Thursday, November 28, 2019

How suspense is created and maintained in the opening scene of the matrix Essay Example

How suspense is created and maintained in the opening scene of the matrix Paper The Matrix that was created and produced by the wachowski brothers, was revolutionary at the time that it was created and is still being looked upon for being the pioneer of the camera shot bullet time. It was widely reviewed and was quoted the action film of the millennium by Total Film.One way that the directors create suspense is using visual effects. An example of this is bullet time, a revolutionary idea that involves over one hundred and fifty still cameras to create a slow motion picture that creates suspense and creates a certain aura of mystery when you first see it shown.Another way that the directors create suspense is to choose their locations very easily to try and emphasize the importance and aim of a particular scene. One scene that they achieved this was in the nightclub. The reason that they chose a nightclub was to create a sense of safety in numbers. The packed club is less likely to be attacked because of all the people and therefore is a safer place to talk and s hare information that is exactly what they did.The choice of character plays a big part in the creating of suspense. Two characters that achieve this very well are the Agents and Neo. The Agents appear to show no emotion. They wear very bland clothes and always appear very powerful. The first time that you see the Agents you do not know if they are good or bad and the directors turn tyhis confusion into suspense very well. Neo is also used to create suspense, as he is not the usual action hero. He is not incredibly muscular like other action heros such as Arnold Schwarzenegger. He is also a lot more intelligent than others using brain not brawn which separates The Matrix from other stereotypical action movies.Sound effects and music are used a lot throughout the movie. The use of sound effects can be very useful for setting the tone and scene and the directors of The Matrix have achieved this very well and appropriately. For example, when Trinity is running across the roof tops whil e being chased by the agents and the police. The music that is used in this scene follows the movement of Trinity. Therefore, when she slows down as does the music. In addition, when there is a tense moment the music slows down even further and a different style is music is shown as to make it seem out of the ordinary to what you have been watching. This trick creates more suspense than just the tension of the jump. Another time that they use sound effects is when the numbers came up on the screen. The numbers that appear on the screen are zoomed in and so does the music it makes the brain think that it is being pulled into the numbers. We are then shown a police officers torch. The way that this works is that the numbers are shown by zooming in. The audience focus in on the numbers and they realise the question why are the numbers significant?.A good example of editing is when the typing on the computer monitor wakes up Neo. The computer typing then tells him to follow the white ra bbit. When we are first shown this there is no real significance about a white rabbit, this leaves the audience wondering about how it will become significant. A few moments later, the information becomes noticeable as the director uses a point of view shot to create a sense of importance. At first, you are shown Neo catching his eye on something; you then see the rabbit on the shoulder through the point of view of Neo. Although the point of view shot, is what makes you see what he is seeing without the shot before when you see him notice it the point of view shot would not have had the same effect.Editing is also used after just before this when trinity leaves the matrix. The agents talk amongst themselves and they say the search has already begun the next thing that you see is the computer screen in front of Neo with the word search flashing on the screen to bring attention to it as it is being said as the two scenes mould together. This technique is very effective and the directo r has achieved this very well leaving the suspense building until later on in the story.Colour and lighting also plays a big part in the creating of suspense throughout the whole movie. Probably the best example of this is in the opening sequence. When the police officers run through into a dark room and their torches focus in on Trinity. This gives her the center of attention. The directors have deliberately set this scene in a dark room and by using the directed beam of the torches; they have been able to create a sense of importance around Trinity.Voice-overs are not the best way of creating suspense in my opinion but the directors do use it and they do achieve a certain element of suspense using it. One example of the directors using voice-overs is when Trinity jumps across the rooftops. She makes a giant leap and one of the chasing police officers proclaims thats impossible just those two words bring you closer to the screen in anticipation that she might not be able to make it .Setting and scenery plays a huge part in the creating of suspense and the directors accomplish this very well. A very good example of the use of settings and scenery is when we first see Trinity. This is in a hotel room; it is very and with no distinctive distractions other than Trinity a chair and a laptop. This focuses all attention on where trinity is sitting and on to what she is doing. It is also a very small space that comes into effect when they start fighting as the small space makes the action more intense with only a small space for them to fight in.Another piece of voice over happens right at the start of the film. A total blackout with just to people talking makes you concentrate more on what they are saying. A character that we dont know yet says Morphius believes that he is the one just this simple piece of dialogue insights us a range of different questions who is morphius?, Who is he?, what is the one? and who is it who is speaking?. Even from the start of the of th e movie we are being already in the thick of it trying to work out things that we do not even know about.I feel that the actual plot and dialogue creates the best suspense in the matrix, as without that the other pieces that are used would not make sense. The way that the directors have set out and structured this movie makes it truly brilliant. However, for me it is the plot and the dialogue that separates it from the rest.

Sunday, November 24, 2019

Fun Family History Activities for Family Reunions

Fun Family History Activities for Family Reunions Like many families, you and your relatives may have made plans to get together this summer. What a great opportunity for sharing stories and family history.  Give one of these 10 fun family history activities a try at your next family reunion to get people talking, sharing and having fun. Memory T-Shirts If you have more than one branch of an extended family attending your reunion, consider identifying each branch with a different colored shirt. To further incorporate the family history theme, scan in a photo of the branchs progenitor and print it out on an iron-on transfer with identifiers such as Joes Kid or Joes Grandkid. These color-coded photo t-shirts make it easy to tell at a glance who is related to who. Color-coded family tree name tags offer a more inexpensive variation. Photo Swap Invite attendees to bring their old, historic family photos to the reunion, including pictures of people (great, great-grandpa), places (churches, cemetery, the old homestead) and even previous reunions. Encourage everyone to label their photos with the names of the people in the photograph, the date of the photo, and their own name and an ID number (a different number to identify each photo). If you can get a volunteer to bring a scanner and laptop computer with a CD burner, then set up a scanning table and create a CD of everyones photos. You can even encourage people to bring more photos by offering a free CD for every 10 photos contributed. The rest of the CDs you can sell to interested family members to help defray costs of the scanning and CD burning. If your family isnt very tech-savvy, then set up a table with the photos and include signup sheets where people can order copies of their favorites (by name and ID number). Family Scavenger Hunt Fun for all ages, but an especially good way to get the kids involved, a family scavenger hunt ensures plenty of interaction between different generations. Create a form or booklet with family-related questions such as: What was great-grandfather Powell’s first name? Which Aunt had twins? Where and when were Grandma and Grandpa Bishop married? Is there someone born in the same state as you? Set a deadline, and then gather the family together to judge the results. If you wish, you can award prizes to the people who get the most answers correct, and the booklets themselves make nice reunion souvenirs. Family Tree Wall Chart Create a large family tree chart to display on a wall, including as many generations of the family as possible. Family members can use it to fill in the blanks and correct any inaccurate information. Wall charts are popular with reunion attendees as they help people visualize their place within the family. The finished product also provides a great source of genealogical information. Heritage Cookbook Invite attendees to submit favorite family recipes- from their own family or one passed down from a distant ancestor. Ask them to include details on, memories of and a photo (when available) of the family member best known for the dish. The collected recipes can then be turned into a wonderful family cookbook. This also makes a great fundraising project for the following years reunion. Memory Lane Storytime A rare opportunity to hear interesting and funny stories about your family, a storytelling hour can really encourage family memories. If everyone agrees, have someone audiotape or videotape this session. Tour of the Past If your family reunion is held near where the family originated, then schedule a trip to the old family homestead, church or cemetery. You can use this as an opportunity to share family memories, or go a step further and recruit the clan to clean up the ancestral cemetery plots or research the family in old church records (be sure to schedule with the pastor in advance). This is a particularly special activity when many members are attending from out-of-town. Family History Skits and Reenactments Using stories from your own family history, have groups of attendees develop skits or plays that will retell the tales at your family reunion. You can even stage these reenactments at places that are of importance to your family such as homes, schools, churches, and parks (see Tour into the Past above). Non-actors can get into the fun by modeling vintage clothing or ancestral outfits. Oral History Odyssey Find someone with a video camera who is willing to interview members of the family. If the reunion is in honor of a special event (such as Grandma and Grandpas 50th Anniversary), ask people to talk about the guest(s) of honor. Or, ask questions on other select memories, such as growing up on the old homestead. Youll be surprised how differently people remember the same place or event. Memorabilia Table Set up a table for attendees to bring and display treasured family memorabilia- historic photos, military medals, old jewelry, family bibles, etc. Be sure all items are carefully labeled and the table is always hosted.

Thursday, November 21, 2019

Investigate the root causes of major Engineering disasters that have Essay

Investigate the root causes of major Engineering disasters that have occurred since 1800 - Essay Example In engineering, most disasters that have occurred portray a possibility of overlooking one or more provisions of safety with some being caused by poor decision-making and ignorance. The Chernobyl Power plant disaster The Chernobyl Nuclear power plant disaster of April 26, 1986 although blamed on negligence on the part of operators had some engineering aspects that could have contributed in the disaster, in addition to the operation negligence. The Chernobyl plant used RBMK reactors that have been blamed for a number of negative features that may compromise the safety of the reactors and their operations. The RBMK reactors have neutron fields with high sensitivity levels towards movement of control rods, which results from having a high number of absorbers in the reactor core aimed at compensating for any extra reactivity (Malko, 1991). When some absorbers are withdrawn, especially affecting most of the absorbers in the peripheral zones, there results a local criticality. Moreover, RB MK reactors involve occurrence of huge positive reactivity that leads to a reduction of the period required to achieve stabilization of the power produced at the core to about 3 minutes (Medvedev, 1990). These factors make operations of a RBMK reactor problematic and uncertain in maintaining the safety of the reactor. Frankel (2010) observed that the Chernobyl reactor was designed to use graphite moderators that were typically unsafe, in addition to use of graphite rods. As a result, any possible loss of water in such a RBMK reactor posed great danger. Contrary to the operations of Pressurized Water Reactors (PWR), any water that circulates in the pipe network is only required to serve the purpose of cooling the reactor core only and not to moderate the core and cool it (Frankel, 2010). In PWR reactor cores, removal of the core cooling water would cause the entire chain reaction to abort. However in an RBMK-0100 reactor such as the one used in Chernobyl, in case water is lost due to closure of the supplying pumps as was the case, the graphite moderating rods continue to propagate and facilitate nuclear chain reactions (Frankel, 2010). Such mechanism, when considered alongside the loss of cooling water in the nuclear reactor core, would lead to overheating of the core in the shortest time possible. In such a case, the event of a core meltdown becomes the only possible event. In addition, in the Chernobyl RBMK reactors, the control rods were not designed as drastic safety features. Control rods are necessary for absorbing neutrons towards reducing or stopping chain reactions from taking place. However, in the Chernobyl RBMK reactors, control rods required about 20 seconds to reach the bottom of the core from their highest position (Medvedev, 1991). This was contrary to modern reactors that have well designed control rods, which  require one second or less, to reach the core of a nuclear reactor stopping any chain reaction. Therefore, in Chernobyl nuclear react or, the design and engineering of the entire core overlooked key safety mechanisms that could have prevented possible meltdown. The result of overlooking these safety considerations was the 1986 disaster. This was

Wednesday, November 20, 2019

On what basis should the presence of mental disorder influence Essay

On what basis should the presence of mental disorder influence decisions in the criminal justice system - Essay Example It should be noted that the latter law was abolished during the nineteen sixties; however some individuals may still be liable to such conditions. (UK government, 2008) In the guilty bust insane verdict provided for in the 1883 Lunatics Act, the law states that when a certain individual was accused of a crime and that sufficient evidence is given in order to support those accusations as to make that respective individual guilty, then that person may be found guilty but insane of it was also proven that that respective individual was insane. The special verdict can be passed even when the person under consideration seems to be in good mental health at the time of the trial but it was affirmed that during the process of committing the criminal Act, this was not the case. (The BBC, 1999) Back in the year 1907, The House of Lords held that there should be no appeal against such cases that an accused had in fact committed the act owing to the fact that the suspect does not posses a guilty mind to carry out that Act. The latter decision was validated during Felstead [1914] AC 534. It should be noted that this law was applicable throughout much of this century until the nineteen sixties. At that time, Northern Ireland passed a law of not guilty on the basis of insanity. This was known as the Mental Health Act. Additionally at that time, the Insanity Act of 1964 was passed in England and Wales where a guilty but inane verdict was changed to one known as the guilty by reason of insanity. In the Criminal Appeal Act of England and Wales (1968) it was put forward that there sections 12 and 14 allowed for appeals. On the other hand, there were of appeals against the guilty but insane verdict within Northern Ireland. (Giddens, 1998) In the Criminal Cases Review Commission, there was a need to look into some of the issues to be

Monday, November 18, 2019

Evaluate the social, cultural and political context of the Beatle's Essay

Evaluate the social, cultural and political context of the Beatle's WHITE ALBUM - Essay Example The hairstyle they wore in the first part of their musical career is normally known as the ‘beatle-hairstyle’ (Hecl 2006, p. 5). They also wore round-rimmed glasses, which are referred to as ‘lenonky’ in Czech Republic. It is the type of glasses, which their famous leader, John Lennon, used to wear through the last part of the group’s career and also afterwards. Allusions to their lives and songs are normally replicated in films and TV series and most likely, a number of individuals, who have learned English, have misspelled the phrase ‘beetle’ with an ‘a’ (Hecl 2006, p. 5). The Beatles are considered to have transcended pop music, which became an element of cultural history of the world then and today. In this thesis, I will dwell upon this legendary group as not just a musical, but a cultural phenomenon, as well. The paper will evaluate the social, cultural and political context of the Beatles White Album. In order to make the reader understand the full influence of this album, this paper will also explain their rise to fame against the background of their era and to confirm that their music had an extensive effect on culture generally both in and outside England. The legacy of the 60s has been undeniably very significant for the growth of culture and society in what is usually referred to as ‘civilised nations,’ and the transformations society went through make the 60s one of the most essential parts of the 20th century, as well as a milestone people have to pass by when they endeavour to study the years that came after (Hecl 2006, p. 6). The 60s were in lots of respects ground-breaking. The changes influenced not only the civilised nations (particularly Europe and the United States) but less developed countries in South America and Africa, as well (Keith 2009, p. 15). This paper, however, will dwell on the former. Thus, it is clear that the late 50s and 60s led to significant

Friday, November 15, 2019

Depression and Monoamine Neurotransmitters

Depression and Monoamine Neurotransmitters Depression is no longer seen as a disorder of monoamine neurotransmitters discuss this assertion in the light of the current neurobiological hypotheses of depression The most common mental health disorder not only in United Kingdom but everywhere around the world is depression. Even more disturbing is the fact that depression disorder is estimated to affect around 10% of the people in England. Moreover, approximately 5 to 15 percent of men population and 10 to 20 percent of women population in the USA will suffer from depression during their life. Or to put it more simply, one in five adults worldwide will experience depression at some point of their lives (Kessler et al, 1997). World Health Organization described depression as state of sadness which is accompanied by loss of pleasure or interest in almost every activity. It also includes feelings of guilt, low self-worth, tiredness, poor concentration and disturbed sleep and appetite. According to the criteria of Diagnostic and Statistical Manual of Mental Disorders (DSM) for depression, a person suffers from depression if it experience at least five of the symptoms during the same 2 weeks perio d. These symptoms include depressed mood, loss of interest, weight loss or weight gain, lack of energy, feelings like worthlessness and thoughts of death or suicide etc. Apart from the mental suffering that depression brings, it is also considered as one of the most often reasons for deaths. In 1996 suicide was listed as one of the leading causes of death in the USA (Mireault Deman, 1996). In other words, depression was the reason for more than 30,000 people to take their lives, which was even more than the one infected with the AIDS virus. Even more disturbing is the verifiable truth that most of the investigators believe that the number of deaths because of depression are more than the ones listed due to the fact that those who kill themselves sometimes do it in a way that looks not like a suicide because of depression (Nemeroff, 1998). The financial costs due to depression are also extremely high. Only in UK costs for the economy are estimated at around  £8.6 billion a year. R ecent research revealed that consultations with the GP for treating a depression are estimated at around  £30 million a year and moreover, treating it in hospitals costs more than  £200 million a year. Furthermore, anti-depressants are also one of the leading costs for NHS  £270 million for the last year only (Mentalhealth.org.uk, 2016). Results of recent studies also showed that the major depressive disorder increase the risk of future hearth attack or stroke (McManus, Meltzer, Brugha, Bebbington and Jenkins, 2009). Having explained how important the problem of depression is to our society, it is now important to review the hypotheses and reasons of why people suffer from it. Firstly, this essay will aim to introduce and explain the genetic factors, how the monoamine theory of depression was developed and why in the recent years depression is no longer seen as a disorder of the monoamine transmitters. In addition, this essay aims to discuss how early life stress can increase the risk of depression later in life. One of the oldest explaining of depression provided by researchers is the fact that it runs in families. In other words, geneticist determined that the ones that are blood related to the one suffering from severe depression are much more likely to suffer from this condition too than the general population. Furthermore, family, twin and adoption studies also supported the hypothesis that depression might be inherited (Sanders et al., 1999; Fava and Kendler, 2000). According to the results, around 40% 50% of the risk of depression is on genetic base. Even though the researchers were able to confirm that the risk of depression is partly genetic, there are still many difficulties in finding the vulnerable genes. This is due to the fact that depression is a very complex disorder and it is believed that it involves many genes (Burmeister, 1999). (Nestler et al., 2002). Another reason for the complexity and difficulty in the identifying the faulty gene is that it is also possible that diff erent variants in genes may cause depression in families. Additionally, as the risk of depression is only partly genetic, another important point needs to be considered the nongenetic factors such as individually specific or environmental. Results from a number of studies, including Akiskal (2000) and Fava and Kendler (2000), shed light on the importance of the stress and emotional trauma during the brain development and the importance they have in the etiology of depression. Even though there are a lot of evidences that depression is a stress related disorder, stress itself is not the leading cause of it. As a matter of fact, usually after a stressful event or situations most of the people are not becoming depressed. Indeed, experiencing a serious stress because of physical abuse or rape does not lead to depression but to post-traumatic stress disorder (PTSD). Another important point to consider is also that in general, there are gender differences in the way people respond to a stressor. To put it simply, Kendler, Thornton and Prescott ( 2001) found that even though men and women are more or less equally sensitive to stressful life events, depending on the type of stressor they tend to respond very differently. In their study they revealed that men are much more likely to become depressed after divorce or having troubles in the work place. On the contrary, it was found that women are more likely to have depressive episodes if they have difficulties in relationships, suffer from serious illnesses or death of someone close to them. Having said that, findings again shed the light into the fact that depression is very complex disorder and there are other important factors and mechanisms that need investigation. While genetic researchers continued to look to try to identify the faulty genes, neuroscientists concentrated themselves on the possible brain changes leading to depression. At the beginning most of the work was focused on the neurotransmitters of the monoamine class serotonin, norepinephrine and dopamine in the central nervous system. The reason why researchers became interested in monoamines was because in the early 50s physicians found that depression symptoms appeared in around 20% of patients who were treated with drug reserpine which on the other hand was found to exhaust the supply of the monoamines. In other words, researchers found that these antidepressants were effective for depression as a side effect but they didnt know yet exactly how they worked. Following these results, another research revealed that there is an underlying biological basis for depression and therefore the monoamine hypothesis of depression was proposed. However, it wasnt cleared which of the monoamin es was the most important in depression. At the beginning the theory was called the norepinephrine theory of depression because the scientist thought that the affected neurotransmitter is the norepinephrine. However, several years after the monoamine theory was proposed, there was a research on the hallucinogen lysergic acid diethylamide (LSD) and its action. During the investigation it was revealed that the serotonin receptors are being blocked by the LSD which brought the question whether serotonin might have an important role in the explaining of mood disorders and specifically depression. Therefore, these findings made serotonin the most studied neurotransmitter in the depression disorder. There are several indications that there is an aberrant decreased function of the serotonergic system. The most obvious evidence of reduced serotonin synthesis comes from the studies of Neumeister, Konstantinidis, Stastny et al. (2002) and Neumeister, Nurgent, Waldeck et al. (2004) in which wa s used tryptophan depletion. The results from these studies once again revealed and confirmed that the reduction of serotonin neurotransmitter leads to the development of depressive disorder. Despite the evidences that the studies on serotonin depletion provided, its mechanism in the depressed patients it still unclear. Meyer, Ginovart, Boovariwala et al. (2006) proposed that high amount of monoamine oxidase (MAO) in the brain is one of the reasons that causes the deficiency of the serotonin. Since the hypothesis was proposed various of antidepressants were developed in order to increase the levels of serotonin in the nervous system. However, scientists realized that even though many of the produced antidepressants relieved the symptoms of depression they actually does not affect the serotonin levels. In fact, they were affecting the dopamine, norepinephrine and cholinergic systems but not the serotonin. Furthermore, there were also some drugs that acted only on the norepinephrine system but still they had shown to improve the symptoms of depression. Another important point to consider regarding the serotonin hypothesis is the fact that antidepressants dont work immediately. In fact it can take more than a month to relieve the depression (Onder and Tural, 2002). Therefore, it raises the question if depression is caused because of the low serotonin levels in the brain then why the increasing levels did not change the symptoms right after. Another limitation of the theory i s the fact that the antidepressants does not work on every depressed person. For example recently it was found that antidepressant drugs work in approximately 60 percent of the depressive patients (Gartlehner, Hansen, Thieda, DeVeaugh-Geiss, Gaynes, Krebs, Lux, Morgan, Shumate, Monroe and Lohr, 2007). This again raises the debates whether the low serotonin levels were really responsible for depression. Also, the final problem of the theory is that it is expected that the decreased levels of serotonin in human brain will low the mood. However, several studies were not able to conclude it. Actually, it was found that despite the fact the serotonin is increased by the antidepressants, the lack of serotonin in the brain does not cause the depression (it is like having a stomachache and taking a pill to reduce the pain, however not taking the pill does not mean it started to hurt you because of that), (van der Veen, Evers, Deutz and Schmitt, 2007). Following this discussion it is important to conclude that the depressive disorder is not entirely caused by the serotonin levels in the brain. The monoamine theory of depression does not sufficiently explain the pathology and treatment of depression. It is a fact that human brain is a very complex place and there is a high probability that depression is caused by a combination of factors. Nowadays, it is generally accepted that mood disorders such as depression are definitely occurring as a result of combinations of factors such as genetic, biological and environmental. The discussion above made it clear that the low serotonin levels are not the cause of the depression. Even though antidepressants do not work on everyone, it is essential to examine the other things that these drugs are doing in the brain. Interestingly, recent study has found that the antidepressant drugs not only increase the levels of neurotransmitters in the brain but in fact they can also stimulate the birth of new neuron cells in the brain which is also called neurogenesis (Lucassen, Meerlo, Naylor, van Dam, Dayer, Fuchs, Oomen and Czeh, 2010). Over the past decade, researchers are arising their interest on the fundamental process called neuronal plasticity (or neuroplasticity) which allows the brain to receive information and also to respond in an appropriate way to the same stimuli. The most studied examples of the neural plasticity are learning and memory or in other words the hippocampus of the brain. However, the structures of the brain and the neural plasticity in it can be also activated by various of other stimuli. An example of these include the environmental, pharmacological, social and behavioural. In other words, brain can be stimulated to produce new cells by positive emotions, actions, thoughts etc. These include healthy diet, active lifestyle (sport), good and healthy relationships, sex or in generally being happy stimulate the brain to produce new cells. Pharmacological stimuli such as antidepressant drugs have also been found to increase the formation of new cells and then neurons. On the contrary, bad life style like binge drinking, smoking, having a stressful relationship, poor diet and chronically experience stress is associated with loss and death of brain cells, which on the other hands is believed to play an important role in the pathology of depression. Furthermore, according to the neurogenic hypothesis of depression, the reduced neurogenesis in the adult hippocampus lead to depression symptoms. Controversially, it has been suggested that the increased formation of new neurons in the adult hippocampus is associated with successful treatment of depression disorder. As a matter of fact it rapidly became clear that neural plasticity is one of the most important process that the human brain is able to perform and moreover it is closely associated with most of the functions of the nervous system (Duman, 2004). Having introduced the topic of neurogenesis or neuroplasticity, it is now necessary to look at the factors that suppress the formation of new cells and what influence the formation of the new one. Over the past 25 years a certain amount of excellent reviews have been written on the topic of depression and stress (Kessler, 1997; Paykel, 2003; Monroe Hadjiyannakis, 2002; Tenant, 2002). Many studies revealed that the experience of stress during the development of the brain is highly associated with impact on emotional and cognitive functions (Ammerman, Van Hasselt Hersen, 1991; Fernald Gunnar, 2009). Examples of stress events associated with vulnerability to stress related disorders later in life include poverty, loss of parent, divorce of parents, substance abuse of any of the parents, physical abuse etc. (Repetti, Taylor Seeman, 2002; Halligan, Herbert, Goodyer Murray, 2007; Lupien, McEwen, Gunnar Heim, 2009; Schore, 2000). Post-traumatic stress disorder, depression and anxiety are all stress related disorders which are considered as important part of chronic early life stress (CES) (Heim, Newport, Mletzko, Miller Nemeroff, 2008; Bremner, Southwick, Johnson, Yehuda Charney, 1993; MacMillarn et al., 2001). Interestingly, recent studies proposed that the loss of the neurons in the hippocampus may contribute to the developing of the depressive disorder. As a matter of fact, the hippocampus is one of the parts of the brain where the formation of neurons is a very essential process that takes place during the life of the humans and animals (Eriksson et al., 1998). Many researchers also reported that the neurogenesis in the hippocampus is able to be influenced by several factors one of which is stress (Kempermann et al., 1997; van Praag et al., 1999). In a number of studies was demonstrated that hippocampus plays a significant role in the pathophysiology of the major depressive disorder (Ho and Wang, 2010; MacMillarn et al., 2001). Moreover, in one recent stud y (Ho and Wang, 2010) confirmed the theory using animal models that stress and shock reduce the cells in the hippocampus and also that the long term use of antidepressant treatment can significantly reverse the effect. Another important evidence supporting the neurogenesis theory are the posmortem studies of the hippocampal tissue. By investigating the hippocampal tissue from depressed patients, researchers found reductions in the neuropil network as well as decline in the neurogenesis of the hippocampus (Sheline, Wand, Gado, Csernansky and Vannier, 1996; Sheline, Gado and Kraemer, 2003). Following the evidences that there is a possible link between the stress, depression and neurogenesis in the hippocampus, a study of Malberg, Eisch, Nestler and Duman (2000) aimed to examine whether the treatment with antidepressant drug will influence the neurogenesis in the hippocampus of an adult rat. It is challenging and difficult to create an animal model that can completely represent the symptoms of depression. This is due to the fact that most of the animals do not have self-consciousness, thinking abilities and most importantly they are not able to indicate the symptoms of the depressive disorders such as the depressed mood, the low self-esteem, the suicidal desires etc. However, many mental disorders including depression, consists endophenotypes which allows to be evaluated in animals. Examples of these endophenotypes that can be observed in the animal model of depression are anhedonia, changes in appetite, behavioural hopelessness, weight gain, changes in sleep etc. (Hasle r et al., 2004). Moreover, brain responses to stress is similar in rodents (Lupien, McEwen, Gunnar and Heim, 2009).   So, in order to examine the effect that antidepressants have on the neurogenesis Malberg, Eisch, Nestler and Duman, (2000) examined adult rats. During the experiments, different kinds of antidepressant drugs were used for a period of 28 days. In order to find out the effects of the drugs on the cells there were two group of rats. In short, to one of the group was given antidepressant and to the other vehicle. To label the dividing cells, four days after the last antidepressant drug treatment rats were given a thymidine analog bromodeoxyuridine (BrdU) and one of them were killed after 24 hours (to measure the cell proliferation) and the other one were killed after another 28 days (to determine the phenotype). The results of the study revealed that continuously treatment with antidepressants increases the formation of new neurons in the hippocampus part of the brain of an adult rats. Another very important finding that this study demonstrated is the fact that antidepressants are increasing the neurogenesis after a chronic treatment (28 days) and not a straight after the intake of the drug (short term).   These results are also consistent with the results of several similar studies (Santarelli, Saxe, Gross, Surget, Battaglia, Duman et al., 2003;). Furthermore, few recent studies also examined the effects that antidepressant drug therapies have on the cognitive functions of healthy humans. Results in one of the studies (Mowla et al., 2007) demonstrated that antidepressants positively influence the memory and other cognitive functions in the old patients that have cognitive problems. Several other researchers also demonstrated that antidepressant drug treatment of depression is associated with improvements in memory and also the cognitive functions (Allain et al, 1992). To summarize, the neurogenesis theory has been supported by many researchers that also include animal studies. As stated earlier, antidepressant drugs were found to increase not only the levels of the neurotransmitters in the brain (serotonin, norepinephrine and dopamine) but also to increase the formation of the new cells in the brain on in other words the neurogenesis. It is generally widely known that during the life of a person new neurons are growing in the hippocampus. On the other hand, it was also found that stress is able to reduce the neurons in the hippocampus of the brain. However, nowadays there are a lot of evidences that taking antidepressant drugs for at least month will significantly increase the neurogenesis in the brain which at the same time will reduce the depression symptoms. In contrasts with the monoamine theory, neurogenesis theory takes the right amount of time to have an effect on the brain. Furthermore, many researchers are now trying to investigate the pa rt that neurogenesis plays in depression disorder. This at the same time will help to increase the production of new cells directly, rather than focusing the antidepressants on the neurotransmitters. However, there are still many debates whether there are real changes in the neurogenesis in the brain of the people suffering from depression (Werry, Enjetu, Halliday, Sachdev and Double, 2010). Further investigation of the neuroplasticity and the antidepressant treatments will lead to better understanding of the disorder and the development of new treatments. References Akiskal, H. (2000). S27.05 Temperamental dysregulations in mood disorders. European Psychiatry, 15, p.s268. Ammerman, R., Van Hasselt, V. and Hersen, M. (1991). Parent-Child Problem-Solving Interactions in Families of Visually Impaired Youth. Journal of Pediatric Psychology, 16(1), pp.87-101. Allain H, Lieury A, Brunet-Bourgin F, Mirabaud C, Trebon P, Le Coz F et al (1992). Antidepressants and cognition: comparative effects of moclobemide, viloxazine and maprotiline. Psychopharmacology (Berl) 106: S56-S61. Bremner, J., Southwick, S., Johnson, D., Yehuda, R. and Charney, D. (1993). Childhood physical abuse and combat-related posttraumatic stress disorder in Vietnam veterans. The American Journal of Psychiatry, 150(2), pp.235-239. Burmeister, M. (1999). Basic concepts in the study of diseases with complex genetics. Biological Psychiatry, 45(5), pp.522-532. Duman, R. (2004). Neural plasticity: consequences of stress and actions of antidepressant treatment. Pharmacological aspects, pp.157-166. Eriksson, P., Perfileva, E., Bjork-Eriksson, T., Alborn, A., Nordborg, C., Peterson, D. and Gage, F. (1999). Neurogenesis in the adult human hippocampus. Nat Med, (4), pp.1313-1317. Fava, M. and Kendler, K. (2000). Major Depressive Disorder. Neuron, 28(2), pp.335-341. Fernald, L. and Gunnar, M. (2009). Poverty-alleviation program participation and salivary cortisol in very low-income children. Social Science Medicine, 68(12), pp.2180-2189. Halligan, S., Herbert, J., Goodyer, I. and Murray, L. (2007). Disturbances in Morning Cortisol Secretion in Association with Maternal Postnatal Depression Predict Subsequent Depressive Symptomatology in Adolescents. Biological Psychiatry, 62(1), pp.40-46. Heim, C., Newport, D., Mletzko, T., Miller, A. and Nemeroff, C. (2008). The link between childhood trauma and depression: Insights from HPA axis studies in humans. Psychoneuroendocrinology, 33(6), pp.693-710. Ho, Y. and Wang, S. (2010). Adult neurogenesis is reduced in the dorsal hippocampus of rats displaying learned helplessness behavior. Neuroscience, 171(1), pp.153-161. Kendler, K., Thornton, L. and Prescott, C. (2001). Gender Differences in the Rates of Exposure to Stressful Life Events and Sensitivity to Their Depressogenic Effects. American Journal of Psychiatry, 158(4), pp.587-593. Kessler, R. (1997). THE EFFECTS OF STRESSFUL LIFE EVENTS ON DEPRESSION. Annual Review of Psychology, 48(1), pp.191-214. Konstantinidis, A., Stastny, J., Ptak-Butta, J., Hilger, E., Winkler, D., Barnas, C., Neumeister, A. and Kasper, S. (2002). Intravenous mirtazapine in the treatment of depressed inpatients. European Neuropsychopharmacology, 12(1), pp.57-60. Kempermann, G., Kuhn, H. and Gage, F. (1997). More hippocampal neurons in adult mice living in an enriched environment. Nature, 386(6624), pp.493-495. Lupien, S., McEwen, B., Gunnar, M. and Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), pp.434-445. Lucassen, P., Meerlo, P., Naylor, A., van Dam, A., Dayer, A., Fuchs, E., Oomen, C. and Czà ©h, B. (2010). Regulation of adult neurogenesis by stress, sleep disruption, exercise and inflammation: Implications for depression and antidepressant actionà ¢Ã‹Å"† . European Neuropsychopharmacology, 20(1), pp.1-17. MacMillan, H., Fleming, J., Streiner, D., Lin, E., Boyle, M., Jamieson, E., Duku, E., Walsh, C., Wong, M. and Beardslee, W. (2001). Childhood Abuse and Lifetime Psychopathology in a Community Sample. American Journal of Psychiatry, 158(11), pp.1878-1883. Malberg, J., Eisch, A., Nestler, E. and Duman, R. (2000). Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. Neurosci, 20, pp.9104-9110. Meyer, J., Ginovart, N., Boovariwala, A., Sagrati, S., Hussey, D., Garcia, A., Young, T., Praschak-Rieder, N., Wilson, A. and Houle, S. (2006). Elevated Monoamine Oxidase A Levels in the Brain. Archives of General Psychiatry, 63(11), p.1209. Monroe, S. and Hadjiyannakis, K. (2002). The social environment and depression: focusing on severe life stress. Gotlib Hammen, pp.314-40. Morgan, L., Gartlehner, G., Richard, H., Thieda, P., DeVeaugh-Geiss, A., Krebs, E., Monroe, L. and Lohr, K. (2012). P-1102 Comparative effectiveness of second generation antidepressants in the pharmacologic treatment of adult depression. European Psychiatry, 27, p.1. Mowla A, Mosavinasab M, Pani A (2007). Does fluoxetine have any effects on the cognition of patients with mild cognitive impairment? A double-blind, placebo-controlled, clinical trial. J Clin Psychopharm 27: 67-70. Mireault, M., DeMan, A. (1996). Suicidal ideation among older adults: Personal  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚  Ãƒâ€šÃ‚   variables, stress and social support. Social Behavior and Personality, 24, 385-392. Mentalhealth.org.uk. (2016). Mental health statistics: the most common mental health problems. [online] Available at: https://www.mentalhealth.org.uk/statistics/mental-health-statistics-most-common-mental-health-problems [Accessed 4 Dec. 2016]. McManus S., Meltzer H., Brugha T., Bebbington P., Jenkins R. (2009). Adult Psychiatric Morbidity in England 2007: results of a household survey. NHS Information Centre for Health and Social Care. [online] Available at: http://www.hscic.gov.uk/pubs/psychiatricmorbidity07 [Accessed 15 Dec 2016]. Nestler, E., Barrot, M., DiLeone, R., Eisch, A., Gold, S. and Monteggia, L. (2002). Neurobiology of Depression. Neuron, 34, pp.13-25. Neumeister, A., Nugent, A., Waldeck, T., Geraci, M., Schwarz, M., Bonne, O., Bain, E., Luckenbaugh, D., Herscovitch, P., Charney, D. and Drevets, W. (2004). Neural and Behavioral Responses to Tryptophan Depletion in UnmedicatedPatients With Remitted Nemeroff, C. (1988). The neurobiology of aging and the neurobiology of depression: Is there a relationship?. Neurobiology of Aging, 9, pp.120-122. Major Depressive Disorder and Controls. Archives of General Psychiatry, 61(8), p.765. Nemeroff, C. (1988). The neurobiology of aging and the neurobiology of depression: Is there a relationship?. Neurobiology of Aging, 9, pp.120-122. ÃÆ'-nder, E. and Tural, U. (2002). Faster response in depressive patients treated with fluoxetine alone than in combination with buspirone. Journal of Affective Disorders, 76(1-3), pp.223-227. Paykel, E. (2003). Life events and affective disorders. Acta Psychiatr Scand, 108(3), pp.61-66. Sanders, A., Detera-Wadleigh, S. and Gershon, E. (1999). Molecular genetics of mood disorders. In Neurobiology of Mental Illness, pp.299-316. Tennant, C. (2002). Life events, stress and depression: a review of recent findings. Australian and New Zealand Journal of Psychiatry, 36(2), pp.173-182. van der Veen, F., Evers, E., Deutz, N. and Schmitt, J. (2007). Effects of Acute Tryptophan Depletion on Mood and Facial Emotion Perception Related Brain Activation and Performance in Healthy Women with and without a Family History of Depression. Neuropsychopharmacology, 32(1), pp.216-224. Van Praag, H. (2005). The World Journal of Biological Psychiatry. 2(5), p.22. Repetti, R., Taylor, S. and Seeman, T. (2002). Risky families: Family social environments and the mental and physical health of offspring. Psychological Bulletin, 128(2), pp.330-366. Santarelli, L., Saxe, M., Gross, C., Surget, A., Battaglia, F., Duman, R., Daluwa, S. and Weisstaub, N. (2003). Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants. Science, 301(5634), pp.805-809. Schore, A. (2000). Attachment and the regulation of the right brain. Attachment Human Development, 2(1), pp.23-47. van Praag, H., Kempermann, G. and Gage, F. (1999). Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus. Nat Neurosci, 2, pp.226-270. Werry, E., Enjeti, S., Halliday, G., Sachdev, P. and Double, K. (2010). Effect of age on proliferation-regulating factors in human adult neurogenic regions. Journal of Neurochemistry, 115(4), pp.956-964. Y. I. Sheline, P.W.Wang,M. H. Gado, J. G. Csernansky, and M. W. Vannier (1996), Hippocampal atrophy in recurrent major depression,. Proceedings of the National Academy of Sciences of the United States of America, vol. 93, no. 9, pp. 3908-3913. Y. I. Sheline, M. H. Gado, and H. C. Kraemer (2003), Untreated depression and hippocampal volume loss, American Journal of Psychiatry, vol. 160, no. 8, pp. 1516-1518.

Wednesday, November 13, 2019

CSU Chico Research paper :: essays research papers fc

  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   Chico State University Chico State University is a school for a student that is in search of being successful in his/her life. It is a school that can open up a student and help them find what they would want to be, by providing the useful classes of tomorrow. These classes are top-notch and can keep people motivated to work harder, and to strive for their goal†¦ And motivation is something that just about everyone needs.   Ã‚  Ã‚  Ã‚  Ã‚  Chico State University is a college located in Chico, California. Chico State was founded in 1887. â€Å"General John Bidwell, pioneer, statesman, and founder of Chico, donated eight acres of cherry orchard, and construction began on Chico State Normal School.†(â€Å"CSU History†). With out his donation, CSU would not be in existence. In 1890, the school finally opened with ninety student and five teachers. In 1935, Chico School became Chico State College. And then in 1972, Chico State College was changed to a California State University, hence the name â€Å"Chico State University.† The property of CSU has also expanded to one hundred and nineteen acres. On top of that, CSU has eight hundred acres of farmland, and two hundred and forty acres of rangeland. The school colors are cardinal and white, and CSU proudly holds the mascot of the wildcat—small, cunning, agile, the wildcat represents every student that attends CSU. The sports at C SU consist of: track and field, men and women’s basketball, baseball, softball, men and women’s soccer, volleyball, men and women’s golf, and cross county. The men’s baseball team is more notably known for 2004’s CCAA and West Region Championship victories. And the women†¦Lets just say they are putting up a great effort in all of their sports. But the girls teams are not the only teams trying, the CSU Athletic Community as a whole is trying their hardest. The CSU has two types of on-campus housing that they offer—village and residential. The apartment fees are seven thousand four hundred and ninety three dollars for a resident room. For the thematic living program, it costs four thousand nine hundred and ninety nine dollars. The â€Å"apartments are comfortable, affordable, and convenient--the ideal place to live for first-time Chico State students†(â€Å"Housing†). Something like that, should help a student in the choosing of whether or not they would want to go to the college†¦But that is based if the student’s last requirement was how the housing was.