Descriptive Essay on Why Many People Have Pets

Descriptive Essay on Why Many People Have Pets Why Do Many People Have Pets? People decide to buy pets in different situations and for different reasons. Each purchase of pet has its own history and emotions behind, which is also very interesting feature of this reality. I will try to describe the most wide-spread situations and understand the major motives that drive people towards the purchase. Some people want to make new friends so as not be alone. They usually have not very sociable character, or just get into situation when their friends are far away, for instance, when moving to another city or country. In case of elderly people, they also get pets not to feel alone, as their children have already grown up and moved away. This motive is rather clear, to my mind, as a human cannot live outside society – he is either its part, or a loner, who, actually, usually has some pets as company. Another reason for buying pets is the necessity to care about someone. It is another interesting peculiarity of human psychology, and it originates from people’s desire to feel that he is needed and valued by someone. On the whole, it is one of the main missions of people– to bring new life into this world and care about it. But children grow so quickly that people satisfy this need only for about 15 years for each child, which is only a small part of our lives. And pets in this situation can be a perfect option. Besides, a lot of people just like pets – the way they look, behave and love their owners. Almost each person has his own favorite pet; tastes differ, but the motives are still the same. Of course, there are

Accuracy of Bayley Scores as Outcome Measures in Trials of...

Introduction Long-term follow-up of high risk preterm infants has become increasingly important as the proportion of infants surviving has increased steadily over the past several decades. It is well known that these infants are at increased risk of cognitive impairment. (Class) With this increase in at risk survivors, many clinical research questions arise that can only be answered by long-term follow-up studies. (Vohr, Teune) Clinical trials that examine common perinatal therapies should also include a long term follow-up component in their research to examine later neurodevelopmental outcomes in their cohorts. Although there is no prescribed protocol dictating which specific neurodevelopmental tests are to be completed during follow-up, the Bayley Scales of Infant and Toddler Development and all its revisions, is the most widely used test to assess neurodevelopment of very preterm infants in the first three years of life (Luttikhuizen) and is a common outcome measure used in clinical researc h trials. Standardized developmental assessments such as the Bayley that are used in a pediatric clinical trial setting as primary outcome measures need to be reliably administered and scored. Trained test administrators and scorers are generally careful that the tests they are administering are conducted and scored correctly. However, given the range of numerical calculations and transcriptions required in scoring the results of these tests, there is always a chance that errors

Stephen Cranes Red Badge of Courage as Bildungsroman Essay

Stephen Cranes Red Badge of Courage as Bildungsroman In the Red Badge of Courage, by Stephen Crane, the main character Henry Fleming joins the army as a young fledging and ultimately matures to a courageous soldier ready for battle. The Red Badge of Courage is considered a Bildungsroman since the reader traces Henry’s development morally, psychologically, and intellectually. Henry progresses from a feared youth who in the course of a couple of days, in the line of fire, has crossed the threshold to manhood. Henry Fleming’s growth is demonstrated after the first battle when he becomes mentally stronger and surmounts his fear of being a coward. Henry Fleming is a romantic dreamer, inspired by visions of a chivalric†¦show more content†¦He had not been aware of the process. He had slept and awakening, found himself a knight (Hart).† Henry’s hopes and confidence are suddenly crushed when the enemy reappears and Henry finds himself running from his post with the others and his worst fears are realized in this testimonial. Henry is still in the stages of development and although he overcomes his first testimonial, he still is a â€Å"fresh fish† in many ways. Henry suffers from shame when he realizes that his comrades have all held in line. Henry tries to justify with himself that he did the natural thing: run. This was what the squirrel did when he threw a pine at it and it was only natural to run to steer away from danger. Later, Henry encounters the tattered soldier and several men who display their â€Å"red badge of courage.† Henry wishes he had a wound displaying courage. The only wound Henry possesses is in his soul since he has such low self-esteem. It is the death of Jim Conklin, the epitome of courage, that makes Henry begin to realize the realities of war as he is beginning to e ncounter more with death. â€Å"The red sun was pasted in the sky like a wafer (Crane, 71).† The sun seems to be a symbol of Jim’s wound and of courage (Solomon). The death of Jim Conklin represented Henry’s childhood and the tattered soldier represents Henry’s idealized self, which is dying. Henry is deserting the image he had of himself before he joinedShow MoreRelatedRed Badge of Courage Essay1271 Words   |  6 PagesTo Be or Not to Be†¦ A Man The Red Badge of Courage written by Stephen Crane is a prime example of bildungsroman, or a coming of age story. Crane begins with a cowardly boy, Henry Fleming, and ends with an experienced war hero who has learned not just what war really is, but who he really is. Mark Twain once said, â€Å"The fear of death follows from the fear of life. A man who lives fully is prepared to die at any time.† [Epigraph] Although he struggles to learn that being a soldier means more thanRead MoreSymbolic Meaning of the Land in Gone with the Wind6993 Words   |  28 Pages1949 she was killed in a car accident crossing Peachtree Street in Atlanta. Gone with the Wind differs from most Civil War novels by appreciating the South and depreciating the North. Other popular novels about the Civil War, such as Stephen Cranes The Red Badge of Courage, are told from a Northern perspective and tend to exalt the Norths values. Mitchells novel is unique also for its portrayal of a strong-willed, independent woman, Scarlett OHara, who has many same characteristics with Mitchell

Evidence for and against the Serotonin Hypothesis of Depression

Question: Discuss About Evidence For And Against The Serotonin Hypothesis Of Depression? Answer: Introduction The fundamental idea stating the cause of depression as a serotonin imbalance within the body elicits a discussion that can be justified as a hypothesis, which adequately deserves ample evidence to either support or dispute. The serotonin hypothesis of depression, from Dr. Schildkraust in 1965, states that low levels or lack of serotonin within the brain causes depression, a condition that could be treated by antidepressants. The hypothesis, when compared to an earlier belief, is presently discussed that the mood disorders occurring repetitively in depression are brain infections or disorders that result from a variety of factors such as various degrees of biological, genetic and environmental factors that gradually change in the brain (Sanders, 1988). The serotonin hypothesis of depression over the years has stated that low levels of serotonin in the brain nerve cells cause depression. It has led to the development of antidepressant medication such as the Selective Serotonin Reuptake Inhibitors (SSRIs). SSRIs work to maintain a high level of the neurotransmitter serotonin in the nerve cells of the brain by inhibiting its re absorption into the cells releasing it (Moreno and Kramer, 2002). According to Paul Andrews (2004), a professor of psychology and neuroscience at Mc Master University in Canada, the hypothesis might be incomplete since depression patients often find it hard to recover from the serotonin boosting medications. Many scientists have refuted the use of SSRIs in treatment of depression because when you accurately analyze their use, they put an obstacle in the path towards the recovery of a depressed patient instead of helping them. It occurs because, instead of them helping people to overcome depression, they interfere with the mechanisms of recovery within the brain (Louie and Meltzer, 2004). A decrease in the levels of serotonin (5-HT) has been hypothesized as the main pathogenic factor resulting to depression for almost half a century. SSRIs increase the levels of serotonin in the nerve cell spaces known as the synapses in a quick manner. In spite of this, the effect of the antidepressant will take many weeks to develop. According to Paul Andrews (2004), SSRIs work in repairing damage in the brain by the use of hormones and stress chemicals, a gradual process that takes several weeks (Louie and Meltzer, 2004). Moreover, Clomipramine, a tricyclic antidepressant (TCA), showed a similar antidepressant efficacy with other TCAs. It stopped the serotonin uptake with a higher affinity of more than 100 folds and above than other inhibitors by the noradrenalin uptake. Such pharmacological studies have supported and facilitated the hypothesis of depression. This clinical observation of an increase in the release of serotonin contributes to an anti depressant effect that has been repeatedly supported .Nevertheless, for instance, the efficacy of SSRIs versus placebos(slow) may be strong in a moderately depressed in comparison to severely depressed patients (Sanders, 1988). It is difficult to quantify the amount of serotonin used and released in a safe way by the human brain. This can be estimated from evidence about serotonin levels metabolized by the brain and by inferences from animal studies. The best evidence against the hypothesis of depression states that not less but more serotonin is used and released during an episode of depression. This is to say that patients are left in worse conditions after using antidepressants. Furthermore, many forms of depression are beneficial adaptation to stress and are natural thus this might be against the serotonin hypothesis of depression and the use of antidepressants (Louie and Meltzer, 2004). Meltzer and Louie (1987) argue that a pharmacological lessening of the functions of serotonin enhances depression; nevertheless, the primary cause cannot be entirely attributed to serotonin deficiency. In the scientific literature and the lay media, it is frequently assumed that serotonin deficiency causes depression. This theoretically attractive assumption might be an overgeneralization or be premature. Clinical presentations of depression are wide since they include various syndromes which were initially separate and various disease aspects especially in melancholic versus an endogenous depression ( Meltzer and Louie, 1987, p. 136). In such clinical manifestations that are diverse, depression could represent various overlapping sources of pain that arise from unique and distinct causes. Moreover, symptomatology in depression can also arise from diverse neurological (for example the Alzheimers disease), endocrine (Cushing disease) and immunological causes (e.g. interferon treatment). Stressors of life such as social isolation, financial difficulties, childhood trauma and job insecurity are also significant factors in depression that demonstrate the importance of the environment in depression ( Mannl , 1989). In the past 40 years , several anomalies in regards to putative biomarkers of the central serotonin functions have been repeatedly reported in patients with depression, indicating that a deficiency in serotonin could be evidenced in depression especially the severely depressed or in suicidal patients. Iproniazid, a drug developed to treat tuberculosis, surprisingly showed an antidepressant activity in patients diagnosed with TB and who concurrently suffered from depression. Clinical studies indicated that Iproniziad inhibited the monoamine oxidase (MOA) enzyme A and B. These enzymes are responsible in metabolizing serotonin and subsequent monoamines .Furthermore; it also increased the serotonin concentrations in the brain thus helping in supporting the serotonin hypothesis of depression (Louie and Meltzer, 2004). Tryptophan Levels. In many clinical studies, an acute depletion of tryptophan leads to a frequent occurrence of mild depression symptoms even after treatment with antidepressants, this occurs by lowering the serotonin levels in the brain thus it can be a fundamental aspect in supporting the hypothesis. Tryptophan depletion in the brain is somehow a non-selective tool in probing the hypothesis, furthermore, its studies were not effective in alleviating depression (Fairburn and Smith, 1997). Tryptophan is an amino acid which most likely affects protein synthesis. The decrease in its levels probably affects the brain and mood by starving pathways of metabolism for example by impairing the kynurenic acid synthesis or neurobiological and quinoline substances.50 percent of patients diagnosed and treated with interferon alpha develop symptoms of depression after treatment. Another evidence that correlates with this study indicates that interferon alpha enhances the induction of indole amine 2, 3 dioxygenase, thus leading to the decrease in levels of tryptophan in the brain, therefore decrease in serotonin is involved herein (Fairburn and Smith, 1997). Another drug Imipramine, a tricyclic antidepressant (TCA) prototype, was originally developed to treat schizophrenia but unluckily, the drug failed and it did not induce its antipsychotic effect but favorably showed actions against depression symptoms in patients with schizophrenia. Consequently, imipramine was successfully adopted to induce the antidepressant effect on the body. In the 1960, chemical studies showed that other TCAs and imipramine blocked the serotonin reuptake .Within that same period, reports indicated that the precursors of serotonin, induced antidepressant effects and increased the brain serotonin levels in study animals (Fairburn and Smith, 1997). It has been reported that in particular patients, depression is precipitated by chronic depletion of serotonin due to vesicular monoamine transport inhibitor, reserpin. In high doses, it depletes extracellular and storage levels of serotonin, noradrenalin, and dopamine making it consistent to ascribe depressogenic effects of reserpine to one neurotransmitter. Studies have indicated that the link between depression and chronic reserpine treatment remains contentious. Studies done later on chronic reserpine treatments indicated less frequent depressogenic effects, a factor in varying the findings could be attributed to the differential schedules of dosing. In addition to that, chronic reserpine induces a weak antidepressant effect rather than a pro-depressant effect, so the cause of disagreement still lies in establishing whether the probability of depression is elicited by the deficiency of serotonin in neurotransmission (Stanley, 1985). Biomarkers or indirect measures have been used to probe for the brains serotonin system integrity over the last four decades. A primary metabolite of cerebrospinal fluids serotonin is 5 hydroxyindoleacetic acid. It reflects the levels of 5-HIAA utilized as an index of neurotransmission within the brain. Studies have indicated a correlation between depression and low levels of CSF 5- HIAA and regarded them as inconsistent. The finding that is more robust is the relationship between aggression, suicidality or impulsivity with low 5 HIAA (Stanley, 1985). Acute stimulation of serotonin triggers a secretion of hormone prolactin, there is a complex mechanism involved in the release of the hormone, which is not defined. It appears that the mechanism involved includes oxytocin neurotransmitters .The amount of prolactin in the plasma increases fenfluramine, a brain serotonin biomarker, that challenges prolactin, where lower serotonin levels reflect a blunted response by the hormone ( Stanley, 1985). In depressed patients, low 5HIAA indicates that there is a minimal response of plasma prolactin to fenfluramine. Furthermore, inhibiting plasma prolactin due to activation of fenfluramine is more insightful in severely depressed patients. In addition to that, aggression and suicidality are also present. Increased cortical receptors, 5HT2AR of serotonin have been associated with depression, there is also a link between an increase in frontal 5 HT2ARs receptors and suicide. In contrast to this, there is a decrease in hippocampal receptors 5HT2ARs in chronic depressed people therefore indicating that necessarily, up regulation of serotonin receptors does not occur in depressed patients. A large groups of scientists report a lack of association in the levels of frontal cortex 5HT2ARr and suicide (Louie and Meltzer, 2004). In conclusion, the serotonin hypothesis might not be wrong or true but it might be incomplete. The association of serotonin levels with depression as the primary syndrome is not entirely conclusive. Considering the diversity of symptoms, disease severity in patients and the numerous etiology that underlie depression as a syndrome, its extremely difficult to associate depression to a particular body mechanism such as serotonin depletion within the brain. Nevertheless, when we shift focus to the analysis of severe depression or suicidality, an association of serotonin biomarker findings suggest that the serotonin deficiency could be linked to depression in some populations but the link does not essentially prove to be the cause. SSRI antidepressants reveal a superiority that is convincing over placebos entirely in depression that is severe while in adult depressed patients, studies indicate that antidepressants have the least effect against depression. It is therefore much persuading to include a hypothesis on serotonin deficiency (lack or a low level) as significantly a causal factor in particular subsets of depression patients and not completely all cases of depression. 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Journal of Clinical Psychiatry. 51 (1), 5-1. Sanders, B. E. (1988). The serotonin receptors. New Jersey: Clifton Press. Smith, W.K. (1987). The stress analogy. (1st Edition). New York: Mc Graw Hill. Stanley, M. (1985). Correlations between aminergic metabolites simultaneously obtained from human CSF brain. Journal of Life Science, 37 (12), 79-86. Steward, 0. (1988). Principles of cellular molecular and developmental neuroscience. New York: McGraw Hill.