God and Philosophy Essay Example for Free

God and Philosophy Essay Many philosophers will say that God plays an important role in a persons mental being. Others will argue that he doesnt and that we decide by our own mentality. The three thinkers that will be discussed in this paper made a large impact in the philosophical world with their theories and reasons. Descartes, Kant, and Hume are all important players in the world of philosophy, but according to other philosophers, so is God. Rene Descartes, a noted French philosopher, scientist, and mathematician, coined the Latin phrase Cogito ergo sum (I think, therefore I am). He refused to accept the scholastic and Aristotelian traditions that had dominated philosophical thought throughout the medieval period (www. iep. utm. edu). He frequently contrasted his views with those of his predecessors. In his theology, he insists on the absolute freedom of Gods act of creation. In 1641, he wrote Mediations on First Philosophy, which he employed a method called methodological skepticism; where he doubts any idea that can be doubted. God, in Descartes metaphysics, is the bridge from the subjective world of thought to the objective world of scientific truth. The mind, owing its existence to God, is innately programmed with certain ideas that correspond to reality; hence the importance, in Descartes system, of proving the existence of God, the perfect guarantor of our ideas, so that the mediator can move from isolated flashes of cognition to systematic knowledge of the nature of reality (Cottingham, 31). In Meditations, he mentions the idea of a benevolent God. Because God is benevolent, he can have some faith in the account of reality his senses provide with a working mind and sensory system and does not desire to deceive him; however, this is a continuous argument, as his very notion of a benevolent God from which he developed this argument is easily subject to the same kind of doubt as his perceptions (www. wikipedia. com). Descartes sought to retain the belief in the existence of innate ideas together with an acceptance of the values of data and ideas derived from an experience. Next up is Immanuel Kant, a German philosopher that held that there is an objective moral law. Most philosophers view morality very differently. Some think there is an objective moral law, but that it depends on Gods will. Others thought morality was to do with reason, but that the reasoning was all about how to promote some objective, like ones own happiness of welfare of society (Walker, 5). Kant rejected these ideas, because morality is depending on something outside itself- Gods will. Kant inquired whether it could be possible to ground synthetic ? a priori knowledge for a study of metaphysics, because most of the principles of metaphysics from Plato through Kants immediate predecessors made assertions about the world or about God or about the soul. Kants works of 1755 reveal more of his originality and his enduring themes. Universal Natural History, deriving the present state of the planets from postulated initial conditions by reiterated applications of the laws of Newtonian mechanics, manifests not only Kants commitment to those laws, for which he was subsequently to seek philosophical foundations, but also his commitment to thoroughly naturalistic explanations in science, in which God can be the initial source of natural laws but never intervenes within the sequence of physical causes. Kant still holds that the existence of God can be proved as a condition of the possibility of any reality. Finally, Kant further develops his argument that scientific explanation cannot allow divine intervention in the sequence of events, and that God must be seen only as the original ground of the laws of nature. The existence of God is therefore to Kant a necessary assumption for what he sees to be an objectively valid morality. Lastly, David Hume, British philosopher, is considered one of the most influential religious philosophers. Hume questioned the process of inductive thinking, which had been the hallmark of science. He criticized the standard proofs for Gods existence, traditional notions of Gods nature and divine governance, the connection between morality and religion, and the rationality of belief in miracles. He also advanced theories on the origin of popular religious beliefs, grounding such notions in human psychology rather than in rational argument or divine revelation. For Hume, all objects of human reason are divided into two kinds: Relations of Ideas and Matters of fact. All reasoning of matters of fact is founded on Cause and Effect. Cause and Effect play a big role in Humes philosophy. Hume wrote The Natural History of Religion in 1757. Its main theme is the causes and consequences of the religious development of mankind from polytheism to monotheism. Belief in a god or gods is not natural like belief in an external world, since there are races in which it is not to be found (Quinton, 52). Contrary to many critiques Hume does believe that there is a God, however he does not believe that God is all greatness like society commonly assumes and accepts. Hume argues that because one sees an effect that doesnt mean that we can automatically know or assume its cause. This argument can be used to explain the creation of the world. As influential as Hume was, he remains an academic skeptic, making the reasonable judgments of an ordinary life, regardless of lack of academic knowledge. God played an important role in every philosophers thinking. They either tried to provide proof that he does or does not exist, or tried to decipher why so many people followed a man whom they have never even met. Nevertheless, God played an important role in Kants, Descartes, and Humes philosophical thinking. Works Cited Burnham, Douglas and James Fieser. Rene Descartes (1596-1650). The Internet Encyclopedia of Philosophy. 2005. http://www. iep. utm. edu/d/descarte. htm. Cottingham, John. Descartes. New York, Rutledge: 1999. Quinton, Anthony. Hume. New York, Rutledge: 1999. Rene Descartes. http://en. wikipedia. org/wiki/Descartes. Walker, Ralph. Kant. New York, Rutledge: 1999.

Louis Armstrong Essay -- essays research papers fc

Louis Armstrong's Influential Career Louis Armstrong’s Influential Career Louis Armstrong was the most successful and talented jazz musician in history. His influence and expansive career continues to make waves in the jazz world. That is what made him become what he is to many today – a legend. Born on August 4, 1901, in the poorest section of New Orleans, Armstrong grew up with his grandparents due to his parents’ separation. On January 1, 1913 he made a mistake which turned out to be the best thing that ever happened to him. At a New Year’s celebration in downtown New Orleans, Louis Armstrong, also known as â€Å"Satchmo† and â€Å"Satch†, fired a pistol into the air and was placed in the Colored Waifs’ Home. It was there that he was introduced to Peter Davis – the brass band leader who taught him how to play the cornet (Brown 17). Soon after he began playing, Armstrong was made leader of the band – something he was extremely proud of. In June of 1914, Ar mstrong was free to leave the Waifs’ Home. He was hired by various cabarets throughout the city, as well as for picnics, dances, and funerals. It was at one of these places that he was spotted by the famous Joe ‘King’ Oliver. King Oliver found Armstrong stand-in slots at orchestras and other venues. In 1918, he was offered the vacant seat left by Oliver in the band the Brown Skinned Babies. Kid Ory, leader of the band, once said that after Louis joined them he, â€Å"†¦improved so fast it was amazing. He had a wonderful ear and a wonderful memory. All you had to do was hum or whistle a new tune to him and he’d know it right away† (Boujut 21). At the end of 1918 Armstrong married Daisy Parker, a prostitute he had met at a dance hall that he played on Saturday nights. The marriage ended only four years later due to her beating him regularly (Bergreen 87). Louis Armstrong was hired in May of 1919 to play on a riverboat that traveled the Mississipp i River from New Orleans to St. Louis. Armstrong soon became very popular in St. Louis and was in high demand (Collier 124). Two and a half years later, he was thrown off the riverboat and fired due to a fight. After returning to New Orleans, he received a telegram from King Oliver in Chicago. It was an invitation to join The Creole Jazz Band – an offer Armstrong couldn’t refuse. The Jazz Band cut it’s first record in the spring of 1923 and toured throughout Illinois, Ohio,... ...s he starred in which shared the same title. For the next seven years of his life he was in and out of the hospital due to heart and kidney problems. On July 6th, 1971, Louis Armstrong died of a lung infection and heart complications. His last wish, that his trumpet be buried with him, was granted. Louis Armstrong influenced almost all aspects of jazz technique and style. He was the first to improvise and elaborate on a given melody. This technique has since been attempted and copied time and time again. Armstrong introduced a freedom to music that continues to impact popular music (Sadie 601). Without this American genius music would not be what it is today. Bibliography Works Cited Bergreen, Lawrence. Louis Armstrong: An Extravagant Life. New York: Broadway, 1997. Boujut, Michel. Louis Armstrong. New York: Rizzoli, 1998. Brown, Sandford. Louis Armstrong. New York: Watts, 1993. Collier, James Lincoln. Louis Armstrong: An American Genius. New York: Oxford, 1983. Crouch, Stanley. â€Å"Louis Armstrong.† Time 8 Aug. 1998: 170. Sadie, Stanley. ed. â€Å"Louis Armstrong.† The New Grove Dictionary of Music and Musicians. 6th ed. Vol. 1. New York: Macmillan, 1995. Word Count: 1246

Explain the Biological Mechanisms by Which Stress Can Induce Depressive Behaviour

Explain the biological mechanisms by which stress can induce depressive behaviour. Introduction Depressive behaviour is a core feature of several major psychological disorders, most obviously major depression (MD) and depressive episodes of bipolar depression (BP). Depression is also frequently found to be co-morbid with psychotic disorders such as schizophrenia and with anxiety-related disorders (e. g. social phobia or OCD). Depression is the biggest major risk factor for self-harm and suicide, thus posing a real clinical problem to try to understand and reverse the mechanisms involved.Traditional anti-depressant treatment has only shown a modest benefit to placebos in treating the disorder; therefore, more effective drugs that target the right biological mechanisms are imminently needed. The majority of experimental research in the area has used rodents to test medication and model known psychopathological aspects of depression in humans, such as learned helplessness, cognitive def icits and increased co-morbidity with anxiety-related behaviours. There are many factors that may explain why some people (around 16% of the population) will experience a depressive episode in their lifetime and others won’t.Genetic vulnerability and epigenetic changes, psychosocial support, socioeconomic status or even climate-related factors all have to be considered in considering the right treatment for individual cases. Whilst the causal link between many of these and the onset of depression is somewhat inconclusive, the strong association between chronic mild stress (CMS) and depressive behaviour is now a huge area of research, resulting in the stress-induced model of depression.Even where there is evidence for the role of genes in depression, such as allele variants for the 5-HTT promoter region, it is shown to vary as a function of exposure to stressful life events. The mechanisms by which environmental stressors can lead to depressive behaviour have been explored tho roughly, with a strong focus on the role of the Hypothalamus-Pituitary-Adrenal (HPA) axis and its dysfunction in depression. The consequent rise in levels of the glucocorticoid hormone cortisol, following HPA activation, has been shown to become chronic increased in depressed patients.This is thought to be due to the development of glucocorticoid resistance, whereby high levels of cortisol are present in the bloodstream and peripheral tissue but negative feedback to shut down the HPA axis no longer works. Due to the numerous roles of cortisol within the body, several biological processes may be affected as a consequence of CMS that may lead to depressive behaviour. Direct and indirect effects of HPA dysfunction include changes in immune response, neuronal damage, decreased rates of neurogenesis and the serotonin pathways.These processes tend to interact and exacerbate one another; therefore, understanding each proposed biological mechanism of stress-induced depression and their impa ct upon each other is likely to lead to a better treatment outcome. Acute Stress and the HPA Axis The experience of acute mild stress is a normal and adaptive process, triggered by an environmental ‘stressor’ deemed to be potentially harmful. From an evolutionary perspective, this serves to protect the individual from danger via activation of the sympathetic nervous system, preparing the individual for ‘fight or flight’ mode.Stress, as well as input from the amygdala, hippocampus and midbrain, directly activates the ‘stress response’ via the Hypothalamic-Pituitary-Adrenal (HPA) axis. The first immediate response is the release of corticotrophin releasing hormone (CRH) from the hypothalamus, which travels to the pituitary where it binds to CRH Receptor 1 (CRHR1). CRH can also act directly on other brain regions, e. g. the amygdala at this early stage. CRH1 activation stimulates the release of adrenocorticotrophin release hormone (ACTH), which tr avels via the bloodstream to the kidneys, stimulating the delayed release of the glucocorticoid (steroid) cortisol.Cortisol acts throughout the body in all cells, via binding to cytoplasmic glucocorticoid and mineralocorticoid receptors (GR and MR) (see Figure 1). Figure 1: Cortisol can pass through the cell membrane due to its lipophillic properties. Binding of cortisol to the GR complex in the cytoplasm causes dissociation of GR from the complex, resulting in an active GR monomer. Two GRs then dimerise to form a GR dimer. This can act as a transcription factor in itself by attaching to Glucocorticoid Binding Elements (GBE), or it can interact with other Hormone Binding Elements and transcription factors to initiate gene transcription. http://jimlund. org/blog/? m=200910] A rise in cortisol levels, alongside CRH, leads to adaptive changes in behaviour, cognition and immune function. Importantly, this rise is followed by a negative feedback loop of cortisol and CRH acting upon its o wn receptors (NC3R1 and CHR2, respectively) to shut down the HPA axis once the ‘threat’ has been resolved. This homeostatic mechanism terminates the production of any more CRH and therefore brings cortisol levels back to baseline (pre-stressor), vital for returning the individual back to a normal ‘resting’ state.It is this negative feedback mechanism which has been shown to be disrupted in patients with depression. Chronic Stress and Glucocorticoid Resistance In a situation of CMS, the prolonged activation of the HPA axis leads to abnormally elevated cortisol levels. However, chronically elevated cortisol can be dangerous, due to its role in suppressing the immune system and increasing vulnerability to infection. It is possible that in order to counteract the constant influx of circulating cortisol causing potentially unwanted downstream effects, GRs in lymphocytes become unresponsive or resistant to glucocorticoids.This dysfunction of GRs is typically seen in depressed patients and has been shown numerous times using the dexamethasone suppression test (DST). Dexamethasone (a synthetic glucocorticoid) mimics cortisol by binding to GRs and shutting down HPA activity in healthy controls. Therefore, dexamethasone-treated individuals have almost no detectable cortisol over the course of the following day. On the other hand, in depressed patients, the DST doesn’t show any significant repression of HPA activity.Whilst they already show significantly higher overall levels of cortisol, they also show reduced suppression of dexamethasone during the DST. This shows that the GRs are unresponsive to glucocorticoids, leading to the typical feature of glucocorticoid resistance in depressed patients. The Inflammation/Cytokine Hypothesis Glucocorticoid resistance has important implications for immune system function. Under normal acute stress, cortisol suppresses lymphocytes in peripheral tissue from producing pro-inflammatory cytokines by act ivating intracellular GRs and leading to transcription of downstream regulatory genes.Key targets of GR-mediated transcription related to immune function include the upregulation of anti-inflammatory genes annexin-1, IL-10 and I? B? (inhibits NF-? B) and down-regulation of pro-inflammatory cytokine genes, such as IL1-6, 9, 11-13, 16-18 and TNF-?. However, glucocorticoid resistance following chronic stress can mean that lymphocytes stop responding to cortisol, so there is an increase in the proliferation of leukocytes and production of pro-inflammatory cytokines.The proposed mechanism for how these peripherally-generated cytokines are able to affect the central nervous system (CNS) involves several pathways. These cytokines (IL-1? , TNF-? and IL-6) cannot typically diffuse across the blood-brain-barrier, but they can enter the CNS in regions of high BBB permeability or be actively transported across the BBB by endothelial cell transporters. Additionally, without crossing the BBB, cyt okines are able to activate endothelial cells to produce soluble factors (e. g.PG-E2) to indirectly activate neurons, as well as activating certain afferent neurons (e. g. the vagus nerve) that carry information to the CNS about the inflammation. In these ways, peripheral inflammation can cause typical changes in the CNS and ‘sickness behaviour’ seen in depressed patients: lethargy, anhedonia, reduced locomotor activity and sleep and weight disturbances. Support for this proposed mechanism comes from findings that clinically depressed patients show an abnormally high production of pro-inflammatory cytokines (IL-1? IL-6 and TNF-? ), cytokine-based immunotherapy often causes depression in cancer or hepatitis C patients and cytokine administration causes depressive behaviour in animal models. Reversal of this depressive behaviour can be seen by administration of anti-depressants, which target and reduce the inflammatory response in both patients and animal models. In a sim ilar fashion, anti-inflammatories such as cyclooxygenase (COX)-2 inhibitors or omega-3 have strong anti-depressant effects on behaviour. Inflammation-Induced NeurodegenerationAnother approach to modelling stress-induced depression has focused on the controversial findings of clinically depressed patients show changes in volume of structural brain regions, including the hippocampus, amygdala, anterior cingulated, prefrontal cortex and basal ganglia. The mechanisms by which some brain regions, in particular the hippocampus as implicated in stress-induced depression, might decrease in volume appear to be a combination of both neurodegeneration (increased apoptosis of neurons) and a decrease in adult neurogenesis in the subgranular zone of the dentate gyrus (DG).Stress-induced HPA hyper-activity may explain the atrophy seen in some brain regions of clinically depressed patients. Glucocorticoids stimulate the breakdown of tissue into glucose for the quick release of energy; therefore, ch ronically increased levels may result in brain tissue loss in regions where cortisol acts, such as the hippocampus. Furthermore, the link between stress, inflammation and an increase in oxidative stress may also explain a large portion of the neurodegeneration apparent in depression.Inflammation has been shown to increase oxidation and the fact that the CNS has no proper defence against oxidative damage makes it very vulnerable to oxidative stress (OS). This has been demonstrated as a key feature in neurodegenerative diseases and depression, implicating a causal role of stress-induced inflammation in triggering degeneration. The damage caused by OS can lead to mitochondrial dysfunction, which can lead to further intracellular build up of damaging oxidised proteins.The only way for cells to cope in this situation is to activate programmed cell death (apoptosis), or in less controlled circumstances, necrosis can occur, leading to a decline in cell numbers and lateral effects on the ne ural network. This mechanism of oxidative stress-induced neurodegeneration can be slowed down and treated by the application of antioxidant enzymes, which serve a neuro-protective role. These enzymes eradicate free radical oxidising particles and also suppress pro-inflammatory cytokine action.A further damaging feature seen in neurodegeneration and depression is nitrosative stress (NS), which may contribute to neurotoxicity and therefore cell death. An increase in the production of cortisol after acute stress will temporarily cause a suppression of neurogenesis in the DG. Neurogenesis in the DG has been demonstrated to be vital for healthy cognition and memory, impacting mood, the sleep-wake cycle and appetite; all affected in depression. Therefore, CMS leads to prolonged suppression of neurogenesis and may explain the behavioural outcomes typical of depression.The decrease in neurogenesis following exposure to stress may possibly involve the neurotrophin Brain Derived Neurotrophic Factor (BDNF), shown to be greatly reduced in regions that also show a decrease in neurogenesis and related to brain regions typically affected in depression. Animal models exposed to CMS show decreased neurogenesis and BDNF levels in overlapping brain regions and elicit depressive behaviours associated with dysfunction of these regions. Furthermore, anti-depressant treatment that successfully increases BDNF levels also leads to recovery from depressive behavioural symptoms.However, the causation here is not clear; whether the BDNF levels dropping are a result of other stress-induced mechanisms or whether it is partly the cause of the behaviour. Some evidence suggests that anti-depressants can work independently of BDNF restoration. Hagen and colleagues set out to control for possible variables such as age, time of cortisol readings and overall brain volume. Whilst there has been no robust evidence for a link between baseline cortisol levels and hippocampal volume, this study did fi nd that hippocampal volume was negatively correlated with length of depressive episode pre-hospitalisation.Furthermore, better responsiveness (lowering of cortisol levels) after treatment was predicted by greater hippocampal volume (relative to overall brain volume). b) antineurogenic effects and reduced brain-derived neurotrophic factor (BDNF) levels; and c) apoptosis with reduced levels of Bcl-2 and BAG1 (Bcl-2 associated athanogene 1), and increased levels of caspase-3. Stress-induced inflammation, e. g. increased IL-1? , but not reduced neurogenesis, is sufficient to cause depression. Antidepressants a) reduce peripheral and central inflammatory pathways by decreasing IL-1? TNF? and IL-6 levels; b) stimulate neuronal differentiation, synaptic plasticity, axonal growth and regeneration through stimulatory effects on the expression of different neurotrophic factors, e. g. trkB, the receptor for brain-derived neurotrophic factor; and c) attenuate apoptotic pathways by activating Bc l-2 and Bcl-xl proteins, and suppressing caspase-3. It is concluded that external stressors may provoke depression-like behaviours through activation of inflammatory, oxidative, apoptotic and antineurogenic mechanisms.The clinical efficacy of antidepressants may be ascribed to their ability to reverse these different pathways. Neuronal damage and apoptosis Activation of the Kynurenine Pathway (KP) 5-HT Accumulated evidence indicates a role of the hippocampal 5-hydroxy-tryptamine (5-HT) and neuropeptide Y (NPY) in the response to stress and modulation of depression, but it is unclear whether and how the hippocampal 5-HT and NPY systems make contributions to chronic unpredicted mild stress (CUMS)-induced depression.Here we observed that rats receiving a variety of chronic unpredictable mild stressors for 3 weeks showed a variety of depression-like behavioral changes, including a significant reduction in body weight, sucrose preference, and locomotion, rearing and grooming in open fiel d test, and a significant increase in immobility time in forced swimming test. These CUMS-induced behavioral changes were suppressed or blocked by intra-hippocampal injection of 5-HT (31. 25 microg/microl) or NPY (10 microg/microl). These data suggest a critical role of reduced hippocampal 5-HT and NPY neurotransmission in CUMS-induced depression.

A Detective With Whoville Police Department - 805 Words

I am a Detective with Whoville Police Department. I have full police powers and investigate all cases within the city of Whoville. I investigate all crimes and have county and state recourses available for assistance. The first step in the investigation took place when the general manager of the D M food store called the police department to speak with someone in reference to possible employee theft. On February 2, 2016 at 1330 hours, I met with Hugh Downs. He explained to me that he suspected his part time assistant manager, Lowraine James of theft. As the detective assigned to the case, I immediately began an investigation. I asked if the food store had cameras that I could view to see if anything can be seen. I also inquired as to whether the computer history could be checked by appropriate IT personnel. On February 3, 2016, I began reviewing video footage of L. James’s work shift. While viewing the footage, I noticed over the course of James work shift, she would stash cash on the side of the cash register after ringing up several purchases from customers. At the end of her work shift while James was counting monies in the cash drawer, she would separate the money and place some of the money in a bank deposit bag and place the previously stashed cash in a brown paper bag. On several occasions, I also noticed when L. James worked an evening shift, she would carry a medium size box and place it in the trunk of her vehicle prior to the end of her work shift. This took