2012 global estimates of major land deals carried out by governments and private companies.
\\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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The commercialization of public land in the Global South, which refers to the medium and low human development based on the United Nations development program report 2005 [1], has increased dramatically in recent years due to the wide spread leasing and sale of land to foreign companies and governments. The main goal of these investors is to secure food and energy production for their populations as multiple factors threaten their food security at home. On the one hand, the current population will increase worldwide from nearly 7 billion to over 9 billion by 2050 [2], a growth that would require the increase of food production from nearly 6 billion tons (gross) to 9 billion tons by 2050 [3]. Furthermore, competition for land, water, and energy will only intensify along with the need to reduce the many negative impacts of agriculture to the environment [4, 5]. Global food security has been further strained, notably during 2007-08 [6], by the growing volatility of the food market and the political controversy surrounding the use of grain to produce biofuels [7, 8]. Any one of these factors will likely pose significant challenges, but the sum of all of them could constitute a major threat to land ownership.
Overall, these factors have driven a change in perspectives of land ownership. Recent trends indicate that the need to provide food and energy security at home has led international corporations, sovereign wealth funds, foreign governments, private equity firms and domestic actors to buy or lease large tracts of land outside their national borders [9]. These land deals or “land grabbing”, as labeled by many Non-Governmental Organizations and the media, are certainly to be considered a prominent factor in the list of significant drivers of land change in certain parts of the globe, especially in southern hemisphere continents. The need to secure food supply comes as a result of the many international pressures that took place in the mid-2000s; and initiated the rise of food prices by 2006. Among these pressures some that stand out are [10]:
Extreme weather events, such as droughts and floods that affected cereal exports in 2005-06 and decreased cereal production worldwide by 10 percent.
World cereal reserves fell as major cereal producers such as the USA, EU and China reduced holdings of food stocks.
Fertilizer prices and transportation costs increased due to the oil price hike from 2003 to 2008.
The increased demand for the production of biofuels conflicted with food crops as land was diverted for the production of monocultures such as sugar, oilseeds, palm oil and maize.
These, along with other international and local pressures caused concern in the international market leading to an increase in market volatility as speculations of food supply where unfavorable [10]. In response to these price hikes many food-importing countries found a long term strategy to outsource their food production and guarantee their food supply at low costs in the leasing and purchasing of foreign land [11]. For example, China holds approximately 20 percent of the world’s population but possesses no more than seven percent of the world’s arable land [12]. For many years this Asian country has been a net exporter of agricultural goods. In recent years due to its rapid economic growth, higher population income, changes in diets, and limited arable land, among other factors, China has become a net importer of agricultural goods since the beginning of the 2000s. In order to ensure its food security and promote its current economic growth the Chinese government and private corporations are investing in land suitable for agriculture outside its national borders. In the same way some wealthy import-dependent countries, such as Japan and South Korea being directly affected by the 2007-08 food crises, have initiated policies along this line. On the other hand, arid, oil-rich countries from the Gulf States under “harsh climatic conditions, poor soils and scarce land and water” among other limitations [11], such as Saudi Arabia, do so in an attempt to reduce its domestic water use [13]. In recent years the scale of this type of business has increased dramatically with millions of hectares being bought or leased outside their borders. [11]
Due to the increasing global demand for food-stuffs production and alternative energy development, the southern hemisphere is portrayed as an idoneous reservoir of arable land capable of satisfying the international needs, a particular example constitute African countries due to their relatively low population density [9] and cheap land. As mentioned in De Shutter (2009) southern countries in Africa and Latin America are the main targets for investors seeking farmland as it is scarce in Asia [14]. This race to buy land has been described by many as a new neo-colonial approach by wealthy countries to take over the key natural resources of poor countries [15]. Some analysts perceive these land deals as a threat to the livelihood of local communities while others stress the positive effects derived from the income generated in these deals [9]. Such benefits could be perceived as the injection of the much-needed capital to sustain agriculture [16] and therefore the creation of on-farm and off-farm jobs, the development of rural infrastructure such as irrigation canals, and the construction of schools and health clinics that will improve local livelihoods. Along this line of thought, many of the host countries of land deals have encouraged this type of investment and are keen to develop it as a potentially lucrative activity [6].
Global land grabs have recently become a major point of international discussion [17] due to the global struggle to ensure food security [18]. “Land grabbing, generally referred to the mass purchase of agricultural lands by transnational companies or foreign countries” [19], refers to the lease (often for 30–99 years) or purchase of vast areas of land outside their national borders [20] mainly for agricultural production. One of the main drivers of this practice is the current international demand for cheap food after the food price hikes of 2007-08 [13]. During these years the dramatic increase in basic food prices reduced the access to food of millions of people as they reached the highest levels in 30 years [21]. According to global estimates this price hike brought around 915 million people to undernourished levels worldwide, and additional hundreds of millions were added to the count due to the effects of the global financial and economic crisis [10]. Although the highest levels of food insecurity where reached in developing nations many food-importing countries felt the effects of food prices in their own population.
According to Brown (2011), wealthy but food-insecure countries worried about tightening markets [20] are seeking to ensure their food production by leasing and buying land overseas (e.g. the Gulf States). By controlling farm land beyond their national borders these countries are gaining control of the international supply-chain of food-stuffs [22]. This practice is perceived as an innovative, long-term strategy to ensure the food security of its population at cheap prices [20]. The majority of the investors are Asian countries such as China and India, which according to the Food and Agriculture Organization\'s (FAO) 2009 report, are currently food self-sufficient. Likewise import dependant countries, particularly affected by the food crisis, such as Saudi Arabia, Japan and South Korea, are also in the search for fertile farmland in African countries like Uganda, Madagascar, Mali, Somalia, Sudan and Mozambique, as well as in other developing countries such as the Philippines, Indonesia, Laos, Thailand, Vietnam, Cambodia, Pakistan, Burma, Brazil, Argentina, Kazakhstan, Ukraine, etc. [16, 20, 23]. (Table1. Shows the most recent estimates of land deals worldwide linked to the countries that are the major sources of land grabbers).
The governments of ‘host’ countries, such as Madagascar, Sudan and Cambodia, generally welcome foreign investment [24], even though much of their own population lacks sufficient food [17]. Large-scale land acquisition for food security by richer countries is increasingly contested, since it is not considered ethical to export food from countries in which there is widespread hunger. For example, Daewoo Logistics, the South Korean commercial group, failed its attempts to acquire 1.3 million hectares (over half the arable land of the country) of land in Madagascar for the production of maize for human consumption food and palm oil used in biofuels [16]. By doing this the company would have ensured future fuel stocks and guaranteed the countries’ food security “by providing half of its maize imports from Madagascar alone” [25]. Ultimately the deal ran into trouble and was a direct factor in the overthrow of the country’s government in 2009 [16].
Countries involved in land grabbing | Land purchased or leased (including deals still in process in ha) | Number of deals |
UK | 4,941,765 | 40 |
US | 4,162,394 | 42 |
UAE | 3,182,950 | 19 |
India | 2,101,400 | 28 |
China | 1,953,527 | 36 |
South Korea | 1,412,394 | 16 |
Saudi Arabia | 1,132,945 | 20 |
Germany | 525,345 | 22 |
2012 global estimates of major land deals carried out by governments and private companies.
In developing countries, land deals result most of the time in the displacement, dispossession and disenfranchisement of local communities. Most of the land utilized by small farmers in local communities is used under customary tenure arrangements; as a consequence, they often lack formal property titles over the land and can easily risk losing access to it [9]. In addition, most of the deals between foreign investors and local governments are arranged outside the public scope and therefore, smallholders may not even know they are losing their land. Women, who make up 70 percent of farmers in the developing world, are often the most vulnerable to this practice as they may not be able to protect their own land tenure claims in court due to local laws.
The general perception under the land deals scope is that most of the land available for buyers is abundant and underutilized; although in many cases it is already being used [6]. Existing land use it usually overlooked due to the lack of formal land rights of smallholders or their access to proper legal assistance [16]. For example, in Gambela, Ethiopia, the Ethiopian government has signed deals with investors from India, Saudi Arabia, China and other countries since 2008 for large-scale agricultural projects in the region (see Table 1). The deals give foreign investors control of half of Gambela\'s arable land [26]. All land allocations recorded are classified as involving ‘wastelands’ with no pre-existing users. As the Anywaa Survival Organization was able to verify, these are ancestral lands from which indigenous communities such as the Anuak have been dislocated. Without any information or consent for the sale and purchase of such territories, the surrounding communities have lost from these forests their refuge in times of violence, an excellent source of medicinal plants, and a valuable reserve of food during famines [26].
Land grabber | Base | Sector | Hectares | Production | Projected Investment | Status of the deal |
Hunan Dafengyuan | China | Agribusiness | 25,000 | Sugar Cane | ------------- | Completed |
ARS Agrofoods | India | Agribusiness | 3,000 | Cotton, groundnut, sesame, soybean | US $5 million | In process |
BHO Agro | India | Agribusiness | 27,000 | Cereal, oil seeds, pulses | US $8/ha/yr (lease) | Completed |
Karuturi | India | Agribusiness | 311,000 | Maize, palm oil, rice, sugar | US $1.2/ha/yr (after first 7 years) | Completed |
Ruchi Group | India | Agribusiness | 50,000 | Soybeans | US $4 million (lease cost for 25,000 ha) | Completed |
Al Amoudi | Saudi Arabia | Finance | 140,000 | Livestock, maize, oilseeds, rice sugar cane, teff | US $2,500 million | Completed |
Examples of land deals initiated in Gambela since 2008.
These large-scale land deals increase local food insecurity as the export of locally produced agricultural products force farmers to purchase agricultural goods elsewhere as opposed to benefiting from the harvest of their own lands [27]. The country of Ethiopia claimed as the epicenter of current land deals [29], shows the direct relationship between food insecurity and land grabs. Since 1984, Ethiopia has been well known for its extreme food shortages [22]. In 2010 ten percent of its population relied on food aid [27], and in 2011, due to the dearth of rain in the Somali and Oromiya regions, the nation appealed for emergency food aid at the United Nations. Betting on economic growth projections, the Ethiopian government promised that the country would be food self-sufficient within five years. Although the economic speculation is promising it comes at the expense of the displacing and dispossession of the population as the government is closing deals with private investors over the citizen’s lands [22]. The detrimental effects of these land deals were evident during the 2008 famine in which food instability levels increased among the population while food was being exported [30]. The USAID, which has been one of Ethiopia’s largest aid donors, is strong critic to this practice, and argues that the right way to ensure the country’s food security is by guaranteeing the complete ownership of land by its citizens and to stimulate the local consumption [31]. Nevertheless, the irony of these land deals continued as a $116-million food aid package is planned to reach the African nation for a five-year period, while, contradictorily in 2009 there was a simultaneous $100-million Saudi investment to grow and export rice, wheat and barley back to itself [22].
The recent global awareness of anthropogenic climate change and the resulting growing interest in green energy, including biofuels, have been another important motivation for land investments. Currently biofuel production is the dominant reason for land deals in countries such as Madagascar and Ethiopia, where jatropha, palm oil and sugar are major crops. According to the Global Land Report 2010 (GLP) biofuels production is an important driver for the international land investments in Africa [9]. These deals are driven in part by the international demand for renewable fuels and the shifts in energy policy among Southern African countries to fulfill their energy needs with their own natural resources [32]. This growing interest on green energy is leading investors to invest in productive land overseas which results in the opening of new land for agriculture [9]. Many see this as a strategy by the private sector to take advantage of the emerging market of green energy. For instance, countries like China wish to diversify its domestic energy sector [9] due to the increasing demand of oil and its high global prices. Hence, the growing production of biofuels has started to affect the current food production as land deals keep taking place in the international scope.
On the other hand, many Southern African countries have actively embraced the biofuels productions in their lands, as they wish to limit their dependence on future oil imports and exposure to price volatility [32] by becoming oil producers. Mozambique is a perfect example. With the goal of becoming an ‘oil exporting country’ on 2004 the Mozambique government urged farmers to plant jatropha - a Latin American shrub which seeds produce an oil that upon extraction can be refined to produce biodiesel - on all marginal and unused lands [33]. Although there is evidence that this crop will perform poorly under harsh agro-ecological conditions, the building of cultivation and processing facilities for the production of biodiesel derived from this plant have been initiated.
When seeking arable land overseas foreign investor’s main targets are lands with access to irrigation for better potential production of food or biofuels [13]. According to the International Institute for Sustainable Development, the ultimate goal of the purchase or long-term lease of land in foreign countries is the acquisition of the water rights [34]. This practice allows major investor countries facing water scarcity to shift their domestic irrigation water to municipal water supplies [13]. We find China, India, Saudi Arabia, Kuwait, Qatar, and Bahrain among this type of investors group. African and Asian countries rich in land and water resources are the primary targets for their land investments [6]. For example, Central Africa only uses irrigation resources in two percent of its land, making an investment in this untapped water resource a very appealing proposition [35]. However, as abundant as water may seem, predictions from the Intergovernmental Panel on Climate Change (IPCC) suggest that fresh water supplies are likely to be depleted in some parts of Africa. As a result of climate change, lands will become drier, with less rainfall, affecting crop yields and making livestock farming impossible. In this possible scenario the water required to slake the investors’ fields could be considerable [13]. Along this line, biofuels have been described as “one of the thirstiest products on the planet”. For example, to produce one liter of biodiesel from soya (soybeans) requires 9,100 liters of water. As for the production of bioethanol from corn or sugar cane there is a requirement of as much as 4,000 liters of water for one liter of bioethanol. Still, even those biofuels considered to be optimal for arid places require large amounts of water in order to grow [24].
Climate change as defined by the IPCC refers to "... a statistically significant variation in either the mean state of the climate or in its variability... Climate change may be due to natural internal processes or external forcing to persistent anthropogenic changes in the composition of the atmosphere or in land use.” The atmospheric changes associated with this phenomenon can be observed at all spatial levels from local to regional to global. It affects average global surface temperatures and sea levels, soil moisture and local precipitation, among other variables [36]. Currently, human society practices are negatively influencing these variables and thus, exacerbating this atmospheric phenomenon. Practices such as fuel burning and deforestation for agricultural purposes can have great influence in the world’s climates.
As referenced in Cotula et. al (2009), 80% of the global farmland is located in Africa and South America [37]. Most of these areas are either tropical rainforests, protected natural regions or are already used for shifting cultivation or grazing of animals [38]. However, they represent the most suitable regions for land deal investments. But the conversion of tropical forests to crop land, (mostly monocrops) come as an inevitable threat to the region’s biodiversity, carbon stocks and water resources [6]. Tropical forests do not only serve as reservoirs, sinks, and sources of carbon in the world, but also provide several ecosystem services that have impacts on a region’s climate. Among these services are the maintenance of elevated soil moisture and surface air humidity, reduction of sunlight penetration, weaker near-surface winds and the inhibition of anaerobic soil conditions [39]. This environmental arrangement is responsible for the rich biodiversity of tropical ecosystems [40]. However, as tropical landscapes are converted to agricultural and pasture areas, the productivity of this soil decreases as less rainfall, associated with changes in the solar radiation partitioning, is observed [39].
Many studies have demonstrated that changes in land surfaces (such as land clearing for agriculture) can influence both local and regional climates and can even have major impacts on climates in distant parts of the Earth [36]. For example, the Amazon Basin landscape is well known for having a direct influence in the flux and exchange of moisture into the atmosphere, regional convection, and hence regional rainfall. However, recent works have determined that the changes in the forest cover of the region have consequences on climates of distant places. The Sahelian drought associated with the destruction of regional vegetation [36] serves as another example of the relationship between changes in land cover and distant climates. In this sense, land deals can be considered major drivers of ecological impacts at both local and global scales. Such impacts can affect the ecosystem services that sustain human livelihoods as conversion of tropical forests to pastures takes place globally.
Food security defined by the United Nation’s FAO is “a situation that exists when all people, at all times, have physical, social, and economic access to sufficient, safe, and nutritious food that meets their dietary needs and food preferences for an active healthy life” [40]. The definition encompasses four important dimensions of food supplies; -food availability, stability of food supplies, access to food, and utilization of food - all of which are closely linked with impacts of climate change. First, food availability refers to whether or not the agricultural productivity of a region can satisfy food demand in that region. Second, food stability is an indication of how consistently the supply meets that demand. Third, access to food literally means the ability of individuals to buy proper food resources for their dietary needs. Lastly, utilization of food references how well individuals can consume food resources without undue concern for quality and safety of food [41].
Climate change affects almost every aspect of human society and natural environment, especially production of agriculture and food in multiple ways. Since many agricultural regions in the world have already suffered from extended drought and abrupt flood induced by global climate change, weather and climate variability will possibly change conditions of land suitability and agricultural productions [41]. Although temperate regions and higher latitude zones may get benefits of agricultural productivity by increasing temperature due to climate change, negative effects such as heavy rainfall, drought, and increased evapotranspiration on other regions (e.g., rain forest, semi arid region, and Mediterranean region) may hinder food availability in general [42].
Many predictions indicate that global and regional weather fluctuations and extreme weather events are expected to increase in frequency and intensity [43]. Because of the weather fluctuations, crop yields and local food supplies will also fluctuate and thus food stability and security could be adversely affected [41]. For example, extreme weather events like typhoons, hailstorms, and droughts will bring failure of crop yields. Specifically, sub-Saharan Africa and parts of south Asia, where most of high climate variable and arable lands are located, will be exposed to the highest instability of crops and livestock production [44]. Although the FAO predicted that access to food will be getting better in the long term based on falling food prices and increasing income level [45], this prediction might not consider the effects of global climate change that can possibly deteriorate the progress of food accessibility. Thus, if the situations - food prices, amount of crop yields, and supplies - of world food markets change under certain weather events, the ability to access food would also be changed as the recent food crisis in 2007 and 2008 suggests. In addition, the IPCC recently reported that increasing temperature will increase incident of more food poisoning, specifically in temperate areas, and cause food and water-borne diseases [43]. This means that individuals will need to more cautiously select and consume their foods. Thus food utilization, the last key dimension of food security, will also be affected by climate change.
All the key dimensions of food security induced by climate change consequently affect land deals in terms of both “host” and “investor” countries. Many host countries already face food shortages and difficulty to access food within local areas where land deals take place. Since land has shifted to foreign buyers, local communities cannot utilize their immediately surrounding land to produce food [13]. Many foreign investor countries, however, may take advantages of all dimensions of food security such as food availability, stability, accessibility, and utilization. Host countries are willing to sell their land in order to take advantage of short-term economic growth opportunities, due to the large-scale nature of land acquisition by investors. [37]. This tends to increase and accelerate land grabs in developing countries overall. Therefore climate change causes food insecurity in a way that changes temperature and precipitation in the first place and then food insecurity brings us more land grab to mitigate food shortages. Those three elements - climate change, food security, and land grab - are interconnected and, unfortunately, are detriment to each other.
In the previous sections of the chapter, each two of three elements (i.e., food security and land grab, land grab and climate change, and climate change and food security) have been investigated through literature reviews in relation to climate change, food security, bio-fuels, and land grab. Explanations gained by reviewing relationships between each two elements, however, do not efficiently reveal the causal relationship among the elements and how closely coupled they are with each other. In this section, we attempt to describe the causal relationships among them in terms of a vicious circle framework.
Causal relationships among climate change, food security, and land grab make current situation worse in Global South, where people already have been suffering from food shortage and severe weather events, and increase vulnerability to climate change. Each of three elements adversely affects people in Global South in different ways that particularly threaten their livelihood, safety, and health. As discussed in the previous sections many other factors influence each of the three phenomena. For instance, land grab did not evolved due to food insecurity alone but growing global population, green energy demand, economic growth, and political reason [9]. Climate change and food security also have many reasons other than the factors in the Figure 1, however, since climate change, food security, and land grab in the circle are closely coupled, each of three elements will be treated as main driving forces in the vicious circle framework.
Figure 1 shows a vicious circle of climate change, food security, and land grab that is proposed by this chapter based on the review of relevant studies. As noted previously, climate change is likely to affect food security by increasing extreme weather events (e.g. extended drought, frequent and severe flood, cyclones, and hailstorms) which change land suitability for food production. In addition, demands to reduce carbon dioxide and other greenhouse gases, increased by human activities, lead the international society to seek alternative energy sources, biofuels and agrofuels thus esteemed as alternative energy sources that produce less CO2 and greenhouse gases. However, enormous amount of crops and crop fields are required to produce alternative green energy [24]. Since climate change is, again, a common driving force of increasing severe weather events and green energy demands, it degrades food security and increases demand of land grabs in general.
Vicious circle of climate change, food security, and land grab
Along with food security and biofuels, there are many other underlying driving forces that accelerate land grabs such as demographic, economic, technological, political, institutional, cultural, and sociopolitical factors [9]. For example, world population has been increasing about 34% for 2 decades by 2007 and will keep increasing until 2050 under the medium scenario projection of the United Nations [46]. This means that the average amount of land per person will keep decreasing and population disparity at the global scale will consequently increase cross-national land deals [9]. The global economy also acts on land deals when agriculture attracts as an investment opportunity. At the same time, land grab exacerbates local food insecurity; because most of the regions, where land deals take place, have already been experiencing famine for a long time, even if the regions themselves have plenty of fertile lands.
The influence of land grabs to climate change significantly increases with deforestation in tropical rainforests where protected natural areas are also located [38]. Deforestation itself, particularly in tropical rainforest, has an adverse effect on reducing carbon dioxide and greenhouse gases through the process of photosynthesis. For example, some studies show that large amount of trees cleared for palm oil crop field can actually hold up to 150 years of carbon savings, and biofuels, which are initially proposed to decrease carbon dioxide and greenhouse gases, also negatively affect climate change by increasing CO2 and greenhouse gases [24].
Analysis of causal relationship among climate change, food security, and land grab confirms existence of a vicious circle that exacerbates vulnerability of poor and small farmers to climate change, and the safety and health of the Global South. Therefore it is important that efforts should be dedicated to disconnect each element of vicious circle or, if it is possible, focused on changing vicious circle into virtuous circle, since climate change, food security, and land grab have already threatened people there.
Studies have shown that global land deals have increased dramatically in recent years, especially during the food crisis of 2007 and 2008. Some countries that need to guarantee food security and biofuels production as a strategy to cope with impacts of climate change and some other factors (i.e., demographic and economic factors) increased a scale of land deals in Global South. Consequently land deals have increased possibility of the climate change impacts by increasing deforestation. Deepening climate change once again can exacerbate food security and increases biofuels demands. This implies that the relationships between land grabs, climate change, and food security make vicious circle. However, it is not easy to approach for solutions from climate change perspective to ameliorate the vicious circle, while it is relatively easy to approach solutions from land grabs and food security perspective. That is because land grabs and food security are specific issues compared to the climate change discourse - one of the most complex issues of our day. This part of the chapter thus approaches to deal with land grabs and food security issues to dismantle the vicious circle.
As illustrated in Figure 1, climate change, food security, and land grabs are connected, and each element has harmful effects to the one next to it in a predominantly counter clockwise direction. This is why we named the framework as the vicious circle and it has causal relationship among elements. Although climate change, food security and land grabs are the main subjects of our conceptual model, they do not stand alone (see in the boxes of Figure 1). Some of them affect reverse direction (e.g. land grab causes local food insecurity). However, the three elements are core sources of making vicious circle to people in Global South. It is important to dismantle and neutralize this circle, as each element is primarily responsible for the damage done to the next. There are both short-term and long-term policies or strategies that may accomplish this. For example, long-term strategies should be suggested for climate change issues. However, this chapter will not touch any policies and strategies on mitigation, adaptation, and vulnerability directly to climate change, since nature of climate change cannot shortly be improved by any efforts due to the complexity of the climate change itself. Instead, policies for land grab and food security (include biofuels) can be discussed as short-term policies.
Loosely-coupled and disconnected by applying alternative policies over time
First, land grab can be reduced and controlled relatively in short time period, if countries targeted for land deals recognize the outcomes and tradeoffs of these deals (e.g. local food insecurity) and regulate it through alliance with countries in similar condition. In fact, some host countries are already considering alternative policies such as “strict limitations on foreign ownership of land; limitations on farm size/land ownership; limitations on the farm acreage dedicated to a single crop or livestock production (soy monoculture, for example); limitations on the total national acreage devoted to a single crop or livestock production, and; limitations on the strict controls on foreign investment in food and agriculture.” [17]. Second, there might be alternatives for food security that may lead to reduce land grabs. Governments depending on imported food could help domestic farmers to increase production by agronomic research. For instance, farmers in food importing countries switch crop varieties and/or develop new varieties better able to produce in terms of volume, and develop biotechnology as well. Third, as a direct competitor to food production and another driving force of the land deals the biofuel production should be alternated by technologically innovative new energy sources [47], since production of biofuels does not really help reduce greenhouse gases, but increases land grab and worsen climate change. Countries seeking green and new alternative energy sources invest in, hydrogen fuel, wind power, solar power, and tidal power, for instance.
Innovative approaches to increase food and energy security suggested above will likely reduce land grabs. Each of the efforts suggested above will keep reducing issues along the line of vicious circle. Even though only a few short-term policies were suggested here, there might be more solutions and efforts to remove many issues in the vicious circle of climate change, food security, and land grab over time. Therefore, the short-term policies connected with long-term policies to climate change may pragmatically trigger a transformation of the vicious circle into a more virtuous circle or at least weaken the connection between each two of the elements (Figure 2).
There are many studies on the relationship between climate change and food security, food security/biofuels and land grab, and land grab and climate change. However, isolating and addressing one pair of issues at a time masks what is really going on in terms of the vicious circle which keeps each element in the circle locked into a downward spiral. The people in the Global South, especially in Africa, are thus more vulnerable to conditions out of their control. This chapter examined the relationship between climate change, food security/biofuels, and land grab as a concept of the vicious circle. To reduce problems in the vicious circle, first of all, each pairs were examined to figure out issues between pairs respectively. Second, causal relations among the elements were shown and explained as the vicious circle. Lastly, based on the examination, disconnecting solutions, in terms of policies, were briefly suggested.
Despite many other factors, this chapter has only focused on the three elements; climate change, food security, and land grab, as the vicious circle. This does not mean that policies suggested here may solve all the issues on climate change, food security, and land grab, but solve or weaken some issues of them. Furthermore, policies may trigger a disconnecting of the links in the vicious circle or transform the vicious circle into a virtuous circle with other possible policy efforts, and can be starting point of reducing vulnerability of people in Global South.
The authors would like to thank the editor Netra Chhetri who gave us valuable advice and opportunity to write a chapter. We also thank Helme Castro and Evan Palmer for their careful and quick proofreading of our manuscripts.
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"}]'},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.
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