Politics as Usual: What Lies Behind the Pro-Poor Rhetoric

Politics as Usual is a 2010 book by Thomas Pogge. The book is a discussion on issues of global significance and their relationship to poverty. Politics as Usual is based on previously compiled essays. Pogge’s book present an alternate view than the one where „Education, health-care, technology, and political participation are becoming ever more universal, empowering human beings everywhere to enjoy security, economic sufficiency, equal citizenship, and a life in dignity.“ according to Crop. He presents one where Poverty and oppression persist on a massive scale, one where the affluent states and international organizations knowingly contribute and even benefit from these evils.

Thomas Pogge covers a number of political and philosophical topics including Negative Duties, In World Poverty and Human Rights Pogge had argued that Western states are complicit and in Politics as Usual he expands and analyses different aspect of Global poverty.The book notes that the bottom half of the worlds population has seen it’s wealth shrink to 1.1 percent with global household income shrinking to 3 percent, during the same period that the top ten percent have seen their shares rise to 85.1 and 71.1 percent respectively. This is due to the affluent countries having power to formulate policies and the poorest countries must take the blunt of the global repercussions of these policies according to Pogge. This can change due to people in the affluent countries becoming aware of their effect on worldwide poverty and pressuring their politicians to take action, or at least to „do no harm“. He further contends that organizations such as the World Trade Organization have a deeper moral obligation than individuals or governments because they are moral agents of the global poor.

Pogge addresses Islamist terror attacks in New York, London, and Madrid. The attackers may have justified their attacks seeking a greater good but the attacks of innocents failed the greater good test even among the attackers standards. He expands to state that the terrorists were wrong to attack in the name of religion and that the governments are also at fault for the war on terror because they inflict harm upon the innocents without considering the moral implications.

Thomas Pogge contends that we are violating our negative duty not to harm the poor by supporting oppressive regimes which further cements their position. Pogge states that the Universal Declaration of Human Rights gives people specific economic rights and including „Everyone has a right to a standard of living adequate for the health and well-being of himself and his family, including food, clothing, housing and medical care.“, which is violated by the international economic system we now have.

Ruth Jack of The Kelvingrove Review states that Pogge’s argument that world leaders allow the status quo to persist but actively and knowingly collude to maintain it for their own ends is not convincing while Pogge’s statistical analysis of the depth of world poverty are accurate and should be noted.

S. Subramanian states that the book makes for painful reading, not because of the author but because of the topic, it states many crimes against humanity, also described as „unimaginable cost of lives as a result of injustices against the poor addressed by his work“.

Antonio Papasso

Antonio Papasso (Firenze, 11 luglio 1932 – Anguillara Sabazia, 8 febbraio 2014) è stato un incisore e pittore italiano.

Secondo figlio di Giovanni e di Aldina Lollini, negli anni quaranta si trasferisce con la famiglia da Firenze a Viareggio. Terminata la guerra, ancora molto giovane lavora per una società che costruisce centrali termoelettriche. Nel 1955 apre un negozio di elettrodomestici a Viareggio.

Il suo interesse per la pittura ha inizio nel 1968, quando studia storia dell’arte corsi serali e decide di fare il pittore. Nel 1970 si trasferisce a Pisa in una casa colonica presa in affitto, e per un breve periodo si avvicina all’informale. Prende contatto con alcuni membri della nuova avanguardia letteraria Gruppo 63 e collabora con Edoardo Sanguineti e Alfredo Giuliani.

Nel 1976 pubblica la raccolta incisoria Genealogia nella quale raccoglie le maggiori opere del primo periodo, quello informale.

Nel 1978, alla galleria 9 Colonne di Trento, presentati da Claudio Di Scalzo, espone i primi papiers froissés (letteralmente „carte spiegazzate“); nel 1980 sono proposti a Genova presso la galleria Greminger da Roberto Sanesi e nel 1981 a Milano da Gillo Dorfles alla galleria Zarathustra. Dopodiché pubblica una seconda raccolta, intitolata Canta, ed espone le sue opere a Como e a Roma.

Successivamente realizza Stultifera, un’opera incisoria accompagnata da una poesia di Roberto Sanesi. Nel 1982 realizza una collezione di sette stampe a colori intitolata Re/Spira, nelle collezioni del Museum of Modern Art e dalla Bibliothèque nationale de France. Negli anni successivi pubblica due altre raccolte: Racconto, ispirata ad una poesia che Alfredo Giuliani dedicò a Papasso stesso sulla rivista Il Verri, e Forma naturæ (archetipi & c.). Nel 1983 va a vivere ad Anguillara Sabazia a nord di Roma.

Verso la fine degli anni novanta espone le sue opere ad Amburgo, Budapest e, nel 1989, nella galleria Charlton di Roma. Nel 1992 realizza un’altra raccolta, Pro/Memoria, ospitata dalla Bibliothèque nationale de France assieme alla raccolta incisoria Forma naturæ (archetipi & c.), presentata in cartella congiuntamente ad un saggio di Giulio Carlo Argan, e ad altre cinque acqueforti a colori che Papasso firma col nome d’arte „Antigone“. Nel 1999 la mostra personale dal titolo Il colore è mio nella sala consiliare del comune di Bracciano, presentato in catalogo da Edoardo Sanguineti, il quale gli dedica la poesia Pensierini per Papasso.

Dal 1996 al 2002 le opere di Papasso vengono pubblicizzate da Telemarket. Nel gennaio del 2006 due retrospettive: a Roma, presso l’università di La Sapienza e successivamente al Museo storico dell’Aeronautica Militare di Vigna di Valle (Bracciano).

Carta spiegazzata (1975)

Respira (1982)

Altri progetti

Wilkes-Barre (minor league baseball club)

The Wilkes-Barre Barons were a minor league team that existed on and off from 1886 to 1955. They began as an unnamed team in the Pennsylvania State Association in 1886.

The following season the team was known as the Wilkes-Barre Coal Barons and played in the Central League in 1888, but the league disbanded after that season. Two Wilkes-Barre team took the field in 1889 and 1892, with the later sharing representation with Pittsburgh, as Wilkes-Barre Coal Barons/Pittsburgh in the record books. The team then played from 1893 until 1898 in the Eastern League, and from 1898 to 1900 in the Atlantic League.

After spending the 1902 season in the Pennsylvania State League, as Wilkes-Barre/Mount Carmel. Their next incarnation came about in 1905, when they began playing in the New York State League, as the Wilkes-Barre Barons. They played in that league until 1917. From 1923 to 1937, they played in the New York–Pennsylvania League and from 1938 to 1948 they played in the Eastern League. Until 1939, they did not have any affiliations, however from 1939 to 1951 they were affiliated with the Cleveland Indians. The team was briefly named the Wilkes-Barre Indians from 1949 to 1951 and were managed by Bill Norman. They won a league championship in 1950 and made the league playoffs each year they played between 1949 and 1951.

From 1953 to 1955 the team regained the Barons name and once again played in the Eastern League, and in 1954 they were affiliated with the Chicago White Sox. In 1955, they were affiliated with the New York Giants.

Multiple notable players spent time with the team, including Bob Chakales, Harry Simpson, Al Smith, Doug Hansen, Sam Jones, Dave Pope, Jose Santiago, Dave Hoskins and Don Mossi.

One ballpark they played their home games at was Artillery Park.

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Stress (biology)

Physiological or biological stress is an organism’s response to a stressor such as an environmental condition. Stress is a body’s method of reacting to a challenge. According to the stressful event, the body’s way to respond to stress is by sympathetic nervous system activation which results in the fight-or-flight response. Because the body cannot keep this state for long periods of time, the parasympathetic system returns the body’s physiological conditions to normal (homeostasis). In humans, stress typically describes a negative condition that can affect a person’s mental and physical well-being.

There is likely a connection between stress and illness. Theories of the stress–illness link suggest that both acute and chronic stress can cause illness, and several studies found such a link. According to these theories, both kinds of stress can lead to changes in behavior and in physiology. Behavioral changes can be smoking and eating habits and physical activity. Physiological changes can be changes in sympathetic activation or hypothalamic pituitary adrenocorticoid activation, and immunological function. However, there is much variability in the link between stress and illness.

Selye demonstrated that stress decreases adaptability of an organism and proposed to describe the adaptability as a special resource, adaptation energy. In recent works, it is considered as an internal coordinate on the „dominant path“ in the model of adaptation. Stress can make the individual more susceptible to physical illnesses like the common cold. Stressful events, such as job changes, may result in insomnia, impaired sleeping, and health complaints. Research indicates the type of stressor (whether it’s acute or chronic) and individual characteristics such as age and physical well-being before the onset of the stressor can combine to determine the effect of stress on an individual. An individual’s personality characteristics (such as level of neuroticism), genetics, and childhood experiences with major stressors and traumas may also dictate their response to stressors.

Chronic stress and a lack of coping resources available or used by an individual can often lead to the development of psychological issues such as depression and anxiety (see below for further information). This is particularly true regarding chronic stressors. These are stressors that may not be as intense as an acute stressor like a natural disaster or a major accident, but they persist over longer periods of time. These types of stressors tend to have a more negative effect on health because they are sustained and thus require the body’s physiological response to occur daily. This depletes the body’s energy more quickly and usually occurs over long periods of time, especially when these microstressors cannot be avoided (i.e.- stress of living in a dangerous neighborhood). See allostatic load for further discussion of the biological process by which chronic stress may affect the body. For example, studies have found that caregivers, particularly those of dementia patients, have higher levels of depression and slightly worse physical health than noncaregivers.

Studies have also showed that psychological stress may directly contribute to the disproportionately high rates of coronary heart disease morbidity and mortality and its etiologic risk factors. Specifically, acute and chronic stress have been shown to raise serum lipids and are associated with clinical coronary events.

However, it is possible for individuals to exhibit hardiness—a term referring to the ability to be both chronically stressed and healthy. Many psychologists are currently interested in studying the factors that allow hardy individuals to cope with stress and evade most health and illness problems associated with high levels of stress. Stress can be associated with psychological disorders such as general anxiety disorder, depression, and post-traumatic stress disorder. However, it is important to note that everyone experiences some level of stress, and diagnosis of stress disorders can only be performed by a licensed practitioner.

It has long been believed that negative affective states, such as feelings of anxiety and depression, could influence the pathogenesis of physical disease, which in turn, have direct effects on biological process that could result in increased risk of disease in the end. However recent studies done by the University of Wisconsin-Madison and other places have shown this to be untrue, it isn’t stress itself that causes the increased risk of illness or death, it is actually the perception that stress is harmful. For example, when humans are under chronic stress, permanent changes in their physiological, emotional, and behavioral responses are most likely to occur. Such changes could lead to disease. Chronic stress results from stressful events that persist over a relatively long period of time, such as caring for a spouse with dementia, or results from brief focal events that continue to be experienced as overwhelmingly long after they are over, such as experiencing a sexual assault.

Experiments[citation needed] show that when healthy human individuals are exposed to acute laboratory stressors, they show an adaptive enhancement of some markers of natural immunity but a general suppression of functions of specific immunity. By comparison, when healthy human individuals are exposed to real-life chronic stress, this stress is associated with a biphasic immune response where partial suppression of cellular and humoral function coincides with low-grade, nonspecific inflammation.

Even though psychological stress is often connected with illness or disease, most healthy individuals can still remain disease-free after confronting chronic stressful events. Also, people who do not believe that stress will affect their health do not have an increased risk of illness, disease, or death. This suggests that there are individual differences in vulnerability to the potential pathogenic effects of stress; individual differences in vulnerability arise due to both genetic and psychological factors. In addition, the age at which the stress is experienced can dictate its effect on health. Research suggests chronic stress at a young age can have lifelong effects on the biological, psychological, and behavioral responses to stress later in life. Recent studies have shown that severe psychological stress resulting in PTSD can also significantly affect parenting perception, behavior, neural activity and HPA-axis physiology in response to stressful parent-infant interactions. These recent studies support the existence of intergenerational effects of early chronic psychological stress.

In animals, stress contributes to the initiation, growth, and metastasis of select tumors, but studies that try to link stress and cancer incidence in humans have had mixed results. This can be due to practical difficulties in designing and implementing adequate studies.

The term „stress“ had none of its contemporary connotations before the 1920s. It is a form of the Middle English destresse, derived via Old French from the Latin stringere, „to draw tight.“ The word had long been in use in physics to refer to the internal distribution of a force exerted on a material body, resulting in strain. In the 1920s and ’30s, biological and psychological circles occasionally used the term to refer to a mental strain or to a harmful environmental agent that could cause illness.

Walter Cannon used it in 1926 to refer to external factors that disrupted what he called homeostasis. But „…stress as an explanation of lived experience is absent from both lay and expert life narratives before the 1930s“. Physiological stress represents a wide range of physical responses that occur as a direct effect of a stressor causing an upset in the homeostasis of the body. Upon immediate disruption of either psychological or physical equilibrium the body responds by stimulating the nervous, endocrine, and immune systems. The reaction of these systems causes a number of physical changes that have both short- and long-term effects on the body.[citation needed]

Homeostasis is a concept central to the idea of stress. In biology, most biochemical processes strive to maintain equilibrium (homeostasis), a steady state that exists more as an ideal and less as an achievable condition. Environmental factors, internal or external stimuli, continually disrupt homeostasis; an organism’s present condition is a state of constant flux moving about a homeostatic point that is that organism’s optimal condition for living. Factors causing an organism’s condition to diverge too far from homeostasis can be experienced as stress. A life-threatening situation such as a major physical trauma or prolonged starvation can greatly disrupt homeostasis. On the other hand, an organism’s attempt at restoring conditions back to or near homeostasis, often consuming energy and natural resources, can also be interpreted as stress.

The ambiguity in defining this phenomenon was first recognized by Hans Selye (1907-1982) in 1926. In 1951 a commentator loosely summarized Selye’s view of stress as something that „…in addition to being itself, was also the cause of itself, and the result of itself.“

First to use the term in a biological context, Selye continued to define stress as „the non-specific response of the body to any demand placed upon it“. As of 2011 neuroscientists such as Bruce McEwen and Jaap Koolhaas believe that stress, based on years of empirical research, „should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism“.

Stress can have many profound effects on the human biological systems. Biology primarily attempts to explain major concepts of stress using a stimulus-response paradigm, broadly comparable to how a psychobiological sensory system operates. The central nervous system (brain and spinal cord) plays a crucial role in the body’s stress-related mechanisms. Whether one should interpret these mechanisms as the body’s response to a stressor or embody the act of stress itself is part of the ambiguity in defining what exactly stress is. Nevertheless, the central nervous system works closely with the body’s endocrine system to regulate these mechanisms. The sympathetic nervous system becomes primarily active during a stress response, regulating many of the body’s physiological functions in ways that ought to make an organism more adaptive to its environment. Below there follows a brief biological background of neuroanatomy and neurochemistry and how they relate to stress.[citation needed]

Stress, either severe, acute stress or chronic low-grade stress may induce abnormalities in three principal regulatory systems in the body: serotonin systems, catecholamine systems, and the hypothalamic-pituitary-adrenocortical axis. Aggressive behavior has also been associated with abnormalities in these systems.

The brain plays a critical role in the body’s perception of and response to stress. However, pinpointing exactly which regions of the brain are responsible for particular aspects of a stress response is difficult and often unclear. Understanding that the brain works in more of a network-like fashion carrying information about a stressful situation across regions of the brain (from cortical sensory areas to more basal structures and vice versa) can help explain how stress and its negative consequences are heavily rooted in neural communication dysfunction. In spite of this, several important brain structures implicated in playing key roles in stress response pathways are described below:

The hypothalamus is a small portion of the brain located below the thalamus and above the brainstem. One of its most important functions is to help link together the body’s nervous and endocrine systems. This structure has many bidirectional neural inputs and outputs from and to various other brain regions. These connections help to regulate the hypothalamus‘ ability to secrete hormones into the body’s blood stream, having far-reaching and long-lasting effects on physiological processes such as metabolism. During a stress response, the hypothalamus secretes various hormones, namely corticotropin-releasing hormone, which stimulates the body’s pituitary gland and initiates a heavily regulated stress response pathway.

The amygdala is a small, „almond“-shaped structure, two of which are located bilaterally and deep within the medial temporal lobes of the brain. The amygdalae are part of the brain’s limbic system, with projections to and from the hypothalamus, hippocampus, and locus coeruleus among other areas. Thought to play a role in the processing of emotions, the amygdalae have been implicated in modulating stress response mechanisms, particularly when feelings of anxiety or fear are involved.

The hippocampus is a structure located bilaterally, deep within the medial temporal lobes of the brain, just below each amygdala, and is a part of the brain’s limbic system. The hippocampus is thought to play an important role in memory formation. There are numerous connections to the hippocampus from the cerebral cortex, hypothalamus, and amygdala, among other regions. During stress, the hippocampus is particularly important, in that cognitive processes such as prior memories can have a great influence on enhancing, suppressing, or even independently generating a stress response. The hippocampus is also an area in the brain that is susceptible to damage brought upon by chronic stress.

The prefrontal cortex, located in the frontal lobe, is the anterior-most region of the cerebral cortex. An important function of the prefrontal cortex is to regulate cognitive processes including planning, attention and problem solving through extensive connections with other brain regions. The prefrontal cortex can become impaired during the stress response. This has been shown to be the case among post-traumatically stressed mothers in response to video-stimuli depicting mother-child separation versus play and related to a maternal epigenetic signature of the glucocorticoid receptor gene.

The locus coeruleus is an area located in the pons of the brainstem that is the principal site of the synthesis of the neurotransmitter norepinephrine, which plays an important role in the sympathetic nervous system’s fight-or-flight response to stress. This area receives input from the hypothalamus, amygdala, and raphe nucleus among other regions and projects widely across the brain as well as to the spinal cord.

The raphe nucleus is an area located in the pons of the brainstem that is the principal site of the synthesis of the neurotransmitter serotonin, which plays an important role in mood regulation, particularly when stress is associated with depression and anxiety. Projections extend from this region to widespread areas across the brain, namely the hypothalamus, and are thought to modulate an organism’s circadian rhythm and sensation of pain among other processes.

The spinal cord plays a critical role in transferring stress response neural impulses from the brain to the rest of the body. In addition to the neuroendocrine blood hormone signaling system initiated by the hypothalamus, the spinal cord communicates with the rest of the body by innervating the peripheral nervous system. Certain nerves that belong to the sympathetic branch of the central nervous system exit the spinal cord and stimulate peripheral nerves, which in turn engage the body’s major organs and muscles in a fight-or-flight manner.

The pituitary gland is a small organ that is located at the base of the brain just under the hypothalamus. This gland releases various hormones that play significant roles in regulating homeostasis. During a stress response, the pituitary gland releases hormones into the blood stream, namely adrenocorticotropic hormone, which modulates a heavily regulated stress response system.

The adrenal gland is a major organ of the endocrine system that is located directly on top of the kidneys and is chiefly responsible for the synthesis of stress hormones that are released into the blood stream during a stress response. Cortisol is the major stress hormone released by the adrenal gland.

In addition to the locus coeruleus existing as a source of the neurotransmitter norepinephrine within the central nervous system, the adrenal gland can also release norepinephrine during a stress response into the body’s blood stream, at which point norepinephrine acts as a hormone in the endocrine system.

Corticotropin-releasing hormone is the neurohormone secreted by the hypothalamus during a stress response that stimulates the anterior lobe of the pituitary gland by binding to its corticotropin-releasing hormone-receptors, causing the anterior pituitary to release adrenocorticotropic hormone.

Adrenocorticotropic hormone is the hormone secreted by the anterior lobe of the pituitary gland into the body’s blood stream that stimulates the cortex of the adrenal gland by binding to its adrenocorticotropic hormone-receptors, thus causing the adrenal gland to release cortisol.

Cortisol is a steroid hormone, belonging to a broader class of steroids called glucocorticoids, produced by the adrenal gland and secreted during a stress response. Its primary function is to redistribute energy (glucose) to regions of the body that need it most (i.e., the brain and major muscles during a fight-or-flight situation). As a part of the body’s fight-or-flight response, cortisol also acts to suppress the body’s immune system.

Cortisol is synthesized from cholesterol in the adrenal cortex. Its primary function is to increase blood sugar through gluconeogenesis, suppress the immune system and aid in fat and protein metabolism.

Norepinephrine is a neurotransmitter released from locus coeruleus when stimulated by the hypothalamus during a stress response. Norepinephrine serves as the primary chemical messenger of the central nervous system’s sympathetic branch that prepares the body for fight-or-flight response.

Serotonin is a neurotransmitter synthesized in the raphe nucleus of the pons of the brainstem and projects to most brain areas. Serotonin is thought to play an important role in mood regulation. Stress-induced serotonin dysfunctions have been associated with anxiety, fear and depression-like symptoms.

Neuropeptide Y is a protein that is synthesized in the hypothalamus and acts as a chemical messenger in the brain. Traditionally, it has been thought to play an important role in appetite, feeding behavior, and satiety, but more recent findings have implicated Neuropeptide Y in anxiety and stress, specifically, stress resiliency.

The peripheral nervous system (PNS) consists of two subsystems: the somatic nervous system and the autonomic nervous system. When a physical stressor acts upon the body the sensory-somatic nervous system is triggered through stimulation of the body’s sensory nerves. The signal acts as a nerve impulse and travels through the body in a process of electrical cell-to-cell communication until it reaches the autonomic nervous system. Activation of the autonomic nervous system immediately triggers a series of involuntary chemical responses throughout the body. Preganglionic neurons release the neurotransmitter acetylcholine (ACh). This stimulates postganglionic neurons which release noradrenaline. The noradrenaline flows directly into the bloodstream ensuring that all cells in the body’s nervous and endocrine systems have been activated even in areas which the ganglionic neurons are unable to reach.

When a stressor acts upon the body, the endocrine system is triggered by the release of the neurotransmitter noradrenaline by the autonomic nervous system. Noradrenaline stimulates the hypothalamic-pituitary-adrenal axis (HPA) which processes the information about the stressor in the hypothalamus. This quickly signals the pituitary gland and finally triggers the adrenal cortex. The adrenal cortex responds by signaling the release of the corticosteroids cortisol and corticotropin releasing hormone (CRH) directly into the bloodstream.

The central nervous system (CNS) is made up of the brain and the spinal cord. The brain is equipped to process stress in three main areas: the amygdala, the hippocampus, and the prefrontal cortex. Each of these areas is densely packed with stress corticosteroid receptors which process the intensity of physical and psychological stressors acting upon the body through a process of hormone reception. There are two types of corticosteroid receptors: mineralocorticoid receptors and glucocorticoid receptors. The mineralocorticoid receptors (MR) have an extremely high affinity for cortisol. This means that they are at least partially stimulated at all times and therefore are entirely activated almost immediately when a true stressor is disrupting the homeostasis of the body. The second type of receptor, glucocorticoid receptors (GR), have a low affinity for cortisol and only begin to become activated as the sensation of stress reaches its peak intensity on the brain.

Stress dramatically reduces the ability of the blood brain barrier (BBB) to block the transfer of chemicals including hormones from entering the brain from the bloodstream. Therefore when corticosteroids are released into the bloodstream – they are immediately able to penetrate the brain and bind to first the MR and then the GR. As the GR begin to become activated, neurons in the amygdala, hippocampus, and prefrontal cortex become over stimulated. This stimulation of the neurons triggers a fight-or-flight response which allows the brain to quickly process information and therefore deal with life-threatening situations. If the stress response continues and becomes chronic, the hyperactivity of the neurons begins to physically change the brain and have severe damaging effects on one’s mental health. As the neurons begin to become stimulated, calcium is released through channels in their cell membranes. Although initially this allows the cells chemical signals to continue to fire, allowing nerve cells to remain stimulated, if this continues the cells will become overloaded with calcium leading to over-firing of neuron signals. The over-firing of the neurons is seen to the brain as a dangerous malfunction; therefore, triggering the cells to shut down to avoid death due to over stimulation.

Decline in both neuroplasticity and long-term potentiation (LTP) occurs in humans after experiencing levels of high continual stress. To maintain homeostasis the brain is continuously forming new neural connections, reorganizing its neural pathways, and working to fix damages caused by injury and disease. This keeps the brain vital and able to perform cognitive complex thinking. When the brain receives a distress signal it immediately begins to go into overdrive. Neural pathways begin to fire and rewire at hyper-speed to help the brain understand how to handle the task at hand. Often, the brain becomes so intently focused on this one task that it is unable to comprehend, learn, or cognitively understand any other sensory information that is being thrown at it during this time. This over stimulation in specific areas and extreme lack of use in others causes several physiological changes in the brain to take place which overall reduce or even destroy the neuroplasticity of the brain. Dendritic spines found of the dendrite of neurons begin to disappear and many dendrites become shorter and even less complex in structure. Glia cells begin to atrophy and neurogenesis often ceases completely. Without neuroplasticity, the brain loses the ability to form new connections and process new sensory information. Connections between neurons become so weak that it becomes nearly impossible for the brain to effectively encode long-term memories; therefore, the LTP of the hippocampus declines dramatically.

The most important aspect of the immune system are T-cells found in the form of T-helper and T-suppressor cells. Cortisol, once released into the bloodstream, immediately begins to cause division of T-Suppressor cells. This rapid cell division increases the number of T-Suppressor cells while at the same time suppressing T-helper cells. This reduces immune protection and leaves the body vulnerable to disease and infection.

The HPA axis is a multi-step biochemical pathway where information is transmitted from one area of the body to the next via chemical messengers. Each step in this pathway, as in many biochemical pathways, not only passes information along to stimulate the next region but also receives feedback from messengers produced later in the pathway to either enhance or suppress earlier steps in the pathway – this is one way a biochemical pathway can regulate itself, via a feedback mechanism.

When the hypothalamus receives signals from one of its many inputs (e.g., cerebral cortex, limbic system, visceral organs) about conditions that deviate from an ideal homeostatic state (e.g., alarming sensory stimulus, emotionally charged event, energy deficiency), this can be interpreted as the initiation step of the stress-response cascade. The hypothalamus is stimulated by its inputs and then proceeds to secrete corticotropin-releasing hormones. This hormone is transported to its target, the pituitary gland, via the hypophyseal portal system (short blood vessels system), to which it binds and causes the pituitary gland to, in turn, secrete its own messenger, adrenocorticotropic hormone, systemically into the body’s blood stream. When adrenocorticotropic hormone reaches and binds to its target, the adrenal gland, the adrenal gland in turn releases the final key messenger in the cascade, cortisol. Cortisol, once released, has widespread effects in the body. During an alarming situation in which a threat is detected and signaled to the hypothalamus from primary sensory and limbic structures, cortisol is one way the brain instructs the body to attempt to regain homeostasis – by redistributing energy (glucose) to areas of the body that need it most, that is, toward critical organs (the heart, the brain) and away from digestive and reproductive organs, during a potentially harmful situation in an attempt to overcome the challenge at hand.

After enough cortisol has been secreted to best restore homeostasis and the body’s stressor is no longer present or the threat is no longer perceived, the heightened levels of cortisol in the body’s blood stream eventually circulate to the pituitary gland and hypothalamus to which cortisol can bind and inhibit, essentially turning off the HPA-axis‘ stress-response cascade via feedback inhibition. This prevents additional cortisol from being released. This is biologically identified as a normal, healthy stress mechanism in response to a situation or stressor – a biological coping mechanism for a threat to homeostasis.

It is when the body’s HPA-axis cannot overcome a challenge and/or is chronically exposed to a threat that this system becomes overtaxed and can be harmful to the body and brain. A second major effect of cortisol is to suppress the body’s immune system during a stressful situation, again, for the purpose of redistributing metabolic resources primarily to fight-or-flight organs. While not a major risk to the body if only for a short period of time, if under chronic stress, the body becomes exceptionally vulnerable to immune system attacks. This is a biologically negative consequence of an exposure to a severe stressor and can be interpreted as stress in and of itself – a detrimental inability of biological mechanisms to effectively adapt to the changes in homeostasis.

Cortisol can weaken the activity of the immune system. Cortisol prevents the proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor.[35]Cortisol also has a negative-feedback effect on interleukin-1.[36] IL-1 must be especially useful in combating some diseases; however, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of CRH hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor (GRMF),[37] so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone (the endogenous Type I and Type II receptor agonist) orRU28362 (a specific Type II receptor agonist) to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are not affected by cortisol.[38]

Stress is the body’s reaction to any stimuli that disturbs its equilibrium. When the equilibrium of various hormones is altered the effect of these changes can be detrimental to the immune system. Much research has shown a negative effect stress has on the immune system, mostly through studies where participants were subjected to a variety of viruses. In one study individuals caring for a spouse with dementia, representing the stress group, saw a significant decrease in immune response when given an influenza-virus vaccine compared to a non-stressed control group. A similar study was conducted using a respiratory virus. Participants were infected with the virus and given a stress index. Results showed that an increase in score on the stress index correlated with greater severity of cold symptoms. Studies with HIV have also shown stress to speed up viral progression. Men with HIV were 2–3 times more likely to develop AIDS when under above average stress.

Stress affects the immune system in many ways. The immune system protects the body from viruses, bacteria, and anything that is different or that the body does not recognize. The immune system sees these as intruders and it sends messages to attack. The white blood cells, leukocytes, are very important to the immune system. White blood cells have several types including B cells, T cells, and natural killer cells. B cells secrete antibodies. T cells attack intruders and natural killer cells attack cells that have been infected by viruses. These leukocytes produce cytokines which fight infections. But they also are the immune systems communicator in telling the brain that the body is ill. When an individual is stressed or going through a stressful experience the immune system starts to produce natural killer cells and cytokines. When levels of cytokines are higher they combat infections and therefore the brain gets communicated the body is ill and it produces symptoms as if the individual was ill. These symptoms include fever, sleepiness, lack of energy, no appetite, and basically flu like symptoms. These symptoms mean the body is fighting the illness or virus. This is useful for when the body goes through the stress from an injury. But the body has now evolved to do this process during stressful events such as taking exams, or even going through a life changing event such as a death of a family member or a divorce. That is why many times when individuals are stressed because of life changing events or situations such as those, they get these symptoms and believe they are sick when in reality it can be because the body is under stress.

Chronic stress is defined as a „state of prolonged tension from internal or external stressors, which may cause various physical manifestations – e.g., asthma, back pain, arrhythmias, fatigue, headaches, HTN, irritable bowel syndrome, ulcers, and suppress the immune system“.[citation needed] Chronic stress takes a more significant toll on the body than acute stress does. It can raise blood pressure, increase the risk of heart attack and stroke, increase vulnerability to anxiety and depression, contribute to infertility, and hasten the aging process. For example, results of one study demonstrated that individuals who reported relationship conflict lasting one month or longer have a greater risk of developing illness and show slower wound healing. Similarly, the effects that acute stressors have on the immune system may be increased when there is perceived stress and/or anxiety due to other events. For example, students who are taking exams show weaker immune responses if they also report stress due to daily hassles. While responses to acute stressors typically do not impose a health burden on young, healthy individuals, chronic stress in older or unhealthy individuals may have long-term effects that are detrimental to health.

Studies revealing the relationship between the immune system and the central nervous system indicate that stress can alter the function of the white blood cells involved in immune function known as lymphocytes and macrophages. People undergoing stressful life events, such as marital turmoil or bereavement, have a weaker lymphoproliferative response. People in distressed marriages have also been shown to have greater decreases in cellular immunity functioning over time when compared to those in happier marriages. After antigens initiate an immune response, these white blood cells send signals, composed of cytokines and other hormonal proteins, to the brain and neuroendocrine system. Cytokines are molecules involved with cell signaling.

Cortisol, a hormone released during stressful situations, affects the immune system greatly by preventing the production of cytokines. During chronic stress, cortisol is over produced, causing fewer receptors to be produced on immune cells so that inflammation cannot be ended. A study involving cancer patient’s parents confirmed this finding. Blood samples were taken from the participants. Researchers treated the samples of the parents of cancer patients with a cortisol-like substance and stimulated cytokine production. Cancer patient parents‘ blood was significantly less effective at stopping cytokine from being produced.

The immune system also plays a role in stress and the early stages of wound healing. It is responsible for preparing the tissue for repair and promoting recruitment of certain cells to the wound area. Consistent with the fact that stress alters the production of cytokines, Graham et al. found that chronic stress associated with care giving for a person with Alzheimer’s disease leads to delayed wound healing. Results indicated that biopsy wounds healed 25% more slowly in the chronically stressed group, or those caring for a person with Alzheimer’s disease.

Chronic stress has also been shown to impair developmental growth in children by lowering the pituitary gland’s production of growth hormone, as in children associated with a home environment involving serious marital discord, alcoholism, or child abuse.

Chronic stress is seen to affect the parts of the brain where memories are processed through and stored. When people feel stressed, stress hormones get over-secreted, which affects the brain. This secretion is made up of glucocorticoids, including cortisol, which are steroid hormones that the adrenal gland releases, although this can increase storage of flashbulb memories it decreases long-term potentation (LTP). Prolonged Stress can also be harmful to our body. That is because stress releases cortisol, and cortisol causes metabolic activity throughout the body. Metabolic activity is raised in the hippocampus. Overstimulation and toxins then are more likely to kill or damage neurons in the hippocampus. The hippocampus is important in the brain for storing certain kinds of memories and damage to the hippocampus can cause trouble in storing new memories but old memories, memories stored before the damage, are not lost. Also high cortisol levels can be tied to the deterioration of the hippocampus and decline of memory that many older adults start to experience with age.

Studies of female monkeys at Wake Forest University (2009) discovered that individuals suffering from higher stress have higher levels of visceral fat in their bodies. This suggests a possible cause-and-effect link between the two, wherein stress promotes the accumulation of visceral fat, which in turn causes hormonal and metabolic changes that contribute to heart disease and other health problems.

Selye published in year 1975 a model dividing stress into eustress and distress. Where stress enhances function (physical or mental, such as through strength training or challenging work), it may be considered eustress. Persistent stress that is not resolved through coping or adaptation, deemed distress, may lead to anxiety or withdrawal (depression) behavior.

The difference between experiences that result in eustress and those that result in distress is determined by the disparity between an experience (real or imagined) and personal expectations, and resources to cope with the stress. Alarming experiences, either real or imagined, can trigger a stress response.

Responses to stress include adaptation, psychological coping such as stress management, anxiety, and depression. Over the long term, distress can lead to diminished health and/or increased propensity to illness; to avoid this, stress must be managed.

Stress management encompasses techniques intended to equip a person with effective coping mechanisms for dealing with psychological stress, with stress defined as a person’s physiological response to an internal or external stimulus that triggers the fight-or-flight response. Stress management is effective when a person uses strategies to cope with or alter stressful situations.

There are several ways of coping with stress, such as controlling the source of stress or learning to set limits and to say „no“ to some of the demands that bosses or family members may make.

A person’s capacity to tolerate the source of stress may be increased by thinking about another topic such as a hobby, listening to music, or spending time in a wilderness.

A way to control stress is first dealing with what is causing the stress if it is something the individual has control over. Other methods to control stress and reduce it can be: to not procrastinate and leave tasks for last minute, do things you like, exercise, do breathing routines, go out with friends, and take a break. Having support from a loved one also helps a lot in reducing stress.

A study was done and it showed that the power of having support from a loved one or just social support, lowered stress in the individuals. They gave painful shocks to married women’s ankles. On some trials women were able to hold their husbands hand, on other trials they held a strangers hand, and then held no one’s hand. When the women were holding their husbands hand, the response reduced in many brain areas. When holding the strangers hand the response reduced a little but not as much as when they were holding their husbands hand. Social support helps reduce stress but even more if the support is from a loved one.

Lazarus argued that, in order for a psychosocial situation to be stressful, it must be appraised as such. He argued that cognitive processes of appraisal are central in determining whether a situation is potentially threatening, constitutes a harm/loss or a challenge, or is benign.

Both personal and environmental factors influence this primary appraisal, which then triggers the selection of coping processes. Problem-focused coping is directed at managing the problem, whereas emotion-focused coping processes are directed at managing the negative emotions. Secondary appraisal refers to the evaluation of the resources available to cope with the problem, and may alter the primary appraisal.

In other words, primary appraisal includes the perception of how stressful the problem is and the secondary appraisal of estimating whether one has more than or less than adequate resources to deal with the problem that affects the overall appraisal of stressfulness. Further, coping is flexible in that, in general, the individual examines the effectiveness of the coping on the situation; if it is not having the desired effect, s/he will, in general, try different strategies.

Signs of stress may be cognitive, emotional, physical, or behavioral.

Cognitive symptoms

Emotional symptoms

Physical symptoms

Behavioral symptoms

A renewed interest in salivary alpha amylase as a marker for stress has surfaced. Yamaguchi M, Yoshida H (2005) have analyzed a newly introduced hand-held device called the Cocorometer developed by Nipro Corporation of Japan. They state that this can be reliably used to analyze the amylase levels and is definitely a cheaper alternative as compared to the more expensive ELISA kits. The working consists of a meter and a saliva collecting chip, which can be inserted into the meter to give the readings. The levels of amylase obtained have been calibrated according to standard population, and can be categorized into four levels of severity.

Measuring stress levels independent of differences in people’s personalities has been inherently difficult: Some people are able to process many stressors simultaneously, while others can barely address a few. Such tests as the Trier Social Stress Test attempted to isolate the effects of personalities on ability to handle stress in a laboratory environment. Other psychologists, however, proposed measuring stress indirectly, through self-tests.

Because the amount of stressors in a person’s life often (although not always) correlates with the amount of stress that person experiences, researchers combine the results of stress and burnout self-tests. Stress tests help determine the number of stressors in a person’s life, while burnout tests determine the degree to which the person is close to the state of burnout. Combining both helps researchers gauge how likely additional stressors will make him or her experience mental exhaustion.

Both negative and positive stressors can lead to stress. The intensity and duration of stress changes depending on the circumstances and emotional condition of the person suffering from it (Arnold. E and Boggs. K. 2007). Some common categories and examples of stressors include:

During passive activity, patients with generalised anxiety disorder (GAD) exhibit increased metabolic rates in the occipital, temporal and frontal lobes and in the cerebellum and thalamus compared with healthy controls. Increased metabolic activity in the basal ganglia has also been reported in patients with GAD during vigilance tasks. These finding suggest that there may be hyperactive brain circuits in GAD.

Patients with generalised anxiety disorder (GAD) exhibit increased metabolic rates in several brain regions compared with healthy controls. Hyperactive neurotransmitter circuits between the cortex, thalamus, amygdala and hypothalamus have been implicated in the disorder. Hypofunction of serotonergic neurones arising from the dorsal raphe nucleus and GABAergic neurones that are widely distributed in the brain may result in a lack of inhibitory effect on the putative GAD pathway. Furthermore, overactivity of noradrenergic neurones arising from the locus coeruleus may produce excessive excitation in the brain areas implicated in GAD.

Based on early neuroanatomical observations and studies with psychoactive drugs, the septohippocampal circuit has been proposed as a model for anxiety disorders. The circuit that links the septum, amygdala, hippocampus and fornix is thought to process external stimuli and regulate the behavioural response through wider projections in the brain. Hyperstimulation of this putative ‘behavioural inhibition‘ circuit, through dysfunctional noradrenergic and serotonergic neurotransmission, has been implicated in producing anxiety, and increased arousal and attention.

In generalised anxiety disorder (GAD) there is increased noradrenaline transmission from both the locus coeruleus and the caudal raphe nuclei. The locus coeruleus-noradrenaline system is associated with anxiety and may mediate the autonomic symptoms associated with stress such as increased heart rate, dilated pupils, tremour and sweating.

Serotonergic nuclei are found in the rostral and caudal raphe nuclei. Neurones ascend from the rostral raphe nuclei to the cerebral cortex, limbic regions and basal ganglia. The activity of neurones innervating the pre-frontal cortex, basal ganglia and limbic region is decreased in generalised anxiety disorder (GAD). The activity of descending neurones from serotonergic nuclei in the brainstem is unaffected in GAD. This altered neurotransmitter balance contributes towards the feeling of anxiety associated with GAD.

GABA is the main inhibitory neurotransmitter in the central nervous system (CNS). GABAergic inhibition is seen at all levels of the CNS, including the hypothalamus, hippocampus, cerebral cortex and cerebellar cortex. The activity of GABAergic neurones is decreased in generalised anxiety disorder.

There are a number of areas of the brain affected in panic disorder. Decreased serotonin activity in the amygdala and frontal cortex induces symptoms of anxiety, whereas decreased activity in the periaqueductal gray results in defensive behaviours and postural freezing. The locus coeruleus increases norepinephrine release mediating physiological and behavioural arousal, while the hypothalamus mediates the sympathetic nervous system.

Hyperactive neurotransmitter circuits between the cortex, thalamus, hippocampus, amygdala, hypothalamus and periaqueductal gray matter have been implicated in panic disorder. Hypofunction of serotonergic neurones arising from the rostral raphe nucleus may result in a lack of inhibitory effect on the putative panic pathways in the brain. While, overactivity of norepinephrine neurons arising from the locus coeruleus may produce excessive excitation in the regions implicated in panic disorder. Physiological symptoms of the panic response are medicated by the autonomic nervous system through connections with the locus coeruleus and hypothalamus.

The principal serotonin centres in the brain are the caudal and rostral raphe nuclei. Transmission of serotonin from the rostral raphe nuclei to the pre-aquaductal grey, amygdala, temporal lobe and limbic cortex is decreased in panic disorder compared with normal. Serotonin transmission to other target regions of the brain remain unchanged.

In panic disorder there is increased norepinephrine transmission from both the locus coeruleus and the caudal raphe nuclei. The locus coeruleus-norepinephrine system may have a significant role in processing fear-related stimuli or it may affect fear-related processing by stimulating other regions of the brain implicated in anxiety and fear behaviours i.e. amygdala, hippocampus, hypothalamus, cortex and spinal cord.

Physiologists define stress as how the body reacts to a stressor, real or imagined, a stimulus that causes stress. Acute stressors affect an organism in the short term; chronic stressors over the longer term. General Adaptation Syndrome (GAS), developed by Hans Selye, is a profile of how organisms respond to stress; GAS is characterized by three phases: a nonspecific mobilization phase, which promotes sympathetic nervous system activity; a resistance phase, during which the organism makes efforts to cope with the threat; and an exhaustion phase, which occurs if the organism fails to overcome the threat and depletes its physiological resources.

Alarm is the first stage, which is divided into two phases: the shock phase and the antishock phase.

Resistance is the second stage and increased secretion of glucocorticoids play a major role, intensifying the systemic response—they have lipolytic, catabolic and antianabolic effects: increased glucose, fat and aminoacid/protein concentration in blood. Moreover, they cause lymphocytopenia, eosinopenia, neutrophilia and polycythemia. In high doses, cortisol begins to act as a mineralocorticoid (aldosterone) and brings the body to a state similar to hyperaldosteronism. If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.

The third stage could be either exhaustion or recovery:

The result can manifest itself in obvious illnesses, such as peptic ulcer and general trouble with the digestive system (e.g. occult bleeding, melena, constipation/obstipation), diabetes, or even cardiovascular problems (angina pectoris), along with clinical depression and other mental illnesses.[citation needed]

There are a number of areas of the brain affected in phobia. Activation of the amygdala causes anticipatory anxiety or avoidance (conditioned fear) while activation of the hypothalamus activates the sympathetic nervous system. Other regions of the brain involved in phobia include the thalamus and the cortical structures, which may form a key neural network along with the amygdala. Stimulation of the locus coeruleus increases noradrenaline release mediating physiological and behavioural arousal.

One hypothesis about the biological basis of phobia suggests that there is an excess of noradrenaline in the principal noradrenergic pathways in the brain and that this causes a down-regulation of post-synaptic adrenergic receptors. Transmission of noradrenaline from the caudal raphe nuclei and the locus coeruleus is increased in phobia.

The principal centres in the brain are the caudal and rostral raphe nuclei. Transmission of serotonin from the rostral raphe nuclei to the thalamus, limbic cortex and cerebral cortex is decreased in phobia compared with normal. The other major pathways for serotonin transmission which involve the basal ganglia and cerebellum, and project down the spinal cord, remain unchanged.

PTSD is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. This event may involve the threat of death to oneself or to someone else, or to one’s own or someone else’s physical, sexual, or psychological integrity, overwhelming the individual’s ability to cope. As an effect of psychological trauma, PTSD is less frequent and more enduring than the more commonly seen acute stress response. Diagnostic symptoms for PTSD include intrusion, avoidance and hyperarousal — re-experiencing the original trauma(s) through „flashbacks“ or nightmares (intrusion), emotional numbing or avoidance of stimuli associated with the trauma, and increased arousal, such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV-TR and ICD-10) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning.

Sensory input, memory formation and stress response mechanisms are affected in people with PTSD. The regions of the brain involved in memory processing that are implicated in PTSD include the hippocampus, amygdala and frontal cortex. While the heightened stress response is likely to involve the thalamus, hypothalamus and locus coeruleus.

Cortisol works with epinephrine (adrenaline) to create memories of short-term emotional events; this is the proposed mechanism for storage of flash bulb memories, and may originate as a means to remember what to avoid in the future. However, long-term exposure to cortisol damages cells in the hippocampus; this damage results in impaired learning. Furthermore, it has been shown that cortisol inhibits memory retrieval of already stored information.

There is consistent evidence from MRI volumetric studies that hippocampal volume is reduced in posttraumatic stress disorder (PTSD). This atrophy of the hippocampus is thought to represent decreased neuronal density. However, other studies suggest that hippocampal changes are explained by whole brain atrophy and generalised white matter atrophy is exhibited by people with PTSD.

Many areas of the brain appear to be involved in depression including the frontal and temporal lobes and parts of the limbic system including the cingulate gyrus. However, it is not clear if the changes in these areas cause depression or if the disturbance occurs as a result of the etiology of psychiatric disorders.

In depression, the hypothalamic-pituitary-adrenal (HPA) axis is upregulated with a down-regulation of its negative feedback controls. Corticotropin-releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocorticotropin hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands; adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.

Serotonin transmission from both the caudal raphe nuclei and rostral raphe nuclei is reduced in patients with depression compared with non-depressed controls. Increasing the levels of serotonin in these pathways, by reducing serotonin reuptake and hence increasing serotonin function, is one of the therapeutic approaches to treating depression.

In depression the transmission of noradrenaline is reduced from both of the principal noradrenergic centres – the locus coeruleus and the caudal raphe nuclei. An increase in noradrenaline in the frontal/prefrontal cortex modulates the action of selective noradrenaline reuptake inhibition and improves mood. Increasing noradrenaline transmission to other areas of the frontal cortex modulates attention.

The current usage of the word stress arose out of Selye’s 1930s experiments. He started to use the term to refer not just to the agent but to the state of the organism as it responded and adapted to the environment. His theories of a universal non-specific stress response attracted great interest and contention in academic physiology and he undertook extensive research programs and publication efforts.

While the work attracted continued support from advocates of psychosomatic medicine, many in experimental physiology concluded that his concepts were too vague and unmeasurable. During the 1950s, Selye turned away from the laboratory to promote his concept through popular books and lecture tours. He wrote for both non-academic physicians and, in an international bestseller entitled Stress of Life, for the general public.

A broad biopsychosocial concept of stress and adaptation offered the promise of helping everyone achieve health and happiness by successfully responding to changing global challenges and the problems of modern civilization. Selye coined the term „eustress“ for positive stress, by contrast to distress. He argued that all people have a natural urge and need to work for their own benefit, a message that found favor with industrialists and governments. He also coined the term stressor to refer to the causative event or stimulus, as opposed to the resulting state of stress.

From the late 1960s, academic psychologists started to adopt Selye’s concept; they sought to quantify „life stress“ by scoring „significant life events,“ and a large amount of research was undertaken to examine links between stress and disease of all kinds. By the late 1970s, stress had become the medical area of greatest concern to the general population, and more basic research was called for to better address the issue. There was also renewed laboratory research into the neuroendocrine, molecular, and immunological bases of stress, conceived as a useful heuristic not necessarily tied to Selye’s original hypotheses. The US military became a key center of stress research, attempting to understand and reduce combat neurosis and psychiatric casualties.

The psychiatric diagnosis post-traumatic stress disorder (PTSD) was coined in the mid-1970s, in part through the efforts of anti-Vietnam War activists and the Vietnam Veterans Against the War, and Chaim F. Shatan. The condition was added to the Diagnostic and Statistical Manual of Mental Disorders as posttraumatic stress disorder in 1980. PTSD was considered a severe and ongoing emotional reaction to an extreme psychological trauma, and as such often associated with soldiers, police officers, and other emergency personnel. The stressor may involve threat to life (or viewing the actual death of someone else), serious physical injury, or threat to physical or psychological integrity. In some cases, it can also be from profound psychological and emotional trauma, apart from any actual physical harm or threat. Often, however, the two are combined.

By the 1990s, „stress“ had become an integral part of modern scientific understanding in all areas of physiology and human functioning, and one of the great metaphors of Western life. Focus grew on stress in certain settings, such as workplace stress, and stress management techniques were developed. The term also became a euphemism, a way of referring to problems and eliciting sympathy without being explicitly confessional, just „stressed out.“ It came to cover a huge range of phenomena from mild irritation to the kind of severe problems that might result in a real breakdown of health. In popular usage, almost any event or situation between these extremes could be described as stressful.

Enrico Hüllweck

Enrico Hüllweck (Vicenza, 31 marzo 1946) è un politico italiano.

Dal 1998 al 2008 è stato sindaco della città di Vicenza.

Nato a Vicenza, in contrà Porti, figlio di Lydia (di padre vicentino e di madre friulana) e di Carlo Hüllweck (di padre tedesco e di madre italiana). Si diploma al Liceo Scientifico Lioy di Vicenza, e successivamente si laurea in Medicina e Chirurgia all’Università di Padova, specializzandosi in Pediatria, Endocrinologia e Malattie del ricambio (all’Università di Firenze), Scienza della Alimentazione e della Dietetica (Università di Padova), Pediatria sociale, Paidologia e Nipiologia (all’Università di Pisa).

Dopo aver svolto il servizio militare come ufficiale medico, ha iniziato a lavorare come medico pediatra. È stato presidente dell’Ordine dei Medici Chirurghi e degli Odontoiatri di Vicenza dal 1990 al 2000. È stato membro della Commissione Nazionale permanente per il Codice di Deontologia medica ed è stato membro della Commissione di Bioetica della Regione Veneto. Ha svolto anche attività di sindacalista medico ospedaliero come esponente della Confederazione Italiana Medici Ospedalieri (CIMO), della quale è stato Vicesegretario Nazionale dal 1976 al 1996. È stato inoltre iscritto all’Albo dei Giornalisti ed è stato direttore di alcune testate, prevalentemente a carattere politico, sindacale e scientifico.

È stato sposato con Vanna Velo dalla quale ha avuto un figlio, Giorgio, giornalista di TVA Vicenza. La moglie è prematuramente mancata nel luglio del 1998 (a lei dedica il libro di poesie „Le mimose di Vanna“). Dal 2004 è sposato con l’ex architetto comunale Lorella Bressanello. Alla cerimonia in Cattedrale partecipò anche Silvio Berlusconi, in qualità di suo testimone di nozze.

Nella XII Legislatura è stato deputato, venendo eletto nelle elezioni politiche del 27 e 28 marzo 1994 per la Lega Nord.

Dopo la caduta del primo governo Berlusconi aderisce a Forza Italia.

Dal 2007 al 2010 ha ricoperto la carica di presidente della fondazione Teatro Comunale Città di Vicenza.

Dal luglio 2008 al 2011 è stato capo della segreteria Politica del Ministero per i Beni e le Attività Culturali.

Il 13 dicembre 1998, battendo al ballottaggio con il 56,5% dei voti Giorgio Sala (sindaco di Vicenza tra gli anni sessanta e settanta), diviene primo cittadino di Vicenza. Il primo mandato viene ricordato per l’avvio di alcune opere di riqualificazione (Campo Marzo, avvio dei lavori al Parco Fornaci, ristrutturazione della Torre Bissara), per l’inserimento di numerose rotatorie (fino ad allora quasi assenti a Vicenza) con lo scopo di fluidificare il traffico cittadino e per l’imponente evacuazione, nell’aprile 2001, di quasi 80.000 cittadini a seguito del ritrovamento di una bomba della seconda guerra mondiale al Cimitero Maggiore. È stato il primo Sindaco d’Italia a essere nominato „Difensore ideale dell’Infanzia” da parte dell’UNICEF.

Viene rieletto per un secondo mandato dopo il ballottaggio dell’8 e 9 giugno 2003, che lo vede vincente con il 53,8% dei suffragi contro il candidato di centrosinistra Vincenzo Riboni.
In questo secondo mandato porta a termine la costruzione della Tangenziale Sud e quella del Teatro Comunale Città di Vicenza, avvia i lavori per la costruzione del nuovo Tribunale con il nuovo quartiere Borgoberga e quelli di ristrutturazione della Basilica Palladiana. Gli ultimi anni del secondo mandato sono segnati dalle contestazioni a seguito dell’approvazione della costruzione di una nuova base americana all’Aeroporto Dal Molin. Il 13 febbraio 2008, a pochi mesi dalla scadenza naturale del suo secondo mandato, rassegna le sue dimissioni per potersi candidare come parlamentare alle Elezioni politiche italiane del 2008, a cui però non viene eletto.

Josef Zemp

Josef Zemp (* 2. September 1834 in Entlebuch; † 8. Dezember 1908 in Bern) war ein Schweizer Politiker. Von 1863 bis 1891 gehörte er dem Grossen Rat des Kantons Luzern an, von 1871 bis 1872 dem Ständerat. Im Nationalrat sass er von 1872 bis 1876 sowie von 1881 bis 1891. Im Jahr 1887 war er Nationalratspräsident. Im Dezember 1891 wurde Zemp als erster Vertreter der Katholisch-Konservativen (der heutigen CVP) in den Bundesrat gewählt. Er war das erste Mitglied der Schweizer Landesregierung, das nicht der bisher allein regierenden liberal-radikalen Fraktion angehörte. In seine Amtszeit fallen der Rückkauf privater Eisenbahngesellschaften und die Gründung der Schweizerischen Bundesbahnen.

Zemp war das älteste von elf Kindern eines Krämers und Gerichtsschreibers aus Entlebuch. Dort besuchte er die Primar- und Sekundarschule, anschliessend ging er ans Gymnasium in Luzern. An der Ruprecht-Karls-Universität in Heidelberg und an der Ludwig-Maximilians-Universität in München studierte er Rechtswissenschaft. Zemp gehörte der Studentenverbindung AV Semper Fidelis Luzern an, 1857/58 amtete er als Centralpräsident des Schweizerischen Studentenvereins. Nach seiner Promotion 1859 kehrte er in seinen Geburts- und Heimatort Entlebuch zurück und eröffnete dort ein Anwaltsbüro.

1860 heiratete Zemp Philomena Widmer aus Emmen, aus dieser Ehe gingen 15 Kinder hervor. 1863 wurde er in den Grossen Rat des Kantons Luzern gewählt und gehörte diesem als Mitglied der katholisch-konservativen Fraktion (der späteren Katholisch-Konservativen Volkspartei und heutigen CVP) bis 1891 an. Er reformierte die Zivilrechtsverfassung und erreichte, dass der Kanton das Recht zur Besetzung der Pfarrstellen an die Kirchgemeinden abtrat.

Im Juli 1871 folgte die Wahl Zemps in den Ständerat, dem er aber nur knapp eineinhalb Jahre angehörte. Von Dezember 1872 bis Oktober 1876 und erneut von Dezember 1881 bis Dezember 1891 war Zemp Mitglied des Nationalrates. Von 1881 bis 1885 war er Fraktionsvorsitzender der Katholisch-Konservativen, 1887 diente er kurzzeitig als Nationalratspräsident.

Zu Beginn der 1880er Jahre versuchte er, die katholisch-konservativen Vereinigungen der einzelnen Kantone zu einer straffer geführten gesamtschweizerischen «Katholischen Union» zusammenzuführen, er scheiterte jedoch mit diesem Vorhaben an kantonalen Eigeninteressen (dies gelang erst 1912, vier Jahre nach Zemps Tod). Es gelang ihm, die seit dem Kulturkampf vorherrschende Obstruktionspolitik der Katholisch-Konservativen gegen die Liberalen zu beenden und seine Fraktion auf einen realpolitischen Kurs zu bringen. Dadurch erhielt er überparteilich Anerkennung.

Nachdem das Volk am 6. Dezember 1891 den Rückkauf der Centralbahn deutlich abgelehnt hatte, trat Post- und Eisenbahnminister Emil Welti umgehend zurück. Die Freisinnigen konnten eine Regierungskrise verhindern, indem sie den Katholisch-Konservativen einen Sitz im Bundesrat anboten und somit ihren Alleinvertretungsanspruch aufgaben. Die Fraktion einigte sich auf Zemp als offiziellen Kandidaten. Er wurde am 17. Dezember 1891 bereits im ersten Wahlgang zu Weltis Nachfolger gewählt, wobei er 129 von 154 gültigen Stimmen erhielt. Die Wahl Zemps in den Bundesrat zwang die Katholisch-Konservativen, sich von der rein oppositionellen Politik loszusagen und Regierungsverantwortung zu übernehmen. Teile der Fraktion kritisierten den neuen Kurs scharf.

Zu Beginn des Jahres 1892 übernahm Zemp das Post- und Eisenbahndepartement. Als Parlamentarier war er noch gegen eine Verstaatlichung der Eisenbahn gewesen, als Bundesrat vollzog er jedoch einen Gesinnungswandel und schuf die gesetzlichen Grundlagen für den Rückkauf. Der antietatistische Flügel der katholisch-konservativen Fraktion leistete heftigen Widerstand und ergriff das Referendum gegen das Rückkaufsgesetz. Doch das Volk nahm am 20. Februar 1898 die Vorlage mit grosser Mehrheit an. Schliesslich wurden am 1. Januar 1902 die Schweizerischen Bundesbahnen gegründet.

1902 war Zemp Bundespräsident und übernahm für ein Jahr das Politische Departement (in seinem ersten Präsidialjahr 1895 war das sonst übliche Rotationsprinzip ausgesetzt worden, so dass er keinen vorübergehenden Departementswechsel hatte vornehmen müssen). 1894 konnte er die Einführung der umstrittenen Mitteleuropäischen Zeit, 1907 das neue Bundesgesetz über die Organisation der Telefon- und Telegraphenverwaltung durchsetzen. Ausserdem bereitete er die Revision des Postgesetzes vor, die jedoch erst 1910 unter seinem Nachfolger abgeschlossen wurde. Aus gesundheitlichen Gründen trat Zemp am 17. Juni 1908 zurück. Viereinhalb Monate später starb er im Alter von 72 Jahren.

Wilhelm Matthias Naeff | Josef Munzinger | Jakob Dubs | Jean-Jacques Challet-Venel | Eugène Borel | Joachim Heer | Johann Jakob Scherer | Karl Schenk | Emil Welti | Simeon Bavier | Adolf Deucher | Josef Zemp | Robert Comtesse | Ludwig Forrer | Louis Perrier | Robert Haab | Marcel Pilet-Golaz | Enrico Celio | Josef Escher | Giuseppe Lepori | Willy Spühler | Rudolf Gnägi | Roger Bonvin | Willi Ritschard | Leon Schlumpf | Adolf Ogi | Moritz Leuenberger | Doris Leuthard

Jonas Furrer | Daniel-Henri Druey | Josef Munzinger | Wilhelm Matthias Naeff | Friedrich Frey-Herosé | Jakob Stämpfli | Constant Fornerod | Josef Martin Knüsel | Jakob Stämpfli | Jakob Dubs | Karl Schenk | Josef Martin Knüsel | Emil Welti | Paul Cérésole | Johann Jakob Scherer | Joachim Heer | Bernhard Hammer | Numa Droz | Simeon Bavier | Louis Ruchonnet | Adolf Deucher | Adrien Lachenal | Eugène Ruffy | Eduard Müller | Walter Hauser | Ernst Brenner | Josef Zemp | Robert Comtesse | Marc-Emile Ruchet | Ludwig Forrer | Eduard Müller | Arthur Hoffmann | Gustave Ador | Felix-Louis Calonder | Giuseppe Motta | Marcel Pilet-Golaz | Max Petitpierre | Friedrich Traugott Wahlen | Willy Spühler | Pierre Graber | Pierre Aubert | René Felber | Flavio Cotti | Joseph Deiss | Micheline Calmy-Rey | Didier Burkhalter

Troll (olie- en gasveld)

Troll is een verzameling van drie olie- en aardgasvelden op het continentaal plat van Noorwegen. De totale bewezen reserves van de drie velden in het Troll gebied werden op het moment van de ontdekking geschat op 1.800 miljard m³ aardgas en 2 miljard vaten olie.

Het veld ligt op dezelfde noorderbreedte als Bergen op zo’n 65 kilometer voor de kust. De zeebodem ligt meer dan 300 meter onder de zeespiegel. In het gebied komen regelmatig stormen voor waardoor de golven soms tot 30 meter hoog reiken.

In 1979 werd het veld ontdekt door het Nederlands-Britse olieconcern Royal Dutch Shell. Het duurde enige jaren voor de grootte van de velden met zekerheid was vastgesteld en dat het gas met winst kon worden verkocht. Drie jaar later stemde het Noorse parlement in met de ontwikkeling van het veld. Verkoopcontracten werden getekend want een dergelijke grote investering wilde men alleen doen als de afzet verzekerd was.

Het geheel bestaat uit drie velden en beslaat een totale oppervlakte van 700 km². De olie- en gasreserves zitten tussen de 1300 en 1600 meter onder de zeebodem. De drie deelvelden zijn:

Troll East, bevat hoofdzakelijk gas, maar onder het gas zit nog een olielaag van vier meter dik. Het Troll East veld is gigantisch, er zit zo’n 1.300 miljard m³ ofwel 40% van de toen bekende Noorse gasreserves. Het veld kan meer dan 50 jaar gas produceren en kan in 10% van de Europese gasbehoefte voorzien. Tegen de gasprijzen van die tijd, werd de totale waarde van het aardgas geschat op 200 miljard gulden.

Het gas zit in een langwerpig reservoir. Omdat het veld ondiep is, staat er weinig druk op waardoor het gas moeilijk is op te pompen. Vanwege de geringe dikte en de hoge kosten van een productieplatform was het noodzakelijk horizontale boorputten te slaan. Voor de ontwikkeling van dit veld werd het grootste productieplatform gebouwd, Troll A Platform, twee pijplijnen en een gasbehandelingsinstallatie bij Kollsnes. Vandaar brengen pijpleidingen het gas naar het Duitse Emden of het Belgische Zeebrugge. De investeringen voor de installaties bedroegen ongeveer 9 miljard gulden. De nieuwe pijplijnen om het gas naar de afnemers op het Europese vasteland te transporteren hebben zo’n 12 miljard gulden gekost. Het gasveld kwam op 9 februari 1996 in productie.

Door de gasproductie neemt de druk in het veld af. In 2014 werden twee grote compressors, elk met een gewicht van 6000 ton, bijgeplaatst op het Troll A platform. Hiermee wordt de druk in het veld op peil gehouden en Statoil verwacht 83 miljard m³ extra gas uit het veld te kunnen halen. Met dit project komt de gasproductie uit op 30 miljard m³ per jaar.

Dit veld werd in 1979 ontdekt. Troll West Oil Province heeft voornamelijk olie in een laag met een dikte van 22 tot 26 meter. De reserves werden geschat op 1.500 miljoen vaten olie, waarvan op 31 december 2006 nog 288 miljoen aanwezig was. Er is een platform, Troll B, het eerste half-afzinkbaar platform gemaakt van beton. De productie startte in de tweede helft van 1995.

In het Troll West Gas Province ligt een gasveld van 200 meter dik en daaronder nog een 12 tot 14 meter dikke olielaag. Hier ligt ook een half-afzinkbaar platform, Troll C, maar nu gemaakt van staal. Dit veld ligt in het noorden van het gebied en kwam in 1999 in productie. Troll C neemt ook de productie van het nabijgelegen Fram veld voor zijn rekening.

De eigenaren van het project zijn: het Noorse staatsbedrijf Petoro met 56% van de aandelen, Statoil (30,6%), Norske Shell (8,1%), Total E&P Norge (3,7%) en ConocoPhillips (1,6%).

Martin Corey

Martin Corey (born c. 1950 at Lurgan) is an Irish republican convicted for Provisional Irish Republican Army killings during the Troubles and reimprisoned in 2010 for alleged dissident republican activity.

On 27 February 1973, with Peter McVeigh and William Meehan, Corey ambushed members of the Royal Ulster Constabulary in Aghalee. One RUC officer, Constable Raymond Wylie, was killed instantly. Constable Robert McCauley died on 25 March 1973. In December 1973, Corey and his accomplices were found guilty of both murders and sentenced to life imprisonment. He was released on licence from the Maze Prison in June 1992.

From 1995, he worked as a gravedigger.

Corey was taken back into custody on 16 April 2010, after the Secretary of State for Northern Ireland, Shaun Woodward, applied to the parole commission to have his release licence revoked, based on secret evidence linking Corey to dissident republicanism. Corey is a member of Republican Sinn Féin.

The parole commission proceeded to review the evidence at a closed hearing on 25 January 2011 at which a special advocate appointed by Advocate General for Northern Ireland represented Corey. Some evidence was withheld, with only the gist being made available to the advocate. The commission ruled on 15 August 2011 that it was „satisfied that Mr Corey had become involved in the Continuity Irish Republican Army from early 2005 and that he was in a position of leadership in that organisation from 2008 until his recall to prison“.

The decision was subject to judicial review by Justice Treacy, who ruled on 9 July 2012 that the hearing’s reliance on secret evidence violated Corey’s right to due process. Treacy granted Corey bail pending a rehearing by the parole commission. The Secretary of State, Owen Paterson, obtained a stay on Treacy’s judgment, appealing it to the Northern Ireland Court of Appeal. The Appeal court under Declan Morgan ruled that, whatever flaws might be in the parole commission’s process, Justice Treacy did not have the authority to release Corey or grant him bail. In December 2013, the UK Supreme Court upheld the Appeal court decision.

Corey’s continued detention in Maghaberry Prison was opposed by Sinn Féin and Republican Sinn Féin, and described as tantamount to internment. The Committee on the Administration of Justice proposed taking the case to the European Court of Human Rights. A website and social media campaign was launched. In May 2012, Corey was initially denied compassionate leave to attend the funeral mass for his brother. On appeal he was allowed to attend the church service, though not the burial, on condition that he be accompanied by Sinn Féin MLA John O’Dowd and lifelong friend and official spokesperson Jim McIlmurray from Lurgan.

In August 2012, the Prison Ombudsman determined that pieces of artwork confiscated from Corey by prison staff must be returned to him as they did not, as alleged, contain images that glorify terrorist activities.[citation needed]

On 15 January 2014, Corey was released from prison under licence. On the instructions of Secretary of State Theresa Villiers he was taken from the prison in a blacked-out van and released into the custody of his solicitor. „Rule 22“ of the parole commissioners‘ rules prohibits publication of the conditions of such a licence; media reported they included bans on living within 20 miles of Lurgan, speaking to the media, or associating with known members of paramilitary group. His release was welcomed by Sinn Féin and the Social Democratic and Labour Party but criticised by Tom Elliott of the Ulster Unionist Party.

HAL Awards

The „Tribute to Heroes And Legends (HAL Awards)“ is an annual awards ceremony, established to honor entertainers, sports figures and business executives who have not only achieved success in their areas of expertise, but have utilized their celebrity status to benefit the community, via charitable activities and community service. The awards ceremony began in 1990, and the first event was held on September 23, 1990 at the Hollywood Roosevelt Hotel in Los Angeles, CA. Initial honorees included actors, Marla Gibbs, Jo Marie Payton and Zsa Zsa Gabor; recording artists Nancy Wilson and M.C. Trouble and executives from Chrysler, CBS, GM and the Laker Organization.

The HAL Awards were created by celebrated songwriter, and Motown Alumna, Janie Bradford. The event raises money for the HAL Scholarship Fund, which provides funding for performing arts students. One of the organization’s most celebrated scholarship recipient is electronic musician and rapper, Flying Lotus, who has released four albums on Warp Records. Each year, scholarship funds are presented to talented students who have maintained at least a 2.0 grade average and who show promise in the area of performing arts. The scholarship provides the financial assistance these students need to continue their education. The students are honored at the star-studded Hollywood event.

The nine awards that HAL bestows each year include Outstanding Achievement in Music, Theatre and TV/Film, The Icon Award, Legacy Award, Pioneer Award, Cornerstone Award, Pacesetter Award and The Unsung Hero Award. Recipients have included: The Temptations, Smokey Robinson, Isley Brothers, The Whispers, The Originals (band), Thelma Houston, Chaka Khan, The Supremes, The Four Tops, Wesley Snipes, Tyne Daly, Reginald Veljohnson, Craig T. Nelson, Della Reese, Roger Mosley, Regina King, Tyrese Gibson, Ernie Hudson, George Clinton. Notable presenters include Vivica A. Fox, Tom Selleck, David Cassidy, Quincy Jones, Gladys Knight, James Avery, Billy Vera, Ray Parker, Jr., Mel Carter and Berry Gordy. In 2014, New Edition, Eddie Floyd and the Mary Jane Girls were added to the list. The organization also honors songwriters, like Harold Lilly, who wrote Alicia Keyes‘ „You Don’t Know My Name“ and the legendary team of Holland-Dozier-Holland, who wrote numerous Motown hits. Producers, such as Clarence Avant, and Gamble & Huff are also honored as well as influential entertainment industry executives, such as BMI’s Thomas Cain, Universal’s Jim Urie, Jon Platt and new Motown president, Ethiopia Habtemarian. The 2015 event featured tributes to El DeBarge, Bobby Brown, The Dramatics, featuring LJ Reynolds, Dennis Edwards, jazz stylist Barbara Morrison, Brenda Holloway, 90’s chartoppers, Tony, Toni, Tone and Universal executive, Andy Skurnow.

Actress Jo Marie Payton has hosted the event since 1991.

Each year a series of additional events are scheduled leading up to the Awards Dinner and Show. Those events include a Welcome Reception for the honorees and presenters; a Celebrity Breakfast giving fans an opportunity to meet the honorees and purchase autographed items; and the Legends of Soul Concert, featuring R&B artists from the 60’s and 70’s, such as Brenda Holloway, Gene Chandler, Brenton Wood and Al B. Sure.

Linea Wakayama

La linea Wakayama (和歌山線 Wakayama-sen?) è una ferrovia regionale a scartamento ridotto che passa per le prefetture di Nara e Wakayama in Giappone, gestita dalla West Japan Railway Company (JR West). La ferrovia collega la stazione di Ōji con quella di Wakayama.

Linea Kintetsu Ikoma
Linea Kintetsu Tawaramoto (Stazione di Shin-Ōji)

Linea principale Kisei
Linea Kishigawa

Altri progetti

Hanshin (Principale • Namba • Mukogawa • Kōbe Kōsoku)
Keihan (Principale • Ōtō • Nakanoshima • Katano • Uji • Keishin • Ishiyama-Sakamoto)
Kintetsu (Osaka • Namba • Nara • Ikoma • Keihanna • Kyoto • Kashihara • Tenri • Tawaramoto • Minami-Osaka • Dōmyōji • Nagano • Gose • Yoshino)
Nankai (Principale • Kōya • Takashinohama • Aeroporto • Tanagawa • Kada • Wakayamakō • Funicolare Kōya)
Shintetsu (Arima • Sanda • Kōen-Toshi • Ao • Kōbe Kōsoku)