Main neuroprotective agents in ischemia.
\r\n\tMass spectrometry has a significant potential to further advance the clinical analysis and be a diagnostic tool for pathology or being used in the operation room and enable fast detection of tumor's margin.
\r\n\tThis book aims to provide an insight into different application fields of mass spectrometry for clinical research and routine. Modern mass spectrometry enables analysis and quantitation of very complex samples such as serum or tissue proteome or lipidome and the mass spectrometry imaging complements tissue analysis in pathology departments.
\r\n\tFurthermore, mass spectrometry can be used in an operating room as a device for on-site detection of tumor margins and be a valuable help for the surgeon.
\r\n\t
\r\n\tMass spectrometry imaging of tissue is an advanced type of tissue analysis that complements and aids the pathology and the traditional tissue analysis by staining and optical microscopy.
The problem statement is defined as how the bank crash in Arendal (Southern Norway) in 1886 can be explained by corrupt practices from the business and political elite in the town.
We ask if the bank crash in Arendal (Norway) in 1886 can be explained by corrupt practices from the business and political elite in the town. For this purpose, we use a regional-global organizational model as illustration. Chaos theory is used to illustrate corrupt practices using the theory in an untraditional way focusing on bounded rationality as a part of humanistic research from organizational thinking. Thereafter, general principles for the research project are introduced focusing on chaos theory and how reports and documents are used as secondary sources in the data collection process. Findings confirm that corruption took place in the bank crash in 1986 initiated and implemented by the business and political elite in the town. The problem definition is confirmed leading us to believe that the study might be used as a candidate to explain other bank crashes such as the global bank crises setting in fall 2008 having negative effects up to this day with no clean-cut suggestions for how the bank crisis can be solved.
The historical background. Norwegian shipping has a long and proud history in international trade. From the Viking times, it has transported goods from the long coast to Greenland and the Southern Europe stimulating trade and economic growth.
Holland became a large economy in the 1500 and 1600 centuries. Norwegian timber was used to build Amsterdam and Rotterdam as large cities. Trade leads to a large immigration from Norway to Holland, and the opposite [55]. United Kingdom was also a leading player in international trade meaning that new trading routes for Norwegian ships were established and developed.
The First Industrial Revolution, which spanned from the mid-1700s to the mid-1800s, was largely driven by the drivers of international trade in few commodities (particularly cotton). Most businesses tended to remain small and to employ as little fixed capital as possible. The chaotic markets of this area led economists such as Smith [48] to describe market forces as an “invisible hand” that remained largely beyond the control of individual firms, leading to less interest for strategic thinking.
The Second Industrial Revolution, which began in the last half of the nineteenth century in the United States and rapidly expanded to Europe, saw the emergence of strategy as a way to shape market forces and affect the competitive environments. In the United States, the construction of the main railways after 1850 made it possible to build mass markets for the first time [4]. In some capital industries, such as shipping and banking which is the empirical setting of this research, Smith’s “invisible hand” cam was supplemented by what Chandler [5] termed the “visible hand” of professional managers.
Norwegian shipping from 1814 until 1849. Norway got her own constitution, the 17th of May 1814. After the poor country was significantly hurt by the Napoleon War (1807–1814), Norway gradually managed to catch up in the capitalist race far behind super powers like United Kingdom and United States basing their economies on decentralized organizational solutions from the First Industrial Revolution up to modern times ([4, 5, 52, 58]; 105) formalizing the use of explicit and tacit knowledge putting economic growth in the center of attention. The fundaments were laid for an expansion in the shipping industry with Arendal, one of the leading Norwegian towns.
Norwegian shipping expansion from 1850 until 1886 with a focus on Arendal. The Norwegian shipping industry expanded rapidly from 1850 until 1874. There was a great demand for products such as timber from Arendal when the United Kingdom was an engineer of economic growth in Europe, leading to possibilities for business people to take advantage of both economics of scale and economics of scope [4, 5].
Arendal took advantage of the new business environment and expanded the fleet rapidly. From 1850 until 1870, Arendal’s fleet increased by 260% while it barely doubled from 1810 until 1849 [56]. Arendal was the largest shipping town in Norway.
In 1875, Arendal was the richest town in Norway mainly due to an expanding shipping industry ([22], p. 156).
United Kingdom decided to drop the Navigation laws in 1849 as a result of more trade stimulating trade in many parts of the world. Lack of protective steps from United Kingdom meant that it opened up markets also for small countries like Norway. The change in attitude from United Kingdom meant that Norway and Sweden were regarded as one country being involved in a union until 1905 when Norway got her independence. This made trade much easier stimulating shipping between Norway and the United Kingdom [56].
In 1850, Norway had a fleet of 284,000 death weight tons and 1156 ships mainly consisting of sailing ships. The number of crews in the shipping industry this year consisted of 19,000 persons. Twenty-eight years later (1878), the number of death weight tons was 1.5 millions. The number of crew working in the shipping industry was about 62,000 persons. For ships, this meant a yearly growth rate of 5.7%, for the crew an annual growth rate of 4.5% ([22], p. 136).
In the time period 1850 until 1880, Norway went from number eight in the world of shipping to number three in the world, with USA and United Kingdom in the front, a remarkable achievement given the small size of the country ([22], p. 136).
Economic and political turbulence often have positive effects on shipping markets. The Crimean War (1853–1856), the American Civil War (1861–1865), and the Prussian War (“The War of 1870”) made it possible for the shipping industry to achieve handsome economic returns, a fact shipping people learn early in their careers often told by the elderly generation as an illustration as to how tacit knowledge is transferred [43].
Arendal had a strong global orientation of her shipping activities paying attention to changing business regimes, political changes, and social unrest. The shipping industry is dynamic where profits are dependent upon economic, political and social changes (i.e., Blandley, 2000).
Flexibility may be the only option in a changing business landscape [46]. In order to adjust to changing market situations, it is necessary to disregard and even to overturn existing knowledge. Creating new knowledge requires theory building and conceptualization, experimentation and testing, involving successes as well as mistakes and dead ends [29], statement that many shipping executives might agree with.
Trade from Arendal was dependent upon a regional approach from Southern Norway. We build our reasoning based on research conducted by Drucker [10], Handy [18], Bartlett and Ghoshal (1995), and Syvertsen [50, 51] relating regionalization to globalization.
A study of a regional – global model can have a certain degree of validity when studying Arendal in the years from 1850 until 1885. Globalization opens up trading opportunities and the same time as regionalization can support personal and business identity and stimulate trade. It can be wise to have a mental home in global business.
Studies of regionalization have become a popular research approach in the last decades consisting of specialized production, close cooperation, personal contact, and a strong culture, well-defined geographical areas as elements ([39]; Cappchi, 1990).
In the world of regionalization, the value to craftwork becomes an asset in itself as it helps business firms offer tailor-made solutions to carefully targeted market segments (Boynton, 2000). The time of mass production and mass distribution is over, putting regional identity in the center for ship building, ownership over ships, and the operation of the ships, as illustrated in this study using a historical study of the town Arendal in Southern Norway as the empirical setting. In many ways, the idea of market novelty is consistent with the classis market position of differentiation, wherein a firm tries to garner a premium price with a product or a service that customers regard as unique and customized [40].
Business practices often have their own dynamics where contributions from the academic world can give limited insights. Management can thus in many situations be more regarded as an art than a science, by Mintszberg [36] called crafting:
“Craft evolves traditional skill, dedication, perfection through mastery of detail.
What springs to mind is not so much thinking and reason as involvement, a feeling of.
intimacy and harmony with the materials at hand, developed through long experience and commitment. Formulation and implementation merge into a fluid process of learning though which creative strategies evolve.”
Why we use chaos theory in this study? Due to the dynamic character of the shipping industry, well-established theories such as forecasting and behavior patterns of clients seem to change rapidly. Economic turbulence coupled with accelerating globalization, continuous improvements in technologies, and deregulation of markets have a profound impact on business firm’s competition. As a consequence, firms have to organize their operations in new ways and use new mental models when analyzing a changing business environment.
Chaos theory is an approach with a relatively long history with most contributions from natural science, less with a focus on economics and business administration. Still, it can be regarded as a flexible theory chosen as the theory to use in this research project.
What is meant by chaos theory? Chaos theory is a study of complex systems, nonlinear dynamic systems, dislodged from its steady-state condition by trigging events, where outcomes can lead to both harmony and increased tensions [20].Chaos describes a situation where the system is dislodged from its steady-state condition by trigging events [33]. It involves regrouping of elements of a system, for which a new order eventually emerges arising spontaneously from the internal structures [16].
It is possible that economic models can be improved through the application of chaos theory by studying and applying which factors can influence processes leading to economic growth or decline. It has shown to be a difficult task. The results in the field give mixed results in part due to confusion between specific tests for chaos and a more general test for nonlinear relationships [3].
Chaos theory can in our point of view, in contrast to much as the writing on chaos theory, be judged from a humanistic perspective in the way that the concept of bounded rationality [47] is central. This logic breaks with neoclassical economic thinking assuming that actors are rational which often is hard to believe analyzing our daily lives and taking a critical look at strategic decisions such as job changes and buying a new home?
We believe that actors are unable to take decisions in a completely rational manner due to both mental limitations and information-processing constraints [12]. Decisions from the practical world of business are often so complex to comprehend and therefore it is difficult to judge the different alternatives when a decision has to be made. Relatively simple and heuristic decision rules, rules of thumbs and easy procedures and routines are used in order to respond rapidly to a changing shipping market where it can look like that the only constants are uncertainty and short-term competitive advantages (Spencer, 1996).
Why butterfly effects are important in chaos theory? The field of chaos theory was pioneered by Lorentz [33] who studied the dynamics of turbulent flows. It is when a system is in a state of chaos that it is most vulnerable to butterfly effects, which states that small causes can have large effects [33].
This metaphor explains that a butterfly in Amazon can, certainly theoretically, cause a swelling ripple that, in turn, can lead to a gigantic dust storm in Texas. Lorentz [33] discovered the effect when he observed the runs of a weather model with initial condition data that behaved in a perceived inconsequential manner that failed to reproduce results in a consistent manner. The butterfly effect presents a challenge of prediction since initial conditions for a system can never be known to complete accuracy.
On the other hand, scientists have since the contribution of Lorentz [33] argued that the weather system is not as sensitive to initial conditions as previously believed [2, 34]. Research has suggested that the Lorentz equilibriums are highly simplified, seen from a natural science point of view [38].
The objective of the research is to analyze if corruption took place in the bank crash in Arendal in the year 1886 caused by the business and political elite.
In order to draw conclusions, we had to find indicators of corruption using reports and documents as sources in the data collection process. This way of approaching research is consistent with the argument to search for relationships that repeat themselves [11].
Kuhn [29] introduced the concept of paradigm shift in order to focus on changes in thinking that can take place over time. He defines a paradigm as a “scientific umbrella” that might manage to unify theories that might seem to be contradictorily. Chaos theory is new enough and flexible enough so that it can be used for a study of the bank crash in Arendal in 1886, where more research is needed.
According to Howe and Eisenhardt [23], the research questions should drive the research design and not the opposite. Platt [41, 42] warns about becoming “method oriented” rather than “problem orientated.” We have played attention to these advices by having an applied approach on the current study. For us, theory has no value in itself. Theory should confirm or reject the claim found in the problem statement.
Validity refers to the relevance of measures and variables. Cook and Campbell [6] present four types of validity: internal, external, statistical, and construct validity. In an ideal world, one should design one’s study to ensure that all forms of validity are ensured. However, this is not always possible in social science. Internal validity refers to causality between two variables, whether variable A has an effect on variable B. In this research chapter, we ask if the there is a relationship between corrupt practices and the bank crash in Arendal in 1886.
According to Calder et al. (1981), generalizability can be distinguished by effect application and theory application. The two types of application lead to different priorities when designing studies. This study belongs to the first category; this means that the study is more practical oriented than theory driven. We ask if the study can be of interest for other bank crashes. We are particularly interested if the current study can be of interest when studying the global bank crisis from 2008 until the current times.
Since this is a historical study with implications for bank crashes in recent decades, it was necessary to research and draw conclusions from both records and documents ([32], p. 277).
In this research project records included banking statements and shipping contracts. Documents are prepared for personal rather than for official reasons and include diaries, memos, letters, field notes, and so on. Documents, closer to speech, require more contextual interpretations. Records may have local uses that may become distant from officially sanctioned meanings [7].
It has often been assumed that written texts provide a “truer” indication of original meanings than other types of evidence. Indeed, Western social science has long privileged spoken over the written and the written over the non-verbal [7]. Somehow, it is assumed that the words get closer to the minds ([32], p. 277).
However, as Derrida [7] has suggested, meaning does not reside in a text but in the writing and reading it. As the text is reread in different contexts, it is given new meanings, often contradictory and always socially embedded, giving room for subjective interpretations of observations and findings.
Given the explorative way the research took place, we preferred to use a flexible research approach. As the study processed, a similar process outlined by Meyer et al. [35], whereby concepts and research methods were constantly rethought and updated following analysis and findings, followed. Similarly, [24], 99) argued that the researcher has to modify theoretical frameworks during the life of the project.
It has been recognized that the conventional research cycle conceptualization, design, measurement, analysis, and reporting do not hold well in hyperturbulent environments (Chiaburu, 2006, 744). In order to understand organizational phenomena at a more than superficial level, the scholarly literature has called for a more in-depth process research [30].
In our research, we consider change to be a continual process of becoming, rather than a succession of stable states. This viewpoint suggests that social reality is not a steady state, but rather can be regarded as a dynamic process (Beech and Johnson, 2005). Thus, there is a need to observe events and interactions as they unfold over time. This approach suggests that dynamic construction, deconstruction, and reconstruction of meaning make sense over time as contextual forces evolve and as organizational restructuring takes place.
An interpretive approach is regarded as suitable for the investigation of complex and poorly understood phenomena [9] since such an approach implies that the researcher’s task is to “make sense of local actors’ activities” ([49],1426). Thus, the important criterion for assessing interpretive data analysis is its ability to provide reasonable insights into phenomena that demand deeper understandings. Empirical findings illustrate, rather than validate, the theories they reflect [1].
We collected data through secondary sources using records and documents. We collected these data from October 2016 until June 2017, using the Kuben (Aust-Agder Museum and Achieves) in Arendal (Norway) as the main site in the data collection process.
Records can include banking statements and shipping contracts, and intentions of going business. Documents are prepared for personal rather than official reasons and include diaries, memos, letters, field notes and so on. Documents, closer to speech, require more contextual interpretations. Records may have local uses that may become distant from officially sanctioned meanings. ([32], p. 277).
It has often been assumed that what written texts provide a “truer” indication of original meanings than other types of evidence. Indeed, Western social science has long privileged the spoken over the written and the written over the non-verbal. Somehow it is assumed that the words get closer to the minds [7].
However, as Derrida [7] has suggested, meaning does not reside in a text but in the writing and reading it. As the text is reread in different contexts, it is given new meanings, often contradictory and always socially embedded. Thus, there is no “ordinal” or “true” meaning of a text outside the specific historical context. In a similar fashion, different types of texts have to be understood in the context of their conditions of reading and production [57].
In order to analyze the bank crash, we will distinguish between the years before the crash (1872–1886), the crash itself in 1886, and the time after the crash.
The traditional view on the crash. The traditional approach to the decline is that United Kingdom as the main trading partner of Norway went into a decline in 1872 due to high costs in production and distribution and a country not being able to change technology to a more modern capitalist tradition found in Germany and Holland [56]. This led to major decline in supply from Norway, for example, timber to the United Kingdom, having negative effects on the town of Arendal [17].
Sailing ships was a Norwegian trade mark as the people had a competence in both building, owning, and operating such ships. This was to a large extent the case in Arendal where this research takes place. When sailing ships became outcompeted by the dampers, the strategic advantage of sailing ships became less dominating ([22], p. 155).
The traditional point of ship owners from Arendal was to show in the transformation from sailing ships to dampers leading to the bank crash in 1886. Our findings are not in accordance with this argument.
The argument of corruption from the business and political elite in Arendal leads to the crash. The argument is that the elite controlled the business bank Arendal Privatbank, established in 1884 in order to support the business interests of local and regional business. This view point supports the idea that business people were involved in opportunistic behavior manipulating accounts in order to attract more investors and ordinary people to take part in new ventures in Arendal, for example, in shipping, insurance, and wood processing.
Our findings support the argument that the brothers Axel and Oscar Herlofson were involved in business practices allocated through Arendal Privatbank, putting their interests first as investors in a number of industries in Arendal, other parts of Norway and abroad. Our results are in accordance with writings of Torstveit [53, 54] claiming that business practices of the business and political elite had direct effects on the bank crash in Arendal in 1886.
The 1860, 1870s, and 1880s were the swinging years of Arendal. Arendal was the town with the highest incomes in Norway with many people being involved in the shipping industry as investors. The years from 1870 until 1874 ship owners gave an annual dividend on 17% of invested capital on average ([54]).
High earnings in shipping led to unrealistic attitudes toward risk in both business and privately. In the late 1870s, business people had easy access to credit without good security. People guaranteed for each other. Rules and procedures for sound banking were no longer so carefully followed. Shortcuts were taken in conflict with good banking practices. The banks also had far too low capital in relation to the assets not being able to meet toucher market situations [27, 28].
The Herlofson family played a main role in the crash of 1886. With ownership and management in many industries, the family was central in the crash of Arendal in 1886. Axel Herlofson was also involved in politics. He was a member of tax commission from 1874 on, and from 1878 he had a similar position in Barbu, which was at that time a village close to Arendal, now a natural part of the town. He won confidence of ordinary people writing off small amounts of debts in appeals.
Axel Herlofson was a key person in a network of young businessmen called the “Arendal Ring.” They supported each other in business and in social activities operating as a closed group of people with concentration of economic and political power.
At times of increased debt, falling freight rates, and ships of falling quality in 1885, it was only a question of time before a financial collapse would occur. So it did.
Arendal Privatbank went bankrupt the 30th of September 1886. For the first time in Norwegian history, a business bank went bankrupt. It was revealed that Axel and Oscar Herlofson’s debt was 12.5 million croners, more than the annual budget in the larger town in Southern Norway Kristiansand [54].
Axel Herlofson had to quit his job when corrupt business practices were found to be of great disappointment for many people in Arendal. He was arrested in the town of Kristiansand trying to leave the country with money from the bank making the scandal even larger. Corruption was confirmed leaving a prison sentence of 6 years for Mr. Aksel Herlofson [54].
The situation in the savings Arendal Sparebank was also led to bankruptcy; 1.7 million croners were given in credit to business clients with limited degree of financial security. Other clients, particularly from the villages, lost the confidence to the bank and rushed to the bank trying to withdraw cash. A total of 800,000 croners were withdrawn until December 1886, of these 75% where from clients in the villages. Accounts for 600,000 were canceled from the clients. The Board of Directors came to the conclusion that it was not possible to continue in business. The bank went bankrupt on the 13th of December 1986. The same occurred the next day with the financial group Arendl Haanværkeres Laaneindretning. The only bank that survived the financial crisis in Arendal was the small savings bank Tromø Sogn Sparebank [56].
A successful town went into a recession with large negative consequences. Workers from all industries came unemployed. In October 1986, Arendal was at the edge of revolt. Fund-raising campaigns and emergency work were started to reduce the disappointment by ordinary people [54].
The working class emerged as a powerful forces leading to the foundation of the Norwegian Labor Party in August 1887 in Arendal. Other consequence of the bank crash in Arendal in 1886 was changes in the bank legislation. The huge corruption in Arendal taking place meant that public authorities were of the opinion that business people had to be controlled to a large extent [54].
The crash in Arendal in 1886 had large negative effects. It is argued by the people of Arendal that the town, de facto, never recovered from the decline. The neighboring town of Kristiansand in Southern Norway has expanded while Arendal has not had the same positive development.
The bank failure in Arendal had consequences far beyond the local community. The region of Southern Norway was pushed into recession leading to immigration to the USA, particularly to New York and the surrounding areas.
The socialist movement became a strong source of influence in Norway changing the political landscape from the 1920s on broke with the communist bloc within the party in 1923. The Labor Party has since played a major role in Norwegian politics.
As a part of the new political regime, the bank failure in Arendal, the Norwegian Parliament adapted stricter banking laws. The new legislation stipulated requirements for credits and restrictions for how clients could organize loans in the financial sector [54].
The findings must be regarded as preliminary due to little research conducted using the regional-global model as a new to historical events as we have done in this piece of research.
Overall, the research confirms that corruption leads to economic decline in Arendal with large regional negative consequences not only for Arendal as a town but also for the region of Southern Norway.
In order to study the corruption, the regional-global model [51] made sense describing Arendal as a center for shipping until the decline set in the beginning of the 1870s. In the industrialization and urbanization of large countries such as Germany, United Kingdom, and United States, Arendal as a town and Southern Norway as a region had the timber, ice, fish, and other resources that meet the demand internationally.
However, the study of corruption practices is limited to the business elite in Arendal in the 1870 and 1880s. Corruptions might also have taken part in other towns and villages in the region but we have not enough data to draw any conclusions. This is neither the case when it comes to business associates at international markets.
The global part of the regional-global model probably made it possible to hide business practices to a certain extent. In the time period the research project focuses at the 1870s and 1880s in Arendal in Southern Norway, it was probably easier than today to avoid paying taxes in international deals due to less control, also from the public sector. In those years, people from over the class had probably greater possibilities to take advantage of a favorable position. Today with stronger means of social control and an active press, opportunistic behavior have been reduced to a large extent.
The study of the Arendal bank crash in 1886 can have a certain degree of external validity as the bank crash in the USA in 2008 led to a global recession that has negative effects on the economic situation such as employment and loss of main industries.
The case of the Arendal crash in 1886 was a result of adaptive expectations, meaning that price increases, for example, in real estate and on stocks would continue to increase. The assumptions were not illustrated through a fall on the US real estate market. Loans were not possible to be met leading to dramatic consequences for the private households and firms, alike [26].
Many of the loans were given with bad security to clients with weak financial standings, the so-called pub-prime loans. Many banks and other financial institutions ran into problems in many situations leading to bankruptcy [26].
Greed was the main motivation for many of the banks leading poor people with limited financial security into deep trouble. In the years from 2005 until 2007, more than 50% of the allocated loans in the US belonged to the prime loan category indicating opportunistic behavior and maybe also corruption [26].
The research confirms the findings of Geroski et al. [14] arguing that growth rates vary more or less randomly across firms over time. As such, it might be argued that corporate growth is unpredictable. However, their data also indicate that firms’ current period of high growth rates is a reasonable predictor of increases in long-term predictability. Our study confirm such as logic.
The study shed light on the importance of crowd practices when business decisions are taken in closed and secret circles. The important role of the brothers Axel and Oscar Herlofson is mentioned in the chapter in order to explain how corruption could take place and lead to the bank crash.
Crowd-related practices and seemingly new, more “open” organizational form are receiving increased attention in the strategy, organizational design, and innovation literature (Harhoff and Lakhani [19]. In this research line, the current research might help to give a contribution to how crowds function, both as an organization and how such organization helps to understand the environment in which the organization operates (i.e., [13]).
The results must be regarded as pre-limitary. It is the first study that tries to combine a bank crash and corruption to chaos theory and how the regional-global model can be used.
More research in public registers and shipping registers can lead to new insight on how corruption can have led to the bank crash in Arendal in 1886. We are of the opinion that more insights can lead to more insights on other bank crashes, also studies as to how the chances of large bank crashes in the future.
On this journey, chaos theory and butterfly effects can be a candidate for further studies on bank crashes. Deeper insights on chaos theory can give possibilities to gain more insights on bank crashes combining theory with practice, an adequate research tradition from chaos theory building on Greek thinking from the early antique.
Corruption was confirmed studying the bank crash in Arendal (Norway) in 1886. Opportunistic behavior of the business and political elite lead the town into a deep economic recession with negative long-term consequences.
More research on the relationship between bank crashes and corruption can give new insights.
We will suggest certain areas that can push research to new levels of knowledge.
The ambidexterity organization literature and corruption? More research on banking crashes linked to corporate practices can use insights from the ambidexterity organization literature (Birkinshaw and Gupta, 2013, [37]), focusing at strategic decisions and operation in running a company, for example, a business bank or a ship owner company.
Blue ocean strategy and corruption? We are of the opinion that in our search for corrupt business practices, chaos theory can be combined with a blue ocean strategy [25] looking at the business world through untraditional approaches, expanding for mental processes. We believe that people who wish to fight corruption can benefit handsomely from using such a way of approaching corporate practices.
Coase and corruption? Shipping executives must be brave and ask why they exist at all, as Coase [8] did in his article. Coase’s [8] theory of the firm can be regarded as a landmark contribution to help understand organizational boundaries and the competitive dynamics between organizations and markets [15, 44, 45, 59].
Coase, in short, argued that the existence of transaction costs in markets leads to the “emergence of the firm.” His seminal contribution was to highlight how the visible hand of an entrepreneur or a manager ([5, 31]; Baldwin and Von Hippel, 2012) intervenes in markets through price mechanism [21].
While Coese’s theory (1937) made significant contributions to the understanding of firms and markets, it might be argued that Coase has a rather limited view on social processes in his study. We are of the opinion that future studies on corruption in bank crashes can benefit from paying more attention to environmental factors, in accordance with current political winds found in many parts of the world, for example, in Germany, France, and the USA.
More research on bank crashes using the regional-global model. We assume that bank crashes will become a more researched area given the more complex and turbulent business environments. We believe that the regional-global model can be a suitable candidate when researching on bank crashes.
The author wishes to thank his children Alexander and Christina for all the inspiration in this research project. I follow the progress of the kids with great pride and surprise. I am without doubt a very proud father. The gifts of life. Nothing less.
Acute ischemic stroke (AIS) remains the second cause of death worldwide [1], despite showing a mortality rate reduction of 1.19% [2]; only in 2017, there were 6 million 167, 291 deaths; 1, 291,000 more with respect to 1997. During the same period, the survival rate increased by 0.02%; this caused an increment in the disability-adjusted life years percentage (DALYs), which went from 4.17 to 5.29% [2].
\nData from the World Health Organization (WHO) indicate that stroke represents the third cause of permanent adult disability worldwide [3], and is present in 90% of survivors. Motor deficits after stroke account for the high rates of long-lasting disability. The most common impairments are related to speech, or language and communication disorders (aphasia and dysphasia), apraxia [4], swallowing, depression, cognitive impairment, and hemiparesis of the contralateral limb [5] characterized by muscle weakness or spasticity in distal rather than proximal muscles [6]. These deficits ultimately cause chronic disability, affecting the ability to work and the patient’s independence and autonomy for performing daily life activities such as dressing or eating, ensuring they will require long-lasting care, which also deteriorates their quality of life and that of the patients’ caregivers.
\nStroke complications represent a considerable economic burden both individually and as a society; such complications are associated with a substantial increase in household expenses related to a higher requirement of medical attention, medication, lost workdays, and payment to external or additional caregivers, and in several cases, physical rehabilitation. It is estimated that the United States alone had an annual expenditure of 45.5 billion dollars during the 2014–2015 period, which is only expected to increase through 2035, according to estimations of RTI international [7].
\nIt is therefore fundamental to revisit the procedures regarding basic and clinical research points of view, as well as the most recent recommendations issued by the American Heart Association/American Stroke Association (AHA/ASA), which endorse multiple-component quality improvement initiatives including emergency department education and multidisciplinary teams with neurological management experience, thus increasing the application of fibrinolytic treatment IV.
\nThe strategies that are currently being studied in search of treatments for cerebral ischemia can be categorized into four areas: clinical care, neuroprotection, neurorestoration strategies, and rehabilitation therapy.
\nThe term neuroprotection is defined as the intentional intervention, either inhibition or modulation, that takes place at a certain point during the ischemic cascade, to intervene in a specific mechanism of damage to prevent tissue injury from increasing during the acute phase of ischemia [8]. The neurorestoration is developed through the stimulation of neurogenesis and neuroplasticity to restore the tissue and functional integrity of the neural tissue.
\nIn the clinical setting, several recanalization strategies have been explored to restore blood flow to the injured area of tissue as soon as possible, to assure the lesser damage and decrease secondary sequelae to the original lesion. Finally, physical therapy has become a rehabilitation tactic that has positively impacted the recovery of patients’ independence, autonomy, and quality of life, which is worth reviewing.
\nCerebral ischemia is caused by an abrupt and sustained occlusion of blood flow to a large artery that unties a series of biochemical alterations that are known as the ischemic cascade, Figure 1 [9]; during the development of such changes, a set of mechanisms that lead to cell death occurs: ionic imbalance and excitotoxicity, oxidative stress, and inflammation [10].
\nKey points to the pathophysiology of stroke.
The reduction of blood flow leads to a depletion in levels of glucose and O2, which alters aerobic metabolism, increasing lactic acid accumulation. Simultaneously, astrocytes use stored glycogen to provide energy to the neurons in the form of lactate [11]; but, because aerobic metabolism is interrupted at this time, lactic acid continues to accumulate, causing lactic acidosis, which causes ionic dysfunction [12]. Ionic alterations, together with Na+/K+ pump inactivity, give rise to neuronal depolarization, which leads to the opening of the Ca2+ channels and the subsequent release of excitatory neurotransmitters such as glutamate, causing increased activation of ionotropic receptors, especially NMDA, increasing the Ca2+ flux into the cell [13].
\nCa2+ is an essential protagonist within the ischemic cascade since it is capable of activating a significant amount of proteins that lead to cell death, and overproduction of free radicals; such proteins are calpains [14], endonucleases [15], calmodulin [16], and A2 phospholipase (Figure 1) [17]. Activation of these proteins leads to a further increase in free radical production and other oxidant species that directly damage structural molecules and activate inflammatory processes [18].
\nThe mitochondria are where the highest production of free radicals takes place; under normal conditions, superoxide anion (O2\n−) and hydrogen peroxide (H2O2) are produced continuously and eliminated by antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase [19]. Alternatively, under ischemic conditions, reperfusion provides sufficient substrate for different enzymatic oxidation reactions to take place, causing an overproduction of free oxygen radicals (ROS) and the inactivation of antioxidant enzymes [20]. Concurrently, nitric oxide (NO) increases due to the activation of endothelial and neuronal nitric oxide synthases as a result of increased Ca2+ concentration, NO reacts with ROS and forms a highly toxic peroxynitric acid (ONOOH) [21].
\nFree radicals promote mitochondrial membrane permeability and allow for cytochrome c to be released into the cytosol, where the intrinsic pathway of apoptosis becomes activated, the concentration of free radicals also increases lipid peroxidation and protein denaturalization [22], DNA fragmentation, and activate several signaling pathways that lead to neural death, such as PI3K/AKT [23], Bcl2, p53 [24] and others. From the moment of the occlusion, endothelial cells express damage-associated molecular patterns (DAMPs), produce ROS and adhesion molecules that allow for their activation and that of surrounding mast cells and macrophages, which, as a consequence, release histamine, proteases, TNF-a, and chemokines [25]. The production and release of these molecules promote the blood-brain barrier (BBB) rupturing, thus causing peripheral leukocyte invasion into the injured brain parenchyma [26].
\nMicroglial cells are then activated in the non-perfused region of the brain parenchyma [27], microglial cells acquire phagocytic characteristics and a predominantly pro-inflammatory phenotype (M1), which in turn increases the release of interleukin-6 (IL-6), interleukin 1β (IL-1β), tumor necrosis factor-alpha (TNF-α), NO molecules, and prostanoids [28]. Peripheral immune cells such as neutrophils, B lymphocytes, T lymphocytes, and NK are recruited into the injured tissue, this event is thought to contribute both beneficially by inducing the release of anti-inflammatory cytokines and growth factors, and negatively by increasing the lesion through a sustained release of proinflammatory cytokines and free radicals [29].
\nWithin the process of the ischemic cascade, three points are identified that could classify as strategic to restore neuroprotection (ionic imbalance, excitotoxicity, and inflammation); nonetheless, most neuroprotective drugs act in many of the phases of the ischemic cascade, which is why they cannot be classified into a single step of neuroprotection.
\nEarly diagnosis of stroke is a predictor for better clinical outcomes [30]; therefore, its confirmation is a pressing matter for the treatment to begin as soon as possible from the recognition of symptoms onset [31]. Currently, different strategies for acute ischemic stroke are being used in the clinical setting and are part of the AHA/ASA clinical practice guidelines [32].
\nThe differential diagnosis for stroke includes transient ischemic attacks, seizure, syncope, migraine, and brain tumors [33]. To establish a correct and timely diagnosis and to determine the best course of action, the clinician must rely on laboratory testing [34] (blood glucose is usually high, total cholesterol, LDL, HDL, AST, CPK-MB), and although the gold standard for diagnosis is a cerebral angiography, clinicians try to avoid it by choosing different methods such as imaging testing, including the first-line non-contrast CT scans, CT angiography, MRI, and MRI angiography [32, 35, 36]. In the earliest stages of acute stroke, CT scans are less useful for ischemic stroke diagnosis but can rule out hemorrhagic stroke [36]. Other clinical tests such as EKG, EEG, and the National Institutes of Health Stroke Scale (NIHSS) help establish differential diagnosis and treatment plan [35].
\nSpecific and timely reperfusion treatment is essential to determine the course of the clinical outcome and to improve survival. Once the ischemic etiology has been established, and the patient is stable, treatment should start promptly. Currently, two major therapeutic strategies are being used to treat cerebral ischemia to allow for recanalization and reperfusion. The treatment of choice will depend on time to treatment and etiology of the injury; these therapies are thrombolysis using pharmacological agents and mechanical thrombectomy [35, 37, 38, 39].
\nAt present and still after decades, the FDA only approves the use of recombinant tissue plasminogen activator (rTPA), also known as alteplase, as the sole pharmacological option for recanalization [35, 39]. Alteplase initiates local fibrinolysis when administered intravenously by hydrolyzing the peptide bond in plasminogen to form plasmin [40]. The standard IV dosage is 0.9 mg/kg for 60 min, with a 10% bolus over 1 min within 4.5 h of AIS onset [31].
\nAlthough alteplase is the only drug available for thrombolysis, most stroke sufferers do not receive this drug as treatment. There usually is a delay in recognition of the symptoms and the time window in which rTPA must be administered is from 3 to 4.5 h from onset of symptoms, and benefits diminish over time [39, 41], which is why the new AHA/ASA guidelines recommend not waiting for clinical improvement before administration [32]. Also, not all patients are eligible, since candidates must be ≤80 years of age, without diabetes or stroke history, with an NIHSS score ≤ 25, not currently taking oral anticoagulation, and without radiologic evidence of ischemic injury involving more than one-third of the MCA territory [42].
\nComplications that are associated with its use are limited: BBB integrity alterations, and hemorrhagic transformation, granting that other studies have shown it to be well tolerated by patients using warfarin or other anticoagulants [38], in controversy with the new AHA/ASA guidelines that suggest it should not be administered if the patient received heparin 24 h before [32, 35, 43]. Other drugs are also available, such as aspirin, which must be delivered within 24–48 h after stroke onset. Although the guidelines emphasize that it should not be used to replace mechanical thrombectomy or IV alteplase, aspirin continues to be the choice for secondary prophylaxis [32, 44], even when the 2018 guidelines find no benefit from its use for the treatment of an ongoing AIS [32].
\nFurthermore, the FDA approves of endovascular treatments, which are reported to have a time window of up to 8 hours from the onset of symptoms [38].
\nFor patients with large vessel occlusion, less responsive to rTPA, intra-arterial therapy is recommended, since it leads to higher recanalization rates by being able to infuse the drug directly into the occluded area or the clot itself [35, 45]. About 10% of patients with AIS fall into this category, but only a few centers can perform endovascular procedures in proper conditions [46].
\nAlso, endovascular mechanical thrombectomy using contact aspiration (CA) [47], which has been described before [48], and stent retrievers (SR), especially those of new generations [49], for clot rupturing and aspiration has shown significant benefits in large vessel occlusion [50] regarding clinical outcomes and lower complication rates [49]. Notwithstanding, CA alone, without the use of a SR, is associated with a greater need for rescue treatment, and thus, worse outcomes [51]; the SR might also increase the risk for hemorrhagic transformation and neurological deficit [52].
\nIncreased costs of endovascular treatments, as well as their complexity and need for trained personnel, cause patients to have less access to them. Therefore, exploring new pharmacological therapies should be continued.
\nIn the search to find new alternatives of neuroprotective agents, a great variety of molecules have been explored that affect one or several strategic points of the pathophysiology, and that promise good results; some are mentioned below.
\nDuring the onset of AIS, glucose and oxygen concentrations decrease, and this promotes the activation of adenosine monophosphate-activated protein kinase (AMPK). This process upregulates cellular pathways that control energy metabolism through catabolic pathways such as glycolysis and lipid oxidation to increase adenosine triphosphate (ATP) production and decrease its consumption through the inhibition of gluconeogenesis. Observations have been made regarding the fact that the activation of this enzyme for short periods increases neural survival, but its activation for extended periods will lead to cell death through apoptosis, necrosis, and autophagy [53], which is why several drugs that modulate AMPK activation have been tested recently in search for beneficial effects.
\nTo mention some, metformin has been widely studied for cerebral ischemia since it possesses pleiotropic activity and modulates AMPK activation [54]. In 2016, Zhang et al. administered 7 mg/kg of metformin intraperitoneally to C57BL/6 mice for 7 days, before middle cerebral artery occlusion (MCAO). After MCAO, the authors observed that it induced neuroprotection by reducing infarct size, through lower AMPK, results that were not observed if administered for short periods of 1–3 days before MCAO, or after the occlusion; also, these benefits were not found in the case of reperfusion [55]. Also, the neuroprotective effect of metformin was observed in a global ischemia model in rats; after administration, apoptosis decreased, and mitochondrial biogenesis was induced [56]. Other experiments have demonstrated that metformin has the potential to improve memory and learning through the increase in brain-derived neurotrophic factor (BDNF) and p7056k protein [57]. On the other hand, it has also been implicated in the reduction of IL-6, IL-1β, TNF-α, and adhesion molecule levels, as well as a decrease in neutrophil infiltration [58]. Considering these results, it is crucial to clarify how this modulation is carried out since there is some controversy about the mechanism (Table 1).
\nMain neuroprotective agents in ischemia.
\n
Atorvastatin is a statin that has pleiotropic effects, since it allows angiogenesis and synaptogenesis, increases blood flow, blunts atherosclerotic plaque formation, and provides neuroprotection in cerebral ischemia model [59] by reducing aquaporin 4 expression (AQP4) [60], thus, preventing cerebral edema and the increase of infarct size. This statin has also been reported to attenuate cognitive deficit [61] through caspase 3 inhibition and avoiding neural death in the CA1 region of the hippocampus.
\nThere is also a great variety of neuroprotective drugs or molecules that act closer by modulating inflammation, through the promotion of an anti-inflammatory microglial phenotype activation; only the most representative will be mentioned below.
\nDRα1 recombinant protein linked to the MOG peptide has demonstrated the ability to decrease macrophage migration and monocyte activation through its binding to CD74, which translates to a reduction in infarct size [62]. It has also been shown that it reduces proinflammatory cytokine expression, such as IL-1β, I-17, TNF-α, and INF-ϒ, as well as lowers T lymphocyte infiltration and promotes a polarization toward an M2 phenotype macrophage activation [63].
\nCop-1 or glatiramer acetate is a copolymer formed by four amino acids (L-alanine, L-lysine, L-glutamic, and L-tyrosine) that has shown to exert neuroprotective effects by being able to reduce infarct size and improve neurological deficit [64]. Cop-1 increases the expression of IL-10, BDNF, Insulin-like growth factor-1 (IGF-1), and neurotrophin (NT-3) in the choroid plexus [65], and the cortex, which stimulates greater neurogenesis [66]. Mangin et al. and their study group obtained similar results; they reported that Cop-1 is capable of reducing COX-2, CD32, TNF-α, and IL-1β, as well as inducing greater neurogenesis and thus, reducing memory loss in mice with cerebral ischemia [67].
\nOn the other hand, food strategies have also been proposed; for example, diet-induced ketosis has demonstrated its neuroprotective effects. Xu et al. observed, in 2017, that the ketogenic diet induced a reduction in infarct size through the overexpression of transcription factors HIF-1α, pAKT, and AMPK [68]; in 2018 Stefanovic, beneficial effects of administering exogenous β-hydroxybutyrate intraperitoneally were also observed in a model of cerebral ischemia induced by endothelin-1 in rats. He reported that the ischemic penumbra cells had a diminished glucose uptake, which translated into less ROS production, astrogliosis, and neuronal death [69]. Ketone bodies or ketosis is worth further exploration since clinical trials in Alzheimer’s patients with mild cognitive decline have shown improvements in verbal memory after being treated with a ketogenic diet [73].
\nDietary administration with docosahexaenoic acid (DHA) has also proven to have anti-inflammatory and neuroprotective effects in cerebral ischemia through the reduction of proinflammatory cytokine expression, such as TNF-α, IL-1β and IL-6; even, a decrease in macrophage and microglial activation and a decrease in leukocyte infiltration to the lesion site [70]. Similar observations were made by Cai et al. who noted that macrophage, neutrophil, and T and B lymphocyte infiltration was significantly decreased, besides stimulating an anti-inflammatory macrophage (M2) activation [71]; DHA is also capable of inducing neurogenesis and angiogenesis [72], which makes it a promising molecule for future experimental research.
\nMany of the cytokines and growth factors that result from immunomodulation processes are directly involved in neurorestoration processes, the latter understood as the set of strategies that seek to reconstruct the affected neural circuits through neuroplasticity or neurogenesis [74].
\nNeurotrophins are a group of proteins that are involved in the maintenance and survival of the central nervous system [75]; this includes BDNF, NT-3, NT-4, NT-5, nerve growth factor (NGF), and IGF-1. Neurotrophins interact with two types of receptors, Trk (tyrosine kinase receptors) and the p75 receptor that belongs to the TNFR receptor family, implicated in apoptosis processes.
\nAmong the most studied neurotrophins are BDNF and NT-3; BDNF is produced by almost all brain cells and is known to participate in processes of proliferation, survival, and neuronal differentiation. Its receptors are widely distributed [76] and activate critical signaling pathways such as PLCγ, PI3K, and ERK, which ultimately lead to phosphorylation and activation of the transcription factor CREB that mediates the expression of genes that are essential for the survival and differentiation of neurons [77]. NT-3 has also been involved in the processes of cell proliferation and differentiation through the notch pathway [78], as well as participating in processes of memory and learning [76].
\nExperiments have shown that the increase of neurotrophic factors in the ischemia model is commonly related to a better functional or memory recovery and that it is usually associated with neurogenesis or neuroplasticity—as in the case of metformin, which showed an increase in BDNF expression and that induced a more significant recovery of memory and learning [57]. Also, Cop-1 was able to induce the increase of BDNF, IGF-1, and NT-3; which correlated with the increase in neurogenesis [65]; and the experiments of Luan et al. showed that patients with cerebral ischemia who presented higher levels of NGF obtained a better functional recovery at 3 months after the ischemia [79].
\nStem cell transplantation has also been linked to better neurological recovery; although clinical trials have not reported the expected results [80], basic research using stem cells has shown an increase in neurological rehabilitation and suggested mechanisms include the overexpression of BDNF and IGF-1 [81, 82], as well as immunomodulatory cytokines like IL-10, which together induce a polarization toward an anti-inflammatory M2 microglial phenotype [83].
\nIn recent years, there has been an increase in the interest of studying how the external environment has a direct effect on the structure and neuronal function, that is, on neuroplasticity [84], and that is why researchers keep studying what kind of external characteristics (specifically physical and social activity) can increase these factors and thereby obtain more significant benefits.
\nIn 2017, Chen et al. explored whether a specific type of environment stimulated the production of BDNF in rats with cerebral ischemia, and what they observed was that physical stimulation increases the expression of neurotrophic factors more than social stimulation and obtains a higher neurological recovery [85]. Mang, on the other hand, observed that the increase in BDNF after an ischemic event is determined by the type of aerobic exercise and the val66met variant of the BDNF gene [86].
\nThe effects on NT-3 have also been evaluated, and the results have been very similar; there is an increase in its levels with physical stimulation after the ischemic event and a more significant functional recovery [87]. Other proteins have also been associated with neuronal plasticity through axonal growth, such as the growth-associated protein 43 (GAP-43), which has been observed to increase when rats with cerebral ischemia undergo fastigial electrostimulation [88].
\nElectrical stimulation directly into the fastigial nucleus (FNS) has proven to be beneficial in a model of MCAO [89]. The mechanism through which FNS has shown to improve walking balance and neurological scores is due to the activation of the PKA/cAMP pathway, suppressing the expression of Rho-Kinase, and through the overexpression of GAP-43 protein [89].
\nIn this sense, experiments continue to be designed to establish the efficacy of training types and times to modulate inflammation, the production of neurotrophins, and the impact on patient mobility, as in the proposal developed by Scalzo et al. [89] that gives rise to the continued development of a well-founded physical therapy for patients with cerebral ischemia.
\nPost-stroke physical rehabilitation (PR) is of utmost importance as a non-pharmacological strategy for neuroprotection and neurorestoration but, most significantly, should be aimed at restoring and regaining motor impairment during the chronic period [90], and to promote the functional autonomy of the patient [4]. Recovery of body function assessment depends on whether the patients can perform everyday activities on their own and is measurable by several different scales such as UE-FM score for the upper extremity, and the Barthel Index for Activities for Daily Living scale [4].
\nFunctional and cognitive deficit severity is related to tissue integrity [91], and it is not clear whether recovery results from biological processes or physical rehabilitation [91, 92]. Some clinical parameters that can be observed at the bedside, such as early finger extension and shoulder abduction, can act as predictors of long-term (over 6 months) recovery after stroke [93]. Spontaneous recovery of upper and lower limbs occurs depending on the type, location, and severity of the lesion, in approximately 60–70% of cases [93] during the first 2–6 months [4, 94], period after which most people believe they have achieved maximal recovery and stop with either physical or pharmacological therapy [4, 95]. Interventions should be designed according to the stage of neurological recovery the patient is in, with the consideration that early chronicity is not a contraindication for continuing rehabilitation [4].
\nPhysical rehabilitation must start early, if possible, during the first week post-stroke [96], because there is an intensification in neuroplasticity during the early stages [91], employing different mechanisms such as the axon regeneration [88], and the higher expression of growth-promoting genes, such as GAP-43. This lesion-induced plasticity that happens during the first days post-stroke [90, 97, 98] reportedly lasts around 6 months after stroke [4, 91, 95, 97]. Also, therapy must continue after such a period, to take advantage of behavior-induced plasticity [95], which is still possible after 1 year of having had the stroke [4].
\nPR has also been proven to elicit neuroprotection and neurorestoration in other neurological disease models, such as Parkinson’s, through the upregulation of BDNF and GDNF and prevention of inflammatory response [99]. The following therapies are currently under study for neurorestorative purposes during the post-stroke chronic period:
\nEnvironmental enrichment focuses on inducing adaptation to different environments, including toys and complex tasks, to improve functional outcomes [97]. Also, this type of therapy has shown to enhance angiogenesis by increasing CD31 and VEGF [97]. Furthermore, environmental enrichment upregulates BDNF secretion, and other neurotrophic factors [85, 90].
\nWang et al. found improvements in spatial learning and memory, number of synapses, and an increase in the expression of synaptogenesis markers. GAP-43, a protein involved in neural plasticity through axonal growth, is upregulated during the first 28 days after stroke in mice exposed to environmental enrichment. Likewise, other markers involved in synaptogenesis like SYN and PSD-95 achieve better concentrations in the brains of mice treated with environmental enrichment [97].
\nFunctional electrical therapy has been used alongside other types of electrical stimulation to induce repetitive muscular contraction to mobilize certain joints [6]. Somatosensory stimulation might enhance neurorehabilitation after stroke through the stimulation of corticomotoneuronal excitability [6]. It has been proposed that this type of therapy increases muscle strength, reduces spasticity, and facilitates voluntary movements, among other motor benefits [6].
\nGuided self-rehabilitation (GSR) is a method in which the intensity of training can be increased inside the home environment. While combined with conventional rehabilitation, it has proven to be efficacious in engaging the patients in their recovery through a contract between the patient and the therapist, allowing for an increased sense of responsibility and motivation for the patients, who are required to register their progress in a diary [100]. Although not many physical therapists accept such an approach [100], positive changes have been observed after 1 year of GSR and conventional rehabilitation in ultrasound measuring of the soleus’ and medial gastrocnemius’ thickness and fascicle length, as well as clinical improvement, observed in soleus extensibility and ambulation speed [101] in chronic stroke patients.
\nConstraint-induced therapy requires constraining the non-affected limb for 90% of the waking hours, forcing the patient to use the paretic limb, inducing the increase of use-dependent plasticity, although this therapy is not practical for most of the population [6].
\nVideogame- or virtual reality-based (VRb) therapies have been under study for upper extremity functional recovery in acute and subacute or chronic patients [91, 96, 99, 102]; the rationale for such approaches is that they promote motor learning and repetitive, intense movements, and in the specific case of virtual reality, the patient is exposed to interactive visual, auditive, and proprioceptive feedback [91, 102]. Different videogame and VRb therapies have reported improvements in fine dexterity, grip strength [96], and grasp force [99] in upper extremities, and, activities of daily living [91] and cognition [102] in young and elderly patients after several weeks of rehabilitation. Better results have been observed when combined with conventional therapy, although it is still not known whether it enhances or speeds up recovery [91].
\nIn addition to continuing the search for pharmacological agents that allow the neuroprotection and neurorestoration of tissue affected by cerebral ischemia, the development of physical therapy and diet modification offers new horizons that have shown satisfactory results in the clinical setting in short times. However, it has not yet been possible to establish a protocolized treatment that can be added to the health care guidelines; so it is important to continue exploring all possible strategies to improve the quality of life of people who have suffered a cerebral infarction and that of their caregivers.
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Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. 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I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). I am a Reviewer for several refereed journals and international conferences, such as IEEE Transactions on Biomedical Engineering, IEEE Transactions on Industrial Electronics, Optic Letters, Measurement Science Review, and also a member of the International Advisory Committee for 2012 IEEE Business Engineering and Industrial Applications and 2012 IEEE Symposium on Business, Engineering and Industrial Applications.",institutionString:null,institution:{name:"Joseph Fourier University",country:{name:"France"}}},{id:"55578",title:"Dr.",name:"Antonio",middleName:null,surname:"Jurado-Navas",slug:"antonio-jurado-navas",fullName:"Antonio Jurado-Navas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/55578/images/4574_n.png",biography:"Antonio Jurado-Navas received the M.S. degree (2002) and the Ph.D. degree (2009) in Telecommunication Engineering, both from the University of Málaga (Spain). He first worked as a consultant at Vodafone-Spain. 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