmer (2008b: 231), as an example of an “optimistic” view on this, argues that advances in satellite technology have created, if not a public sphere in the traditional sense, at least “a platform for new, interesting flows of trans-European communication.” However, there are also quite a few voices that are less hopeful regarding the possibility of a European public sphere. Sparks (2007a, 2007b) concludes that despite the development of supra-national political bodies such as the EU, there is as yet no sign of a corresponding media system; most media remain confined within the borders of the nation-state. This is commonly used by authors in the field as an argument against the possible development of a European public sphere: since there is no functioning European media system, the prospects of a European public sphere are rather discouraging. And, additionally, since the national realm has considerable power as the point of reference for the making of identity, the chances of creating a common European “us” are minute. The only viable way to enhance political interest at the EU-level among citizens and to instill a sense of European belonging is for national news media to present news about the political institutions of the EU: EU policy-making, EU-level actors, EU politics, etc. The more frequently EU topics appear in various national media, the better the breeding-ground for a sense of community and for the development of “Europeanized national public spheres,” it has been argued. Accordingly, EU topics in national media have been measured quantitatively – the more the EU topics, the more the transnationalization, or Europeanization, of national news media, it has been assumed (e.g. D’Haenens, 2005; De Vreese, 2007; Koopmans & Erbe, 2004; Machill et al., 2006).
I would argue, first, that the sheer presence of EU topics in national news media does not automatically lead to the emergence of a transnational discourse. Following the argumentation above, in order for EU topics in national media to contribute transnational outlooks and not traditional “foreign” ones, they have to be, in one way or another, discursively connected to local and/or national conditions. These connections should not be interpreted in terms of mere domestications of EU topics (what will happen with Swedish moist snuff when the EU legislates against it?), which rather reproduce national outlooks (Sweden and the EU), but through the discursive intermingling of EU and national horizons, for instance the forging of a common European “us,” as in the example presented below (Sweden in the EU). Secondly, it is not only EU news in national media (whether intertwined with national horizons or not), that might contribute to a sense of EU belonging. Instead, such topics tend to impose themselves on national media from above as “Europeanization projects” (Lauristin, 2007). I would suggest that the everyday reporting of events or phenomena of transnational scope is just as relevant an object of study since such events, due to their borderless character, have the potential to trigger discursive transformation. According to Beck (2006), it is transnationalized threats and the suffering they cause that by necessity pave the way for a global outlook, since traditional dichotomies such as internal and external, national and international, and us and them lose their validity when confronted with these kinds of dangers (cf. Nohrstedt, 2010); a new cosmopolitanism becomes essential in order to survive in “world risk society” (Beck, 2009). The transnationalization of risks and crises such as climate change, terrorism, and financial crises pushes even national media – slowly and unsteadily perhaps, and most likely not at the same pace everywhere, yet nevertheless – in the direction of transnational modes of reporting. These transnational outlooks could well be in embryonic stages, not entirely explicit in nature, but instead common-sensical and “banal” in the words of Billig (1995), and deeply embedded and naturalized in the everyday language of news. This means that they are difficult to capture empirically without the aid of sensitive discourse analytical tools (Olausson, 2010; cf. Berglez & Olausson, 2011).
Some authors (e.g. Schlesinger, 2008) dismiss the entire notion of a European identity and argue that there are too many obstacles, such as the lack of a common language, history, and worldview, for such an identity to evolve. However, it is not very productive to cling to this “cultural” conception of identity, which can only lead to the discouraging conclusion that a European identity is a rather unachievable project. Instead, identity could be treated in a more modest way which does not demand cultural homogeneity; from such a perspective, identity concerns the identification with a political “us,” in relation to some given events, phenomena, or issues more than others (Mouffe, 1995, 2005). Thus, European identity could simply be treated as, in the words of Habermas and Derrida (2003: 293), “a feeling of common political belonging” as is illustrated by the empirical example presented next.
Elsewhere (Olausson, 2010), I have shown how the embryo of a European political identity is being forged in Swedish news reporting on climate change. In the construction of this transnational outlook, the discursive transcendence of national identity is pivotal and occurs when the national and the transnational become so closely entwined that they merge into a common “us.” Admittedly, this study also confirms the common conclusion of media research that national identity holds a hegemonic position in national news media. In this case, it is constantly reproduced through, for instance, elements of national self-glorification such as “If any country can manage this, Sweden can,” and “Sweden is one of the countries that have succeeded best.” The national outlook is also nourished through domestications of the climate issue, for example when maps of Sweden recurrently fade in and out between images of flooded areas and other alleged consequences of the changing climate on the television screen.
However, it is also evident that the national mode of reporting does not entirely preclude the emergence of transnational outlooks. As a matter of fact, it seems as if national identity functions as a necessary anchoring mechanism in the construction of a common European “us” which momentarily dissolves the distinction between the national and the transnational. Sweden and the EU are on the one hand mentioned in the news reporting as two separate entities, but on the other hand they are also closely tied to each other in the sense of their all being part of the group of “climate heroes.” In contrast to the “climate villain,” the USA, “we,” the EU, take climate change seriously and make earnest efforts to mitigate it, the message reads. The quotation from the broadsheet Dagens Nyheter “Perhaps it is not unknown to us in Sweden and Europe that greenhouse gas emissions cause great changes in the world climate” implies how national identity is transcended and incorporated into a European identity, how a common “us” is established.
Thus, the already established and naturalized national outlook becomes a means to introduce a transnational counterpart, which is not yet an integral part of everyday thinking and discourse. In the news program, Rapport, produced by the Swedish public service broadcaster, SVT, a sense of European community in relation to the climate issue takes shape through an intriguing blend of national and transnational identity positions. In the initial phrase of the reporter’s statement a “we” that transcends the national and includes the European sphere is constructed: “Exactly the way we do things within the EU…” However, when the reporter continues, this European “we” becomes integrated within the national: “…says our Swedish Minister for the Environment,” with “our” here referring to the national community.
The purpose of these brief empirical examples of the construction of a European political identity is to demonstrate that national and transnational outlooks are not engaged in discursive struggles where the destruction of one or the other is the inevitable outcome (Laclau & Mouffe, 1985). As Sparks (2007a: 150) suggests, the local, national, and global exist alongside each other in news discourse and tensions do arise between them, but “the evidence does not support the contention that one is being undermined by the other two.” I would even go so far as to claim that they in fact are highly dependent on each other: in order for less established transnational outlooks to become naturalized and integrated in everyday thinking and discourse, they need to become anchored within the familiar and established national horizon (Olausson & Höijer, 2010). Thus, there is reason to suppose that national and transnational discourses work interactively and that they mutually (re)construct each other (cf. Delanty, 2000; Olausson, 2007).
In this chapter, I have put forth the argument that the research field of global media needs to acknowledge not only the trans-boundary nature of media technology but to a greater extent the very knowledge production of the global that takes place not least in national media. When the given assumptions about what exactly the “global” in “global media” refers to are changed from being a matter of geographic reach to becoming a discursive feature, then it is possible to discover transnational and even global “embryos” in several as yet relatively unexplored media contexts, as has been shown (cf. Berglez, 2008).
As noted by Volkmer (2003), there is still a remarkable focus on the cultural impact of new communication technologies in the sociological debate on globalization. Cultural transformation has also been a dominating issue, not least in the disagreements between the fields of international communication and cultural studies over the cultural imperialism thesis. Hafez (2007) for his part, regards absence of cultural transformation generated by cross-border communication as a sign that a truly global media does not exist. Before there is reason to talk about global media it must be clarified “whether receiving cultures are changed by transmitting cultures in the process of cross-border communication through the Internet, satellite broadcasting, international broadcasting or through media imports and exports” (Hafez, 2007: 14). Thus, it seems that without the evidence of cultural transformation generated by cross-border communication, the notion of global media remains utopian.
It is true that the discourse perspective on global media, as proposed here, says little about cross-border communication and cultural transformation, but it does not totally exclude these aspects. In particular, this holds true if we go beyond the traditional technology platforms of the news media – newspapers, radio, and television – and widen the focus of research to include web-based forms of news reporting. The digital versions of newspapers, for instance, offer links to other websites around the world, hyperlinks which enable user interaction, etc. The digitalization of (national) news allows, to a greater extent than previous technologies, for cross-border communication and perhaps also cultural transformation (Berglez, 2011; Heinrich, 2008). But, what is deemed even more important here is political transformation – how the nation-state logic of political identity loosens up, is transgressed, and transforms into transnational political identities in certain contexts, as in the example above of the discursive construction of EU-identity in relation to climate change. I would argue that the discourse perspective contributes knowledge of a fundamental ingredient, both in a global public sphere and in what Berglez (forthcoming) describes as a global political culture, namely how and under what circumstances the media – national or transnational – provide their audiences with a global interpretative framework capable of including politically relevant interconnections between various geopolitical scales (cf. Volkmer, 2003).
A central aspect of this line of reasoning is the idea of late modernity being characterized by contingency in every respect, which means that everything that exists right now could take quite a different form in another situation and context (Mouffe, 1995). The contingent character of today implies that it is not reasonable to expect the media, be they national or transnational, to produce global knowledge all the time – the reporting on certain objects or phenomena, such as global risks, is probably more inclined to assume global characteristics than the reporting on local events such as a traffic accident. But it is also true that the media do not reproduce the nation-state logic throughout their reporting. And the same goes for the media audience; our national identity positions are, in all probability, activated in relation to quite a few of the events and phenomena reported in the media, but in certain cases and under certain circumstances, possibly in relation to distant suffering or global risks such as climate change, we accept global outlooks provided by the media and take on transnational identities, if not for more than a brief moment (e.g. Olausson, 2007, forthcoming). The national and global, as shown, are not mutually exclusive, but reinforce and reconstruct one another. Thus, it is rather unproductive to understand the media as contributing to either the stability of the nation-state or the fluidity of globalization, since they most likely contribute to both of these conditions depending on context and circumstances, and in a dialectic fashion. Stability and fluidity are two sides of the same coin.
The discourse approach to global media studies, for which I argue in the present chapter, is certainly not the perspective that provides us with the only “correct” version of reality. However, this perspective is currently somewhat obscured by the dominant view on global media as consisting of transnational media networks and technologies, and there is reason to draw attention to the discursive aspect of global media, which is something qualitatively different from technological reach. Nonetheless, I would like to bring this chapter to a close by emphasizing the fruitfulness of there being a variety of theoretical perspectives that pose different kinds of questions about global media and together enrich the research field. Considering their, in all essentials, complementary nature, the diversity of theoretical perspectives and approaches is indispensable for an integral explanation of global media.
Distinct diseases have different etiology pattern and this chapter covers the chromosomal diseases, cancer, neurodegenerative diseases, pulmonary diseases, obesity-induced insulin resistance, lymphoblastic leukemia, viral immunology and infectious diseases. These communicable and non-communicable diseases negatively affect structure-function of the organism and specific symptoms are associated with these conditions. Pathogens or internal dysfunctions may lead these diseases. The chapter provides pathology of selected diseases from each class along with the molecular mechanisms.
\nDown syndrome (DS) is the most common chromosomal genetic disorder. The disease is caused by the trisomy of human chromosome 21 (HSA21) and is also the most genetic mental disability [1]. The HSA21 mosaic can also lead to DS. Maternity age is an important aspect in the formation of an individual with DS [2]. The main cause of this disease is the absence of normal chromosome separation during meiosis and the production of gametes with two copies of chromosome copies instead of a single copy. As a result, DS individuals have trisomy 21 in some body cells, and a normal number of chromosomes in others. This is called mosaicism and is seen in approximately 4% of DS individuals. The term mosaicism was first reported in 1961 [3] and can occur in two ways: either a normal zygote is exposed to an early mitotic error following fertilization, which results in trisomy 21 in some cells, or an early mitotic error in some cells allows it to return to normal karyotype [4].
\nHSA21 is the most studied human chromosome, and since the long arm of chromosome 21 has been fully sequenced, a significant progress has been made in understanding its functional genomic units. HSA21 is the smallest chromosome and the overall gene density per megabase is about 15 genes per Mb (for the human genome) [5]. HSA21 is also very rich in long encoding RNA (lncRNA) genes, and, one of the poorest for genes encoding microRNA (miRNA). Also, the gene density is average for pseudogenes encoding the protein per Mb [6]. HSA21 is a weak chromosome in non-encoding RNAs (ncRNAs) and long nuclear elements (LINE). Interestingly, HSA21 shows significant enrichment for proteins found in cytoskeleton structures. These cytoskeletal proteins are known to play a role in neurological disorders, especially Alzheimer’s neuropathology [7].
\nIndividuals with DS occasionally develop the myeloproliferative disorder (TMD), a disease that is mostly unique to DS. Almost all TMD cases were found to contain somatic mutations on the X chromosome, in the GATA1 transcription factor [8]. Certain features of DS contain genes on other chromosomes causing gene and trisomy mutations and working together to reveal the disorder in HSA21. Studies have shown that the formation of Trisomy 21 precedes the formation of GATA1 mutations [1]. This may indicate that Trisomy 21 either increases genomic discrepancy leading to GATA1 mutations, or it supplies a selected medium for hematopoietic cells containing GATA1 mutations.
\nMany hypotheses have been proposed to explain the genotype–phenotype relationship in DS. One of these is the ‘gene dosage effect’ hypothesis putting forward that the phenotypes arise directly from the dosage imbalance of the genes. Overlapping this hypothesis, the ‘DS Critical Region’ (DSCR) was announced in the 1990s. [9, 10]. Many of the DS features can be called into a subset of the critical genes in the DSCR region, suggesting that DS phenotypes are mainly caused by the dosage imbalance of only a few genes on HSA21. Genomic regions affecting the presence of certain DS phenotypes have been identified and high-resolution genetic maps of DS features have been created [11]. Olson et al. studied the DSCR regions in mice to test its hypothesis. They concluded that dosage imbalance of some individual genes on HSA21 directly affects certain phenotypes, but they stated that more studies are needed [12].
\nThe “amplified developmental instability” hypothesis suggests that dosage imbalance of the HSA21 gene leads to a non-specific impairment of cellular homeostasis [10]. Extra chromosome materials may also contribute to phenotypes by disrupting chromosomal regions. Some data on monozygotic twins for TS21 suggest that differential expression between normal and trisomic twins can be regulated across chromosome domains. This study shows that some DS phenotypes can be enlightened by the modification of the chromatin structure in the nucleus [13]. Monozygotic twins affected by DS but showing incompatible phenotypes have been reported in some cases, suggesting the role of epigenetics in the phenotypic variability of DS. For example, DNA methylation (controlling gen expression) has been shown to change in Trizomy of chromosome 21 (TS21) samples [14].
\nTurner syndrome (TS) is a disorder in mosaic karyotypes associated with complete or partial loss of the X chromosome. Seen especially in women, TS is associated with short stature, delayed puberty, ovarian dysgenesis, infertility, congenital malformations of the heart, type 1 and type 2 diabetes mellitus, osteoporosis, and autoimmune disorders. It occurs in almost every 2500 live female births. Fetuses affected by TS are 99% estimated to result in fetal death. Approximately half have monosomy X (45, X) and 10% have a repeat (isochromosome) of the long arm of the X chromosome. Most of the rest has a mosaic in more cell lines for 45X. TS, which is associated with a missing X chromosome, was first identified about 100 years ago [15].
\nRelated genes: Shox gene (short length homeobox protein-coding) located on X and Y chromosomes, it is a gene responsible for TS phenotype. This gene does not undergo X inactivation, and a decrease in the expression of SHOX explains some of the TS-related growth deficits. The gene product controls the expression of natriuretic peptide B (NPBB) and FGFR3 (fibroblast growth factor receptor 3) and regulates the proliferation and of chondrocytes, and also cooperates with SOX5, SOX6 and SOX9 and some other genes [16].
\nThe TS genome is hypo-methylated with less hypermethylation sites and there are RNA expression changes that affect the X chromosome genes and autosomal genes compared to women who are 46 XX. Known escape genes are expressed differently in individuals with TS and other X chromosome genes such as RPS4X and JPX (CD40LG and KDM5C) in particularly, KDM5C (encoding lysine-specific demethylase 5C) can participate in the transcriptional profile of neuronal genes and play role in different neurocognitive profiles [17]. 40S ribosomal protein S4 (RPS4X) also plays an important role in TS, bringing together multiple protein complexes. In addition, the Y paralog of RPS4X (RPS4Y) may also have a role since it is normally expressed as duplicates [18].
\nMany different studies show that women with TS have increased mortality compared to the pool of a wide variety of related diseases [19]. The most obvious increase in morbidity is caused by autoimmunities like diabetes mellitus or thyroiditis, osteoporosis, cardiovascular diseases, hypertension, congenital malformations, especially endocrine diseases including heart diseases, digestive system and anemia [20].
\nIt is still unclear which chromosomal regions or genes make up the phenotypical properties of TS. The physical symptoms of TS were thought to be due to the absence of normal sex chromosomes before inactivation of the X chromosome, or the haplo-insensitivity of the genes in the pseudo-autosomal regions of the aneuploidy [21]. It is thought that a complete phenotype results in the loss of short arm (Xp) in the X chromosome. Aneuploidy itself can cause growth failure. Loss of a region in Xp22.3 was found to be related to neurocognitive problems in TS [22]. Loss of the SRY gene locus in the short arm of the Y chromosome leads to the phenotype of TS, even if it does not cause a population of 45 X cells. It has also been suggested that an area in Xp11.4 is important for the development of lymphedema [23].
\nCancer can be defined as the uncontrolled cell growth with the most basic explanation. Cell stacks that grow uncontrollably are called tumors. Benign tumors grow much slower and usually do not metastasize, while malignant tumors can spread to other organs through metastasis, and lead to multiple organ damage and eventually death. Tumor cells acquire characteristic features such as sustaining growth signals in the process of cancer, avoiding growth suppressors, resisting cell death, ensuring replicative immortality, initiating angiogenesis, and activating invasion and metastasis [24].
\nCancer cells acquire these abilities in the process due to genetic instability and inflammation caused by environmental and hereditary effects. Many studies show that viruses, in addition to many environmental factors such as radiation and chemicals, induce cancer. Chronic inflammation has been shown to trigger oncogenic mutations, genetic instability, tumor growth, and angiogenesis through angiogenesis and cause local immunosuppression [25].
\nTwo types of gene groups involved in cancer are oncogenes, which trigger cellular growth and uncontrolled proliferation, causing increased genetic instability with increased expression and tumor suppressor genes that cause cancer as a result of decreased control of their expression, cell division, and growth. Proto-oncogenes include RAS, WNT, MYC, ERK, and TRK genes. A mutation that may occur on a proto-oncogene or a regulatory region of the gene (e.g., promoter region) can cause an increase in the amount of protein with the change in protein structure [26]. Expressions of oncogenes can also be regulated with miRNAs [27]. Mutations occurring in these regulatory miRNAs can cause activation of oncogenes [28]. Cancer cells increase cell growth-division by activation of oncogenes, as well as suppress preventive control mechanisms of tumor suppressor genes that control this process.
\nMutations in tumor suppressor genes cause loss of function. Therefore, they occur in both alleles. To inactivate the gene and its protein, wide-ranging effects, such as deletions, frame-shift mutations, insertions, should be seen rather than point mutations [29]. Tumor suppressor genes include retinoblastoma (RB) [30], TP53, BRCA1, BRCA2, APC, and PTEN. Many side factors such as transcription complexes, changes in cellular metabolism, microenvironment can guide the course of cancer [31].
\nThe development of cancer is a multi-stage process consisting of initiation, promotion, and progression. Cancer-inducing events are usually caused by genetic mutations. Mutant cell proliferates rapidly in the promotion stage and acquires features that allow malignant behavior in the progression stage. Production of telomerase and expression of p53 are examples of malignant behavior [32]. Then, the process proceeds in the form of dysplasia formation, where new blood vessels are formed (angiogenesis) with cellular transformation. Angiogenesis facilitates the intravasation of cancer cells after undergoing an epithelial-mesenchymal transition (EMT) [33]. EMT gives an invasive phenotype to cancer cells and is managed by various transcription factors (such as SNAI, SLUG, ZEB2, ETS1, TWIST) [34]. These transcription factors also regulate each other for the protection of EMT [35].
\nNormal cells only use anaerobic glycolysis when oxygen is absent or limited, while cancer cells can convert glucose to lactate in the presence of oxygen. Otto Warburg discovered that cancer cells exhibit a differentiated metabolism ability [36]. Warburg effect is biochemical properties that help identify cancer cells. On the other side, cancer cells are generally highly glucose-dependent. Glucose intake of cells is enabled by overexpression of different isoforms of membrane glucose transporters in cancer cells [37]. It has been shown that the benefit of the Warburg effect for cancer cells is not just the formation of glycolytic ATP, but also the production of many glycolytic intermediates before anabolic processes such as NADPH and amino acids [38]. Cancer cells are also able to metabolize glutamine to synthesize some amino acids they need, use it as a nitrogen source and for fatty acid synthesis in hypoxic conditions [39]. Therefore, blood glutamine levels increase in some cancer cases [40]. Lactic acid is used to produce citric acid and maintain cancer progression in neighboring cancer cells. This is called the “Reverse Warburg effect” [41].
\nTumor micro-environment, consisting of fibroblasts, adipocytes, endothelial cells, and macrophages, is a good source for tumor growth. Tumors “steal” energy-rich metabolites from their micro-environment [42]. Monocarboxylate carriers (MCTs) are used for L-lactate transfer between cancer cells and their microenvironment [43]. Tumors have heterogeneous structures with hypoxic and aerobic regions. A “metabolic symbiosis” behavior has recently been found between the two regions [44]. Lactate is produced by glycolysis in hypoxic tumor cells. This product is obtained by aerobic cancer cells by MCT1. Aerobic cells convert lactate to pyruvate with lactate dehydrogenase isoform B (LDH-B) enzyme.
\nWhen glucose consumption is not enough to meet the energy need of cancer cells, they begin the fatty acid oxidation (FAO) [45]. For example, prostate cancer, leukemia, and large B-cell lymphoma, increasing palmitate and FAO uptake in cells are among the most commonly used bioenergetic pathways [46, 47, 48]. Normal cells usually receive fatty acids by diet, while tumors show an increase in de novo fatty acid synthesis [45].
\nPyruvate plays a pivotal role in the regulation of metabolic reprogramming, especially in tumors [49]. Pyruvate dehydrogenase (PDH) converts cytosolic pyruvate into mitochondrial acetyl-CoA, which is the first substrate of the Krebs cycle. Pyruvate dehydrogenase kinase (PDK) negatively regulates PDH. This reaction slides glucose from oxidative to glycolytic metabolism [50]. Lactate dehydrogenase (LDH) is the primary metabolic enzyme converting pyruvate into lactate. LDH plays an important role in arranging food interchange between stroma and tumor. Studies have shown that inhibition of LDH is important for treating advanced carcinomas [51]. Mitochondrial hyperpolarization is a mutual property of several tumor cells [52]. Tumor cells, which have more negative mitochondrial structures, are more selective targets in drug therapies [53].
\nBrain tumors are cancer tissues that grow abnormally and prevent the brain or central spinal system from performing its normal functions. Primary brain tumors originating from brain tissue can usually spread only to other parts of the brain, and occasionally to other organs. Tumors that form in another tissue in the body migrate to the brain are called metastatic or secondary brain tumors. These types of tumors occur more frequently than primary brain tumors. They are termed after their tissue of origin [54].
\nThe most prevalent primary tumor types in adults are glioma, astrocytomas, oligodendroglioma, meningioma, schwannoma, pituitary tumors, and central nervous system (CNS) lymphoma.
\nRetinoblastoma mutations are found in almost 75% of brain tumors and are mostly associated with glioblastoma, and Tp53 mutations are found in more than 80% of advanced gliomas [55]. Primary glioblastomas have EGFR tyrosine kinase mutations, tumor suppressor PTEN gene mutations, DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) protein abnormalities [56, 57]. While IDH1 mutations in the control mechanism of the citric acid cycle are seen in advanced glioblastomas, IDH2 mutations are usually shown in oligodendroglioma [58]. Mutations in the BRAF oncogene are common in pilocytic astrocytomas, pleomorphic xanthoastrocytomas, and gangliogliomas [55]. In some glioblastoma tumors, telomere length is maintained by mutations in the TERT promoter and ATRX gene [59].
\nWHO groups glioma patients based on the presence of two genetic changes; first, mutations [60] in the family of genes encoding isocitrate dehydrogenase (IDH), and second, loss of two specific parts of the genome (1p and 19q co-deletion) [61]. The presence or absence of these changes gives a clue about the patient’s prognosis and appropriateness of various kinds of treatments.
\nApproximately 40% of people with astrocytoma, oligodendroglioma, or IDH mutation bear a hereditary variation. This variation is a single nucleotide polymorphism (SNP) in the 8q24 region of the genome [62]. There is another SNP in the 11q23 region, which enhances the risk of IDH-mutant brain cancer. Approximately 5–8% of gliomas are familial, POT1 gene mutations have been found in 6 of 300 families with glioma [63].
\nNon-coding RNAs (ncRNAs) play important roles in regulating tumor malignancy in glioma [64, 65, 66]. According to healthy brain tissue, mir-21 expression increases in glioma and mir-21 acts as an oncogene [67, 68]. It has been reported that mir-124 and mir-137 act as tumor suppressors in glioblastoma multiform cells [69]. Hotair, SOX2ot, CRNDE, Malat1, H19, GAS are lncRNAs that have been recently shown to regulate glioma [70, 71]. Glioma cells also express the circRNAs, for example, circBRAF, bircFBXW7, circSMARCA5. These regulate proliferation, migration, and invasion of glioma cells [72, 73, 74]. The exosomal ncRNAs, mir-21, mir-148a, lncRNA PU03F3, lncRNACCAT2 can be used as circulating biomarkers of glioma patients [75, 76, 77, 78]. circRNAs and the exosomal ncRNAs were also reported as potential biomarkers for the diagnosis and prognosis of glioma patients.
\nAs a characteristic of almost all neurodegenerative diseases, abnormal protein assembly gathers these diseases under the prion concept [79]. Prion protein, known as PrP, was introduced to define protein pathogens and distinguish them from viruses and was identified as a proteinaceous infectious particle known to resist inactivation. Even back at that time, its importance was foreseen in terms of shedding light on the etiologies of chronic degenerative diseases [80]. Self-propagation is an important characteristic of prions that is also observed in abnormal protein assembly in Alzheimer’s Disease (AD) [81, 82]. Aggregation of proteins in neurodegenerative diseases was believed to occur spontaneously in autonomous cells, however, it was later understood that this aggregation begins in a particular region and propagates across other regions developing the disease further. Transmission of these prion proteins across neuronal cells takes place trans-synaptically [82].
\nAs described more than a 100 years ago, abnormal protein assembly forms the basis of neurodegeneration with AD being one of the most common neurodegenerative diseases. The pathology of abnormal protein assembly starts with misfolding of native proteins that gather to form seeds which eventually lead to aggregation and development of protein fibrils. The pathophysiology of AD involves amyloid plaque inclusions of β-amyloid (Aβ) peptides and neurofibrillary lesions of tau protein. Tau inclusions may also be characteristics of other neurodegenerative diseases, which do not necessarily show the same implications. Altering the native forms of this protein may contribute to its pathology and cause damage to its host cell.
\nMost cases of this disease are sporadic, while dominantly inherited mutations are also seen to a lesser extent. Back in the 1990s, missense mutations of APP, encoding amyloid precursor, were shown to cause AD [83, 84, 85, 86, 87]. Mutations in this gene also increase the aggregation tendency of encoded proteins. Many studies have demonstrated phenotypes associated with neurodegeneration when this protein is overexpressed.
\nThere are six isoforms of microtubule-associated protein tau ranging from 352 to 441 amino acids, encoded by the MAPT gene as a result of alternative mRNA splicing. One half has three repeats and the other has four repeats, altogether establishing the microtubule-binding domain and also the core of tau filaments in case of pathology [88]. All isoforms have been observed in the brains of AD patients. Diseases that have isoforms with only three or four repeats, but not both, lack the Aβ peptides seen in AD and therefore do not carry the symptoms specific to the disease [70]. Tau inclusions may be of a variety of conformations, which can also be caused by different mutations on the MAPT gene, explaining the existence of numerous tauopathies [89, 90, 91, 92, 93].
\nAβ peptides are encoded by the amyloid precursor protein gene, APP, and are widely expressed as type 1 transmembrane glycoproteins. As a result of alternative mRNA splicing, there are three major transcripts named APP695, APP751, and APP770 [94, 95]. β- and γ-secretase enzymes take part in the production of Aβ peptides in sequential endoproteolytic cleavage. β-secretase is responsible for cleaving the N-terminus of the peptide thus removing the portion that remains on the extracellular side. This cleaved peptide is endocytosed and intracellular aggregation builds up which is later released into the extracellular space [79]. γ-Secretase is a membrane-embedded enzyme that is able to cleave many transmembrane proteins including C-terminus of the Aβ peptide. It a complex enzyme of four proteins; presenilin (PS) forming the catalytic core, presenilin enhancer-2 (Pen-2) enabling maturation of PS, anterior pharynx-defective (Aph-1) stabilizing the complex, and nicastrin possibly being the receptor for the enzyme’s substrate [96, 97]. PS and Aph-1 each have two variants resulting in at least four different enzyme complexes, which give rise to various cleaved Aβ peptides. Additionally, γ-secretases cleave the peptide in three different sites. Different protein variants and cleavage sites produce Aβ peptides of different profiles, some of which may be more susceptible to aggregation [98].
\nOverall, it is important to target the pathways leading to abnormal protein assembly and only then treatments may be proposed based on these mechanisms. Once the first protein inclusion is formed, it is essential to keep an eye on the time frame until the disease symptoms come forth. When techniques sensitive enough to catch the first protein inclusion are developed, then tracking its transformation into filaments can be helpful in designing novel preventive approaches. Understanding this cascade will also contribute to planning more efficient therapeutic methods.
\nAsthma and chronic obstructive pulmonary disease (COPD) are common disorders characterized by progressive chronic inflammation in the lungs. They have unique characteristics with dissimilarly involved cells, mediators, and inflammation. They also have distinct responses to corticosteroid treatment. Roughly 15% of COPD patients have characteristics of asthma [99]. Also, a comparable ratio of asthma patients has traits of COPD that is currently the fifth leading cause of death worldwide [100]. Many risk factors are linked to COPD including smoking tobacco, air pollution, indoor cooking while tobacco smoking (including passive smoking) making up around 80% of the cases [101]. There are many types of cells and mediators that have a significant effect during the pathogenesis of asthma and COPD.
\nMacrophages have a crucial role in coordinating the inflammatory response activated by cigarette smoke extract in COPD cases [102]. They discharge inflammatory mediators including tumor necrosis factor (TNF)-α, IL-8, other CXC chemokines, monocyte chemotactic peptide (MCP)-1, LTB4 and reactive oxygen species (ROS) [103]. However, the role of macrophages in asthma is not certain. Allergens via low-affinity IgE receptors may activate macrophages causing an inflammatory response through the discharge of a definite arrangement of cytokines. On the other hand, macrophages also excrete anti-inflammatory mediators, such as IL-10 that is thought to decrease in subjects with intense asthma [104].
\nActivated neutrophils were shown to be enhanced in some subjects with severe asthma and COPD in their sputum and airways [105]. Among the serine proteases secreted by neutrophils are neutrophil elastase (NE), cathepsin G, proteinase-3, matrix metalloproteinase (MMP)-8 and MMP-9, leading to alveolar destruction [103]. The mechanisms of neutrophilic inflammation in asthma and COPD are not clear. Demonstration of priming in COPD occurs at neutrophils in the peripheral circulation. Many chemotactic signals exhibit the capacity for neutrophil recruitment in COPD. These include LTB4, IL-8 and related CXC chemokines, comprising GRO-α (growth-related oncoprotein) and ENA-78 (epithelial neutrophil activating protein of 78 kDa) which are enhanced in COPD airways [106]. Although the mentioned mediators might be sourced from alveolar macrophages and epithelial cells, neutrophils have the capacity of being a vital source of IL-8 [107].
\nAirway and alveolar epithelial cells in COPD can be a vital point of source of inflammatory mediators and proteases 5. Cigarette smoke activates epithelial cells which produce inflammatory mediators, including TNF-α, IL-1β, GM-CSF and IL-8 [108]. Epithelial cells play an important role in airways defense and tissue repair processes. Goblet cells, a type of epithelial cell, in mucus catch bacteria and inhaled particulates [109]. Epithelial cells release antioxidants and antiproteases. Immunoglobulin A is carried by epithelial cells, hence involved in adaptive immunity [110]. On a side note, native and adaptive immune reactions of the airway epithelium are triggered by cigarette smoke and damage by other harmful agents, increasing sensitivity to infection.
\nThe main role of dendritic cells is to introduce innate and adaptive immune reaction by activating macrophages, neutrophils, T and B lymphocytes among others [103].
\nLymphocytes are directly involved in the pathogenesis of both asthma and COPD. Both airway and parenchymal inflammation exist in asthma and COPD patients [111]. Most lung lymphocytes are T cells which are in the respiratory tract of ordinary humans. Activated T lymphocytes are characteristic in both asthma and COPD, but CD4+ type-2 T lymphocytes are the major player in asthma whereas CD8+ type-1 lymphocytes are specific to COPD [111]. CD4+ T lymphocytes can generate many cytokines involved in mediating cell functions and cell–cell communications. This is done through impressing physiologic cell properties such as proliferation, differentiation and activation of other immunocompetent cells, chemotaxis, and connective tissue metabolism [112]. On the other hand, CD8+ T lymphocytes exist in the respiratory mucosa and are activated in response to foreign antigens [111]. Specifically, the cells in the respiratory mucosa have an important role in anti-viral immunity. Another lymphocyte type is B cells which are the minority (<5%) lymphocytes. The main function of B cells located in the lungs is the production of immunoglobulins for local defense mechanisms [113].
\nApart from these mentioned cells, there are crucial molecular mediators in the pathogenesis of asthma and COPD. The first family of mediators is transforming growth factor (TGF) family. The TGF-β subfamily is composed of five parts that exhibits plenty of effects pertaining to asthma and COPD. A recent study shows that overexpression of TGF-β1 in mice causes Smad3-dependent pulmonary expression of procollagen, antiproteases and fibrosis [114]. TGF-β exhibits chemotactic signatures for monocytes, macrophages and mast cells. Research shows an abnormal pulmonary expression of TGF-β1 in subjects suffering from COPD. Protein and mRNA expression of TGF- β1 are abundant in the lung tissue, including airway epithelial cells, of mild to moderate COPD patients. TGF-β1 has the role in pathogenesis of COPD because of its increased expression in parallel to the number of macrophages [115].
\nAnother mediator family is the fibroblast growth factor (FGF) family with 23 members in humans. Their functional receptors are named from FGFR1 to FGFR5 [116]. FGFs have many functions such as development, tissue homeostasis, and repair. In addition to further growth factors, FGF-1, FGF-2, and FGF-7 and their receptors FGFR1 and FGFR2, are located abundantly in the lungs [101]. Research shows that increased expression degrees of FGF-1, FGF-2, and FGFR1 were detected in vascular and epithelial areas in the lungs of COPD patients. FGF-1 causes higher collagenase expression and lower collagen I expression in lung fibroblasts which prompt tissue remodeling.
\nAnother family of mediators is the vascular endothelial growth factor (VEGF) family. There are seven units in this family capable of attaching to related cellular receptors. VEGFs have many functions including paracrine acting, angiogenic factors, prompting mitogenesis, emigration, and permeabilization of the vascular endothelium [101]. VEGF and its receptors assist in tissue remodeling as well as disease intensity in incessant lung diseases such as asthma [117]. COPD patients have increased pulmonary VEGF expression in bronchial and alveolar epithelial located around the vascular smooth muscle and alveolar macrophages. Additionally, unlike healthy subjects, COPD patients exhibit elevated levels of VEGFR-1 and VEGFR-2 expression inside the endothelium [118]. Furthermore, VEGFR-2 and VEGF expressions are decreased in COPD patients. Compared to VEGFR-2, VEGFR-1 has a higher affinity for VEGF which leads to VEGFR-1 scavenging VEGF from VEGFR-2. This phenomenon culminates VEGFR-1 activation and in the case of endothelial apoptosis, increased MMP activity as well as vascular and alveolar decimation [101]. This suggests the importance of harmony among VEGF, VEGFR-1, and VEGFR-2 during the pathogenesis of COPD subordinary types.
\nFinally, cytokines and chemokines are mediators supplying a chemotactic gradient which has the potential to activate macrophages, CD8+ T cells and neutrophils for COPD patients. It is known that inflammatory cells of both native and gained immune systems are significant in the COPD pathophysiology. This is where cytokines and chemokines are the key drivers [103, 119]. Different types of cytokines arrange chronic inflammation in asthma and COPD. T2 cytokines which are IL-4, IL-5, IL-9 and IL-13 interfere with allergic inflammation. Other types of cytokines including TNF-α and IL-1β accelerate the inflammatory response [120]. In asthma and COPD patients, chemokines are instrumental in drawing inflammatory cells from the circulation into the lungs [121].
\nObesity is a serious health problem that has become epidemic all over the world, especially in developed countries. It is characterized by hypertrophied adipocytes that secrete various adipokines and hormones, chronic inflammation in all tissues, and systemic insulin resistance resulting in type 2 diabetes, hypertension, and hyperlipidemia. In addition to these metabolic diseases, it can cause diseases such as cancer, atherosclerosis, obstructive sleep apnea syndrome, steatohepatitis, and musculoskeletal problems [122]. The obesity rate is 20% in women and 18% in men in developed countries [123]. It affects complex metabolic pathways in all tissues as a result of chronic and progressive inflammation, leads to insulin resistance, endothelial dysfunction and lipotoxicity.
\nThe pathophysiology of obesity includes complex interactions of numerous adipokines, hormones and pro-inflammatory cytokines with the central nervous system and metabolic organs (such as liver, pancreas, and muscle) as a result of genetic-environmental interactions.
\nGenetic etiology: Obesity is generally present in a polygenic etiology. Many studies have investigated the genetic background of body mass index (BMI) and waist/hip ratio (WHR), which are the best measurements of obesity. The results of these studies have been presented collectively in genome-wide association studies (GWAS) [124]. Although, single gene defects (monogenic) are rare in obesity, including especially melanocortin-4 receptor, leptin and leptin receptor genes [125].
\nDysregulation in hypothalamic control: The center of food intake and energy regulation in the central nervous system is the arcuate nucleus (ARC) in the hypothalamus besides the autonomic nervous system and brain stem. The balance between the opposing effects of orexigenic and anorexigenic neurons is important. Agouti-related protein (AgRP) and neuropeptide Y (NPY) (AgRP/NPY) neurons are orexigenic that promotes appetite and eating. Pro-opiomelanocortin–producing (POMC) peptide and cocaine-and-amphetamine–regulated transcript (CART), collectively known as POMC/CART neurons are anorexigenic that suppress appetite and eating. Oxygenic pathways that increase energy balance become more effective in obesity [126].
\nAdipose tissue dysfunction and systemic inflammation; The most important pathophysiological mechanisms of obesity and obesity-related insulin resistance are adipocyte dysfunction (visceral adipose tissue; VAT) and low-grade chronic systemic inflammation. In particular, white adipocyte tissue in obese subjects contributes to the regulation of food intake, energy metabolism and other functions by secreting adipokines from adipose tissue, which provide the necessary signals to the central nervous system, hypothalamus, liver, pancreas, muscle tissue, and other systems to regulate appetite, food intake, and energy balance [125]. Leptin is the most important adipokine that stimulates anorexigenic POMC/CART neurons and induces production of pro-inflammatory cytokines (TNF-alpha and IL-6) by macrophages and monocytes. In the case of hyperleptinemia, leptin resistance develops by the inhibition of the JAK2/STAT3 signaling pathway, which later increases oxidative stress and inflammation, causing insulin resistance, hyperlipidemia and hypertension [127]. Resistin is a pro-inflammatory adipokine produced by the resistin gene (RETN), which activates SOCS3, causing the insulin signaling pathway to be inhibited and consequently induces insulin resistance [128]. Other adipokines like Retinol binding protein 4 (RBP4), Angiopoietin-like protein 2 (ANGPTL2), Visfantin, Adiponectin, Lipocalin 2, Serum Amyloid A, Angiotensinogen, Renin, Angiotensin-Converting Enzyme, Acylation-Stimulating Protein, and Vaspin, are increased, and adiponectin, and Apelin are decreased in obesity, altogether stimulating inflammation, lipolysis, releasing free fatty acid (FFA) and causing insulin resistance as a result [129].
\nGastrointestinal hormones and microbiota: Gastrointestinal hormones and gut microbiota play a significant role in the complex pathophysiology of obesity. Ghrelin produced in the stomach induces starvation and food intake by stimulating orexigenic AgPR/NPY neurons in the hypothalamus. Although the effect of ghrelin cannot be fully explained, it is thought to increase in obesity, stimulate growth hormone release (GH), increase gastrointestinal motility and insulin secretion [130]. Decreased GLP-1, Peptide YY, pancreatic polypeptide, and increased amylin and cholecystokinin cause appetite inhibition and gastric emptying delay, resulting in excess energy [129]. Besides hormones in the gastrointestinal tract, changes in microbiota-gut-brain axis and their effects on metabolic organs are also important. Occurring as a result of nutrition and gene–environment interactions; chronic systemic inflammation resulting from intestinal microbiota dysbiosis (increase in Firmicutes-Bacteroides ratio), microbial fermentation products, increase in short-chain fatty acid formation and intestinal permeability, decrease in butyrate-producing bacteria rate, leads to an increase in proinflammatory response in metabolic organs, impaired fat metabolism and glucose metabolism [131, 132].
\nİmpaired insulin sensitivity and oxidative stress; The beginning of insulin resistance is the first step in the pathophysiology of T2D. Anabolic effects such as glycogen and protein synthesis, glucose transport, adipogenesis are formed by phosphatidylinositol-3-kinase (PI3K)/Akt pathway activation as a result of insulin binding to its receptor (INSR) synthesized in the pancreas [133]. On the other hand, insulin shows mitogenic effects with mitogen-activated protein kinases/Ras pathway (MAPK/Ras).
\nAdipokines, FFA’s, pro-inflammatory cytokines (TNF-a, IL-18, IL-1β, IL-6), synthesized as a result of inflammation in adipose tissue in obesity, also cause systemic inflammation in metabolic tissues such as liver and muscle. As a result, decreased GLUT-4 expression, activation of Ser/Thr kinases with insulin receptor substrate (IRS) phosphorylation, production of ceramides and proinflammatory cytokines, suppressing of cytokine signaling-3 (SOCS-3) expression, insulin pathways and effects. On the other hand, increased production of reactive oxygen radicals and production of toxic doses NO with inducible nitric oxide synthase (iNOS) activation, affect mitochondrial and endoplasmic reticulum functions. Activation of pro-inflammatory pathways increased oxidative stress, mitochondrial dysfunction, ER stress affects lipid metabolism, insulin mechanisms of action and other metabolic pathways, causing insulin resistance, Type 2 diabetes, hypertension, and hyperlipidemia [134].
\nBeta-cell dysfunction: In addition to peripheral insulin resistance in obesity, serious reductions in beta cell function are also observed. An increase in fat accumulation in islet cells due to chronic lipotoxicity disrupts the function of beta cells by blocking calcium channels. Chronic hyperglycemia due to disruption in glucose metabolism and systemic inflammation due to an increase in oxidative damage and lipotoxicity, disrupt insulin secretion pathways and cause changes in apoptosis gene expression. Hyperinsulinemia in obesity, impaired insulin signaling pathway, oxidative stress, lipotoxicity in islet cells, loss of beta-cell function and apoptosis may lead to the formation of type 2 diabetes [122, 135].
\nObesity has become a pandemic all over the world as a result of rapidly changing lifestyles and genetic heritage in the last century. Despite the findings in recent studies on the development and complications of obesity, it is difficult to say that the subject of etiology and pathophysiology is still not fully understood. Especially omics technologies, big data on environmental gene interactions, neuroendocrinology, and neuropsychological studies will reveal findings that open up different horizons. However, due to its complications from deadly metabolic diseases to cancer, rapid preventive measures should be taken, and effective treatment models should be developed.
\nAcute lymphoblastic leukemia (ALL) is a heterogeneous malignancy emerging from lymphoid precursors. It is characterized by the proliferation of immature lymphoid cells with somatic mutations including chromosomal rearrangements, and aneuploidy [136]. ALL has two peak points; first point occurs at ~5 years of age (80%), and the second point occurs at the age of ~50 (20%) [137]. The basic mechanism underlying the development of ALL is similar in children and adults, while they have the frequency of different genetic subtypes. Molecular analysis of genetic changes in leukemia disease provides a great advantage in order to understand prognosis and pathogenesis of ALL [138].
\nThe diagnosis of ALL depends on the presence of at least 20% lymphoblast in bone marrow. Immunophenotyping by flow cytometry (FCM) identifies the subtype of ALL that may be B-cell precursor (BCP), mature B-cell types, or T-cell ALL. Chromosomal abnormalities are a characteristic of lymphoblastic leukemia, which are found in B or T cell lineage. The most common abnormality found in adult B precursor ALL is the t(9;22) BCR-ABL translocation, while the t(12;21)(p13;q22) TEL-AML1 translocation is most commonly found in childhood B precursor ALL [139]. On the other hand, the discovery of mutations in the receptor tyrosine kinase FLT3 contributes to the understanding of leukemogenesis mechanism in hyperdiploid ALL (20% of cases). Based on this finding, targeting specific tyrosine kinase inhibition may be useful in the management of leukemia [140].
\nSmall-molecule kinase inhibitors have a clear benefit in the treatment of many cancer types including leukemia. Imatinib mesylate, a small-molecule inhibitor of BCR-ABL kinase, is highly effective in the treatment of chronic myelogenous leukemia (CML) [141]. Although the single kinase inhibitor is a remarkable treatment option in a different type of leukemia, it will need to be combined with either other targeted therapy or chemotherapy because of the resistance to small-molecule inhibitor [142]. Unlike ALL, Chronic Lymphocytic Leukemia (CLL) is defined the accumulation of monoclonal B cell with a special immunophenotype in the bone marrow, blood, and other lymphoid organs where B lymphocytes express CD19, CD23, CD5, low-level CD20 and surface immunoglobulins [143]. The standard treatment procedure of ALL and CLL includes consolidation therapy following chemotherapy in pediatric patients. For adult patients, unlike pediatric patients, the allogeneic hematopoietic stem cell transplantation is frequently preferred as consolidation therapy [144]. Because the patients resistant to chemotherapy are not respond to treatment well enough, novel therapy approaches such as Chimeric antigen receptor-modified T cell (CAR-T) therapy have developed in order to overcome chemotherapy resistance and improving the outcome of patients [145]. CAR-T cells, as immunotherapeutic tools, are genetically engineered to express a chimeric antigen receptor recognizing an antigen that is located in the special cells such as a tumor [146]. CD19 antigen on B lymphocytes was considered the initial target for CAR-T cell therapy. However, specific antigen loss might cause the failure of CAR-T cell therapy in CLL. CD19–20 co-targeting CAR-T cells were designed to kill both CD19-positive and CD19-negative CLL and it was shown that these cells were very effective in killing CLL cells. In one of the first reported in pediatric ALL the clinical trials, CAR-T cells targeted the CD19 antigen of B cells are designed with CD3ζ and CD28 costimulatory domain [147].
\nThe origin of a pathogen has a crucial role in developing vaccines and blocking transmission. This may last many years due to its elusiveness as seen in HIV-1, SARS, and MERS [148, 149, 150]. According to a recent report, it was emphasized that SARS-CoV-2 is able to infect T cells, which are targeted by HIV [151]. Another report alleged that the motif insertions of spike glycoprotein, similar to HIV-1, may help increase the range of host cells of SARS-CoV-2. HIV-1 envelope glycoprotein contains mutable insertions and deletions not necessary for biological function. Only 1 and 2 insertions are matched in only a few HIV-1 strains and this reveals that four insertions are scarce. Thus, HIV-1 cannot be assumed as the source for those insertion sequences in the SARS-CoV-2 genome due to their inefficient identities and scarceness in the HIV-1 sequences [152].
\nThe reported cases showed that there have been 3,162,284 COVID-19 cases in at least 212 countries and approximately 7.1% of which was resulted in death as of April 30, 2020 [153]. It is known that SARS-CoV, MERS-CoV, and SARS-CoV-2 are the members of coronoviridae family of the Nidovirales order, which comprises a relatively positive-sense, single-stranded RNA genome of around 26–32 kb [154]. 5o-methylguanosine cap at the beginning, a 3o-poly-A tail at the end, and a total of 6–10 genes in between exist in their genome [155, 156].
\nThis family has extremely expressive instability and recombination rate, which is similar to RNA viruses, so it is practically unfeasible to prevent their distribution among humans and animals worldwide; nevertheless, the fact that the virus is exceedingly pathogenic to humans is closely related to random genetic recombination in the host. Although there is a strict genetical relation between SARS-CoV-2 and SARS-CoV, it is explicit that SARS-CoV-2 has a unique feature providing rapidly spread worldwide [157].
\nSARS-CoV-2 genome sequence is much more resembles a SARS-like bat rather than SARS-CoV [158, 159]. Two open reading frames translating the replication- and transcription-related gene into two large non-structural polyproteins [156]. Ribosomal frameshifting contributes to translate two different but overlapping open reading frames. Besides these nonstructural proteins, the subgenomic RNA also encodes the viral genome packaging protein N (nucleocapsid), and the viral coating proteins M (membrane), E (envelope), and S (spike) as the structural proteins. Viral coating proteins, which interact with host surface receptors, is generally preferred as the therapeutic target blocking protein–protein interaction [160, 161]. TMPRSS2, the human serine protease, enables S Protein of both SARS-CoV and SARS-CoV-2 to prime, and these two viruses use the angiotensin-converting enzyme 2 (ACE2) receptor in order to bind the host cell as the first step of the viral entry mechanism. Unlike SARS-CoV and SARS-CoV-2, the cell entry of MERS-CoV depends on the binding of its own spike protein to DPP4 (dipeptidyl peptidase 4). The RT-PCR analysis of the throat swabs is essential to the diagnosis of COVID19 pneumonia, and it takes 3.5 h to provide the results [162].
\nClinical management puts emphasis on the importance of supportive care and prevention of complications due to a lack of specific treatment for COVID-19 pneumonia. On the other hand, potential antiviral therapies for the purpose of rapidly dealing with this pandemic are taking place on several clinical trials. These trials focused on three main targets that include enhancing the host immune system, blocking the virus spike protein-host cell surface receptor interaction, and vaccine development [163].
\nHPV genome, which is a double-stranded circular DNA, has the early (E) genes that are responsible for replication and transcription, and the late (L) genes that are responsible for viral capsid proteins. In the early stage of HPV infection, the highly expressed E1 and E2 proteins provide the maintaining of viral replication and transcription within the cervical cell [164].
\nHPVs, unlike SARS coronaviruses, are non-enveloped viruses and don’t have a specific host cell receptor that initiates the viral infection. Additionally, HPVs have many different genotypes such as HPV type 16 and type 18 which are known as the reason for cervical cancer. HPV infection may cause low-grade cytological changes on Papanicolaou smears, or low-grade squamous intraepithelial lesions [165]. When malignant conversion considered, viral oncoproteins E6 and E7 attach, respectively, tumor suppressor protein p53 and Rb have a crucial role [166]. Until today, many vaccine developments studies have been carried out to protect HPV malignant type 16 and 18. For example, the clinical vaccine Gardasil 9 provides effective protection against vaginal, cervical, and vulvar diseases caused by HPV type 16,18 and also its 5 other different types [167].
\nThe chapter outlined the unique mechanism of each disease. Depending of the origin of the disease; deficiency, hereditary, infectious and physiological diseases may be treated diversely but the perturbation effect can only be eliminated with proper intervention. Current amelioration may be improved by biochemical methods only if the molecular mechanism is clearly understood. Therefore, molecular medicine provides unique solutions to diagnose and treat disease by elucidating macromolecular interaction and abnormalities in cells and tissues. The chapter summarizes current findings and methods to alleviate and cure the diseases.
\nBYK, EK, KUC and ENYT acknowledge YOK100/2000 bursary and thanks to Turkish Council of Higher Education (YOK).
\nNone.
Thanks to Assistant Prof. Dr. Lütfi Tutar for carefully reading the manuscript.
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\\n\\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\\n\\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\\n\\nAnd for any purpose, provided the following conditions are met:
\\n\\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
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LICENSE | \\n\\t\\t\\tUSED FROM - | \\n\\t\\t\\tUP TO - | \\n\\t\\t
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The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\\n\\nContent reuse:
\\n\\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
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\\n\\nReposting & sharing:
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\\n\\nRepublishing – More about Attribution Policy can be found here.
\\n\\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\\n\\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\\n\\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\\n\\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\\n\\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\\n\\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\\n\\nUnder the following terms:
\\n\\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\\n\\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\\n\\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\\n\\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
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\\n\\nReposting & sharing:
\\n\\nOriginally published in {full citation}. Available from: {DOI}
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\\n\\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\\n\\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\\n\\nShare — copy and redistribute the material in any medium or format
\\n\\nUnder the following terms:
\\n\\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\\n\\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\\n\\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\\n\\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\\n\\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\\n\\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\\n\\nPolicy last updated: 2016-06-08
\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
\n\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\n\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
\n\nAgreement samples are listed here for the convenience of prospective Authors:
\n\n\n\nDEFINITIONS
\n\nThe following definitions apply in this Copyright Policy:
\n\nAuthor - in order to be identified as an Author, three criteria must be met: (i) Substantial contribution to the conception or design of the Work, or the acquisition, analysis, or interpretation of data for the Work; (ii) Participation in drafting or revising the Work; (iii) Approval of the final version of the Work to be published.
\n\nWork - a Chapter, including Conference Papers, and any and all text, graphics, images and/or other materials forming part of or accompanying the Chapter/Conference Paper.
\n\nMonograph/Compacts - a full manuscript usually written by a single Author, including any and all text, graphics, images and/or other materials.
\n\nCompilation - a collection of Works distributed in a Book that IntechOpen has selected, and for which the coordination of the preparation, arrangement and publication has been the responsibility of IntechOpen. Any Work included is accepted in its entirety in unmodified form and is published with one or more other contributions, each constituting a separate and independent Work, but which together are assembled into a collective whole.
\n\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\n\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
\n\nVideo Lecture – an audiovisual recording of a lecture or a speech given by a Lecturer, recorded, edited, owned and published by IntechOpen.
\n\nTERMS
\n\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\n\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\n\nAnd for any purpose, provided the following conditions are met:
\n\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
\n\n\n\n
LICENSE | \n\t\t\tUSED FROM - | \n\t\t\tUP TO - | \n\t\t
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The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\n\nContent reuse:
\n\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\n\nContent adaptation & reuse:
\n\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\n\nReposting & sharing:
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\n\nRepublishing – More about Attribution Policy can be found here.
\n\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\n\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\n\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\n\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\n\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\n\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\n\nUnder the following terms:
\n\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\n\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\n\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\n\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
\n\nContent reuse:
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\n\nReposting & sharing:
\n\nOriginally published in {full citation}. Available from: {DOI}
\n\nAll Book cover design elements, as well as Video image graphics are subject to copyright by IntechOpen.
\n\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\n\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\n\nShare — copy and redistribute the material in any medium or format
\n\nUnder the following terms:
\n\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\n\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\n\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\n\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\n\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\n\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\n\nPolicy last updated: 2016-06-08
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