Birth Mark By Hawthorne Essays - The Birth-Mark, Nathaniel Hawthorne

Birth Mark By Hawthorne Nathaniel Hawthorne wrote a time of great change in America. In the mid-nineteenth century, Americans began to experience a shift in focus from the once stringent religious outlook to a more scientific view of the world and its natural wonders. Americans, however, did look at these new scientific discoveries with much hesitation, questioning their long-term effects on society as a whole. Hawthorne' s work, "The Birth Mark echoes these sentiments and combine natural faith with a confidence in science to make a very interesting tale. This tale and its morality convey a message to the reader that there is a price for tampering with the natural order of things. This story opens by explaining how educated and knowledgeable Aylmer is, and the narrator even suggests that he may have the power to alter nature. " We know not whether Aylmer possesses this degree of faith in man's ultimate control over nature (Birthmark, 1262 )."As Aylmer tries to use science to alter nature, or in this case, the birthmark on his wife's cheek, his plan backfires and his wife dies. The death of Georgiana shows that knowledge is dangerous if used in the wrong way. The influence of the evolution of culture has caused men to educate themselves, and learn extensive amounts about science. However, some men like Aylmer take advantage of their intelligence and try to play the role of God. Aylmer allowed his mind to consume his heart, resulting in the senseless death of his beautiful wife. Culture teaches men that if they learn enough that they can manipulate nature; however, in the Birthmark, Hawthorne shows that intelligence still can't overcome nature and thus culture is self-destructive. The fact the whole story is about removing a physical flaw from Georgiana's face when she is already obviously beautiful demonstrates the degree to which Aylmer has allowed this pursuit of knowledge and culture to destroy his ability to perceive nature's beauty. In this text, Georgiana and her birthmark represent nature, and culture is represented by Aylmer. Culture has taught men to question the flaws of women that they once found intriguing, therefore Aylmer is challenging nature when he tries to remove it. Aylmer is so wrapped up in this culture that he treats Georgiana as property. Her opinion about the removal of the birthmark was of little concern to him. Therefore, culture asserts that it is not only a separate entity from nature but that it has superior qualities. Because of Aylmer's belief that culture is superior to nature, the Creator of nature and culture alike chose to punish him. The punishment was not in an effort to be vengeful, but to show him what should have been important to him was not the birthmark on Georgiana's face, but the beauty that she possessed both inside and out that made him desire to spend the rest of his days with her. "...he failed to look beyond the shadowy scope of Time, and living once and for all in Eternity, to find the perfect Future in the present (Birthmark, 1273);" therefore, he was forced to spend eternity without the one that truly loved him?unconditionally. Bibliography Michelson, Bruce. Norton Anthology of American Literature. The Birtmark, pp1261-73.

Today, our world is faced with many diseases. Some Essays

Today, our world is faced with many diseases. Some Essays Hiv Today, our world is faced with many diseases. Some havent been discovered and some have no cures. The immune system fights off many of these diseases, but what happens when it fails us? One of the most deadly, incurable disease the world is faced with today is the Human Immunodeficency Virus (HIV). There is no none cure yet. Viruses cause colds and the flu. Viruses are microscopic particles that invade the cells of plants, animals, fungi, and bacteria. They often destroy the cells they invade. How do viruses reproduce? A virus first enters a cell in one of three ways: direct penetration, endocytosis, or membrane fusion. The virus takes over the cells machinery and is thus forced to make the viruss proteins and RNA. When the virus has entered, viral RNA is released in to the cell and reverse transcriptase occurs. Reverse trancriptase is when the cell makes a DNA copy of the viral RNA. It then produces the proteins and genes the virus needs to be assemble. The virus can then be released by three ways: lytic, lysogenic, and persistent. A virus, although not considered to be alive, does have a life cycle. First the virus attaches to a cell, which it recognizes by its surface markers. Then it penetrates the cell and gets inside. Next, it replicates and makes copies of itself. It then assembles itself back together and the new viruses are released. A virus cannot replicate by itself; it has to infect a cell. The virus is always the same size. It doesnt have a metabolism. A virus has three different shapes it can be: helical, polyhedral, and enveloped. It is made up of nucleic acid (RNA or DNA), and surrounded by a protein coat. Certain viruses can survive harsh conditions. Pathogens, disease-causing agents, have to enter the body to cause illness. There are several ways for them to get into the body: through the genitals, breaks in the skin, and natural openings. The immune system usually stops these invaders from getting in. The primary way to stop pathogens is by the skin. But, the skin has natural openings where they can get in. The eyes, ears, nose, mouth, and genitals are all natural openings. The second line of defense is at these natural openings. The pathogens get stuck in the mucus lining of the nose and mouth or are killed by the saliva and stomach acids; tears from the eyes; earwax; and acidic secretion of the vagina all stop pathogens but they dont get them all. The third line of defense is the Tortiory Response. There are two different kinds, innate (which you are born with and is non-antigen specific and acquired (which you acquire through life and is antigen specific). Innate has three different reposes to it. The first: phagocytic cells eat live viruses, bacteria and, dead cells. The second: natural killer cells are non-specific and destroy all infected cells. The third: interferon binds to the surface of surrounding healthy cells and activates their genes to create an antiviral state. Acquired immunity has different parts to it: macrophages (ingest viruses and expresses information to other cells; intructs and recognizes), T4-cells (instruct), T8-cells (respond), B-lymphocytes (respond), and lymphokines (rate control). There are two different kinds of acquired immunity: humoral and cell mediated. The humoral response involves the production of antigen-specific antibodies. Those antibodies neutralize he virus, help macrophages ingest and T8-cells to destroy it, and cause the destruction of the viral envelope. Colonal selection is part of the humoral response. The T4-cells get the right B-cells and activate them. The B-cells produce antibodies quickly then start to divide. Once they divide, they are called plasma cells and are able to produce 2,000 antibodies per second for 4-5 days. The cell-mediated response develops T8-cells that destroy host cells that have been infected already. T8-cells can tell the difference between regular and infected cells. HIV is a very deadly disease. There are certain risk behaviors associated with the disease. HIV is mainly transmitted by sexual contact or either by IV drug use. Anal sex carries a higher risk of getting it than vaginal or oral sex. The probability is 1/33 to 1/10 people. Vaginal intercourse also caries a high risk. Male to female

International Financial Reporting Standards Essay - 4

International Financial Reporting Standards - Essay Example As such, it does not outline an industry specific platform that guides and regulates its style of reporting. The existence of financial reporting standards acknowledged across the global platform, such as IFRS, is important especially to multinational corporations and global companies that operate in different countries across the world, with subsidiaries and interests in countries with different approaches to financial accounting and reporting. Therefore, the existence of such internationally acknowledged reporting standards enables these corporations to consolidate their financial statements, especially when returning the profits from subsidiaries to the parent company. A good example of such a multinational corporation that has overseas subsidiaries is the MacDonald’s Chain of Restaurants, whose mother company is in the united states but is has a global presence with its restaurants located in major markets across the world such as Asia and Europe. Despite the numerous benefits that come about to international corporations with their use and application of the IFRS guidelines, its application is not so efficient as an accounting practice because it acts merely as a guideline and not as a rule, or a principle, which accountants should follow and adhere to when preparing and reporting financial statements. This rule out the possibility of all companies applying these standards in their reporting and preparation of financial statements because there is no legal means of enforcing these standards. The lack of a strict enforcement mechanism makes it very difficult for international companies to apply IFRS principles in accounting. As such, these companies only follow these rules out of choice, especially because they want to achieve a global look, rather than following the formalities. However, if in the event these companies, especially the multinational

Event Evaluation -Netowrking Event Essay Example | Topics and Well Written Essays - 4000 words

Event Evaluation -Netowrking Event - Essay Example How long did planning the event take? Well the answers were explained in the following context. The following factors were help to illustrate clearly how they planned for the big event within the allotted time. The plan is the event! The key aspect that was considered when in the course of planning for the event was its ability to be successful. This is at the very best considered basing on virtual realities and constraints. Obviously, there were a number of hurdles and numerous challenges that would make the entire plan a nightmwere. To be able to truly achieve their target, they should be able to ensure that all elements were managed at various levels whereby it would be easier to control inputs and outputs. The core factor when they were considering time is to establish the goal of the entire arrangement and then proceed to draw the framework for the work to be done. Acquire adequate service orientation:-This would enable them to device the scenarios involved in acquiring the righ t services and it is worth creating a more definite organizational structure and from then they could build a more flexible planning technique (Ramsborg et al. 2008). With substantial inclusion of various requirements such as acquiring accessories, getting logistical information and assembling the necessary themes for the event, all schedules were correlated through the approximated layout scheduling process. Define organization capacity and flexibility: - The obvious approach to their organization is their ability to operationalize and internalize all the activities with due diligence and to easily get the right way towards establishing the right attributes. In that, they were be able to make all important aspects regarding the plan without having to get any difficulty as the entities needed for the events were always listed basing on important interests. Additionally, the planning process is exponentially maintained within the required capacity whereby the energy and interest is e xplained and recreated to enhance optimum arrangements as required by the resources available and the amount of services needed by the client. The good thing here was that in the Performance Hub, there was an ideal venue for the creation of music, dance or drama, as well as being suited to conferences and corporate events. The Performance Hub is a highly flexible venue and this was evident in the way the organisation of the event was tailored to showcase the capacity and organizational flexibility due to its tailor made state of the art facilities especially made for such events. For instance to show how versatile the event organizational capacity was, there was the options of several venues that included the following: The Black Box Theatre: The Black Box Theatre is one of the best-equipped small theatres in the country. Ideally suited to small performances, the theatre features a raked seating area and high quality acoustics. The 108 seat venue is fully equipped with lighting and sound equipment to support your performance. The theatre has double height loading doors allowing you to bring your set directly into the venue. The Performance Hub can also offer support with a functional box office and catering provision on request. Technical support can

Innovation Management Essay Example | Topics and Well Written Essays - 500 words

Innovation Management - Essay Example Spin-Brush, a unique electric toothbrush received this protection from the United States government that kept it flourishing over its competitors over a great period of time. This right has kept away the many competitors in the market from using the design and packaging of Spin-Brush thereby making the product to remain relevant and outstanding in the market. The ‘try-me’ design in which Spin-Brush has been devised attracts most customers to it and probably many firms would want to exploit that so they could also drive in many consumers. This has been protected by the patent rights that Osher received. Patent has also made it easy to license it with companies such as Crest. Its value has continued to be high since many competitors are kept away from altering it making it be the only product with those features. Customers therefore find it conspicuous compared to other products due to packaging and design. Companies are likely to respond in different ways as they try to counter-neutralise the domination of Spin-Brush so that they may remain relevant in the competitive industry. There is a possibility of lowering the prices of electric brushes that previously sold at higher prices than that of Spin-Brush in order to attract customers. Also, companies are likely to mount promotional campaigns to create awareness concerning their products in the markets (Fox, 2013:147). Spin-Brush producers need to increase even more their advertisements and field demonstrations showing how efficient their product is. A counter-promotional strategy would work best to minimise rise of these other competitive companies since the design and packaging in which Spin-Brush is made favours it over other players in the industry. Other inventions are more likely to come up in areas that are not covered by the patent right such as technological know-how behind the production. Consequently, the

Effect of Adolescent Cannabis Use on Brain Functions

Effect of Adolescent Cannabis Use on Brain Functions Cannabis Use During Adolescence: A Review of Impacts on Brain Functions and Associated Outcomes Recent years have seen a dramatic increase in the social acceptability of cannabis usage in the United States, with several states having already legalized recreational use of the substance and several more projected to do so within the next several years (Leyton, 2016).   Concurrently, there has been an increase in the amount of adolescents who report using cannabis, with recent data indicating that 39% of high school seniors report using cannabis within the past year and 6-7% reporting daily or near daily cannabis use (Johnston & O’Malley, 2015).   Despite increasing utilization of cannabis products for pain management and other ailments (Hwang & Clarke, 2016), some in the scientific community have expressed concern about the potential ramifications of recreational legalization of cannabis.   Chief amongst these concerns is the idea that adolescents will have very easy access to increasingly potent cannabis and synthetic cannabis products (Sobesky & Gorgens, 2016), as a great deal of research has indicated that the use of cannabis poses several risks specific to individuals in the adolescent age range (see Levine, Clemenza, Rynn, & Lieberman, 2017).   This paper will summarize the research examining the impact of cannabis use on the developing adolescent brain and potential associated outcomes, particularly in the areas of cognition/executive function, anxiety and depression, psychotic disorders, and future substance use/dependence.   The Adolescent Brain To understand the impact of cannabis use on the developing adolescent brain, it is first necessary to understand the changes taking place in the brain during this developmental period.   Not surprisingly, the period of adolescence is a time of tremendous change in the circuitry of the brain.   According to Arain et al. (2013), there is a significant amount of neuronal plasticity in the brain during adolescence, meaning the â€Å"wiring† of the brain is extremely adaptable to learning and experience.   Such plasticity, particularly in the prefrontal cortex, lends itself to difficulty thinking rationally and critically, often leading to the impulsive decision-making that is characteristic of the adolescent years.   In addition, the hypothalamic pituitary adrenal (HPA) axis, the system responsible for regulating human responses to stress, also undergoes significant development during the period of adolescence.   Within this system, the amount and duration of adrenocorti cotropic hormone (ACTH) and glucocorticoids released in response to stress increase significantly as compared to other life periods (Romeo, 2013).   Shortly before puberty, a â€Å"surge† of synaptogenesis and neuronal growth occurs in which grey matter in the brain thickens substantially.   From this point throughout the period of adolescence, the brain is continually rewired through dendritic pruning and increased myelination of synapses, particularly in the prefrontal cortex (Arain et al., 2013; Lubman, Bonomo, & Yucel, 2007).   In addition, white matter increases are seen in the corpus callosum (Arain et al., 2013).   Taken together, these changes increase the efficiency of communication within the brain, allowing for the eventual development of more complex cognitive functioning, including improved impulse control, operational thinking, and working memory (Hart, 2007; Lubman et al., 2007).   In addition to the constant rewiring of brain circuitry that occurs during adolescence, the levels of three neurotransmitters – dopamine, serotonin, and melatonin – change during the adolescent period (Arain et al., 2013).   According to Dahl (2003), dopamine and serotonin levels decrease during adolescence, resulting in emotional dysregulation, mood disruptions, and difficulties with impulse control.   Melatonin levels, on the other hand, increase, which in turn increases the amount of sleep that adolescents need to be fully â€Å"re-charged.†Ã‚     Given the massive changes that are occurring in the brain during the period of adolescence, it is a time in which the brain is especially susceptible to the use of substances, (Lubman et al., 2007) including cannabis.   Cannabis’ Action in the Brain Before discussing the specific impacts of cannabis use on the adolescent brain, it is important to understand how cannabis acts in the brain in general.   First, the brain has an endogenous cannabinoid system (endocannabinoid system) made up of the ligands anandamide and 2-arachidonoyl glycerol (2-AG) and cannabinoid receptors known as CB1 and CB2 receptors (Moreira & Lutz, 2008).   CB1 receptors are located throughout the brain, but are particularly populous in the front region of the cerebral cortex, the basal ganglia, the cerebellum, the hypothalamus, the anterior cingulate cortex, and the hippocampus; CB2 receptors are generally found throughout the body’s immune system (Hill et al., 2010; Iversen, 2004).   The endocannabinoid system plays a role in a number of processes, including the regulation of the HPA axis stress response (Hill et al., 2010; Lee & Gorzalka, 2015), neural plasticity, and learning and memory (Lu et al., 2008).   According to Iversen (2004), the psychoactive component in cannabis is Δ9-tetrahydrocannabinol (THC).   THC, as well as increasingly popular synthetic cannabinoids, act as agonists on CB1 cannabinoid receptors in the brain.   Because CB1 receptors are generally presynaptic rather than postsynaptic, cannabinoids control the release of certain neurotransmitters, including acetylcholine, L-glutamate, ÃŽ ³-aminobutyric acid (GABA), noradrenaline (norepinephrine), dopamine, and 5-hydroxytryptamine (5-HT).   The use of exogenous cannabinoids, such as marijuana or synthetic marijuana products, leads to an unnaturally long-lasting activation of CB1 receptors, ultimately inhibiting the release of the aforementioned neurotransmitters in selected areas of the brain (Iversen, 2004).   In addition to its impact on CB1 receptors and associated neurotransmitters, THC also appears to trigger the firing of dopaminergic neurons in the ventral tegmental area of the brain and the nucleus accumbens – areas of the brain that are heavily implicated in the brain’s reward circuit associated with drug use.   This effect is also seen with heroin, cocaine, amphetamines, and nicotine, suggesting that THC may also act on the opioid receptor system within the brain (Iversen, 2004). Impact on Cognition and Executive Function Tasks The literature has focused on several larger areas of impact regarding cannabis use during adolescence, one of these being the potential impacts on cognition and tasks of executive function.   As previously mentioned, the brain undergoes a significant amount of change in the adolescent years, including the frequent re-wiring of neural connections through neural pruning processes, particularly in the prefrontal cortex.   According to Filbey, McQueeny, DeWitt, and Mishra (2015), cannabis use during adolescence disrupts this normal pruning process through its modulation of neurotransmitters and inhibition of microglial processes.   This results in abnormal connectivity within the brain, including a decrease in white matter volume and integrity (Gruber, Dahlgren, Sagar, Gonenc, & Lukas, 2014; Jacobus et al., 2009). Such changes result in a number of cognitive impacts, including increased impulsivity, poorer reaction times, and increased errors on executive function tasks (e.g., planning, organization, self-regulation, etc.) (Becker, Wagner, Gouzoulis-Mayfrank, Spuentrup, & Daumann, 2010; Gruber et al., 2014).   Indeed, studies have indicated that individuals who begin marijuana use in early adolescence are at an increased risk for developing deficits in attention (Ehrenreich et al., 1999) and visual processing (Tapert, Granholm, Leedy, & Brown, 2002), and exhibit a decreased full scale IQ and verbal IQ in adulthood (Meier et al., 2012).   Memory also appears to be affected by adolescent-onset cannabis use (Tait, Mackinnon, & Christensen, 2011), likely via its impact on the hippocampus – a part of the brain heavily implicated in memory functions.   Animal research has shown that the hippocampus is affected by cannabis use especially during the period of adolescence.   In rats, adolescent exposure to cannabis impacted the microstructure of the hippocampus as well as abnormalities in the way that proteins are expressed in the hippocampus (Quinn et al., 2008).   Specifically, it appears that exogenous cannabinoids bind to CB1 receptors and inhibit the release of glutamate, thus contributing to deficits in short-term memory (Hart, 2007) and negatively impacting performance on memory-related tasks (see Levine et al., 2017).   Some animal studies indicate that lower levels of cannabis use (those most reflective of the actual amount that adolescents use) are not predictive of long-lasting hippocampal changes.   However, because current cannabis products are continuing to increase in potency (Levine et al., 2017), hippocampal changes and subsequent memory problems are topics of concern, especially with regard to adolescent users of cannabis.   Working memory also appears to be impacted by cannabis use, particularly in individuals that began using cannabis before the age of sixteen.   Becker et al. (2010) used functional magnetic resonance imaging to examine performance on a working memory task in individuals who began using cannabis before age sixteen (early-onset) as compared to individuals who began using cannabis after the age of sixteen (later-onset).   Results of this study indicated that early-onset cannabis users exhibited increased cortical activity in the parietal lobe as compared to later-onset cannabis users.   The researchers concluded that this increased cortical activity indicated decreased cortical efficiency in response to challenging working memory-related tasks in early-onset, but not later-onset, cannabis users (Becker et al., 2010).   Such findings are consistent with a number of studies indicating that an earlier age of onset of cannabis use is associated with greater risk of negative impacts on cognitive functioning during adulthood (Ehrenreich et al., 1999; Fontes et al., 2011; Meier et al., 2012; Pope et al., 2003).   Impact on the Development of Anxiety and Depression Several studies indicate a connection between adolescent-onset cannabis use and the development of both anxiety and depressive disorders (e.g., Brook, Rosen, & Brook, 2001; Degenhardt et al., 2013; Fairman, 2015; Hayatbakhsh et al., 2007; Patton et al., 2002; van Laar, van Dorsselaer, Monshouwer, & de Graaf, 2007).   Though past researchers have speculated about the directionality of this relationship, studies have consistently indicated that adolescent-onset depression is not predictive of later cannabis use (e.g., Degenhardt, Hall, & Lynskey, 2003; Moore et al., 2007; Womack, Shaw, Weaver, & Forbes, 2016), negating the idea that depressive and/or anxiety symptoms lead to engagement in cannabis use as a method of symptom relief.   Instead, such findings promote the idea that cannabis use during adolescence, in combination with other potential risk factors, increase the risk for the development of anxiety and depressive symptoms in adulthood (Levine et al., 2017).   As with the cognitive changes discussed in the previous section of this paper, it is early-onset use of cannabis that appears to be riskiest with regard to the development of future anxiety and depressive symptoms (Hayatbakhsh et al., 2007; Patton et al., 2002).   In an interesting study by Spechler et al. (2015), fMRIs were used to examine activity in the amygdalas of adolescent users of cannabis.   The researchers showed participants images of both angry and neutral faces, a well-known test of amygdala activity and a well-regarded index of emotional processing.   Results of this study indicated that compared to the control group, adolescent cannabis users exhibited increased amygdala activity in response to the images of angry faces whereas the control group showed the same amount of amygdala activity when shown images of neutral faces.   Spechler et al. (2015) concluded that adolescent cannabis use is associated with increased hypersensitivity to negative affect.   However, in this case, the directionality of the relationship is unclear: it is possible that the sensitivity of the amygdala pre-dated the cannabis use and the cannabis use was engaged in due to its anxiolytic effect.   Conversely, it is possible that cannabis use led to increased sensitivity in the amygdala.   Either way, it appears that adolescent cannabis users are overly sensitive to negative affect and the potential threat that accompanies it, which may explain the increased incidence of depressive and anxious symptomatology in this population.    There are several potential neurobiological mechanisms explaining the relationship between adolescent cannabis use and the development of anxiety and depressive symptoms.   One possibility is the impact of exogenous cannabinoids on the HPA axis system.   The endocannabinoid system regulates the responsivity of the HPA axis, which, as previously mentioned, undergoes significant development during the adolescent years (Hill et al., 2010; Lee & Gorzalka, 2015; Romeo, 2013).   Studies with both human and rodent subjects have indicated that the use of exogenous cannabinoids during adolescence has the capacity to alter HPA axis stress responses, thus impacting emotionality and the development of anxiety-related symptoms (Lee & Gorzalka, 2015).   Lovelace et al. (2015) discuss another neurobiological mechanism that may underlie the relationship between adolescent cannabis use and the development of anxiety and depression.   In a rodent study, these researchers examined maladaptations in the prefrontal cortex due to cannabis use by looking at presynaptic plasticity at glutamatergic synapses in adolescent rats.   The results indicated that exposure to exogenous cannabinoids during adolescence led to over-activation of CB1 receptors, which led to permanent changes in synapses in the prefrontal cortex.   Overall, mice exposed to exogenous cannabinoids during adolescence showed a loss of presynaptic plasticity, which impacts the brain’s ability to adapt to changing environments and thus may contribute to an increased vulnerability of psychopathology during adulthood (Lovelace et al., 2015).   In an interesting rodent study conducted by Rubino et al. (2008), researchers found that exposure to THC during adolescence was associated with decreased density and function of CB1 receptors in the ventral tegmental area, the nucleus accumbens, and the amygdala.   These areas of the brain are implicated in emotional processing and reward and are thus implicated in the development of depressive symptomatology.   The behavior of the rats in this study also mirrored depressive symptomatology.   Specifically, rats exposed to THC during adolescence exhibited both â€Å"behavioral despair† (which the researchers defined as time the rats were immobile) and anhedonia (as measured through decreased consumption of sucrose).   Taken together, it appears that several neurobiological mechanisms are at play in the connection between adolescent cannabis use and the development of anxiety and depressive symptoms.   Impact on the Development of Psychotic Disorders A substantial body of literature has indicated a connection between the use of cannabis during adolescence and the later development of psychotic disorders (e.g., van Os et al., 2002; Henquet et al., 2005; Stefanis et al., 2004).   This is especially true for individuals who are already genetically predisposed to develop psychotic disorders (Henquet et al., 2005) though the connection has also been found in individuals that do not have this genetic predisposition (van Os et al., 2002).   As with the impact on cognition and on anxiety/depressive symptoms, it appears that early-onset cannabis use (Arseneault et al., 2002; Moore et al., 2007) as well as heavier (i.e. daily or near-daily) use pose the greatest risk for the later development of a psychotic disorder (Moore et al., 2007; van Os et al., 2002). Rubino and Parolaro (2014) discuss the possible neurobiological mechanisms behind the connection between adolescent cannabis use and the development of psychotic disorders.   In general, it appears that the use of exogenous cannabinoids during adolescence disrupts the maturational processes occurring in the brain during this time, especially in the hippocampus and the prefrontal cortex – two areas of the brain that are implicated in the psychotic disorder schizophrenia, in particular.   The endocannabinoid system itself undergoes a significant amount of change during the adolescent years; thus, exogenous cannabinoid exposure during this time period has the potential to alter the long-term functionality of CB1 receptors, which then impacts the activity of several neurotransmitters implicated in psychotic symptomatology, especially dopamine (Rubino & Parolaro, 2014). Additionally, being exposed to cannabis during the adolescent period has been shown to disrupt prepulse inhib ition (the ability to accurately perceive and process stimuli) and down-regulate GABAergic activity in the prefrontal cortex – both symptoms commonly seen in individuals with schizophrenia (Morales-Muà ±oz et al., 2014; Zamberletti et al., 2014).  Ã‚   As previously mentioned, individuals who have a genetically predisposed vulnerability to develop psychotic disorders are at an especially high risk to do so if they engage in cannabis use during adolescence (Henquet et al., 2005).   For example, individuals who have a specific variant of the gene for catechol-O-methyltransferase (COMT), which breaks down dopamine – the neurotransmitter implicated in schizophrenia – are at a much higher risk for developing the disorder if they used cannabis during adolescence as compared to individuals who do not have that specific variant of the gene for COMT (Caspi et al., 2005).   Another gene that influences the relationship between adolescent cannabis use and psychosis is the ATK1 gene, which affects dopamine breakdown in the striatum.   According to DiForti et al. (2012), cannabis users with a certain variant of the ATK1 gene were seven times more likely to develop psychosis as compared to individuals with this gene variant w ho did not use cannabis.   Clearly, in individuals that already possess these specific genetic variants, cannabis use during adolescence can be the trigger that leads to the expression of these genes and the development of psychotic symptoms and/or disorders.   In addition, adults with psychotic disorders who used cannabis during adolescence are at a greater risk for relapse of psychotic symptoms, poorer adherence to treatment, and increased rates of hospitalization related to their diagnosis (Hunt, Bergen, & Bashir, 2002; Lewis, Tarrier, & Drake, 2005; Wade et al., 2006).   Impact on the Future Development of Substance Use Disorders   Several studies have indicated a link between adolescent cannabis use and the later development of a substance use disorder.   Again, this relationship is especially strong for individuals that engage in cannabis use in early adolescence and who engage in heavy (i.e., daily or near-daily) use (Fergusson, Boden, & Horwood, 2006; Hall & Lynskey, 2005; Stuart & Green, 2008).  Ã‚   Past researchers have speculated upon various explanations for this trend, including the so-called ‘gateway hypothesis.’   In general, the ‘gateway hypothesis’ assumes that individuals who use â€Å"harder† drugs such as heroin and cocaine almost always started their use of substances with using cannabis, and that this link is explicitly causal (Van Gundy & Rebellon, 2010).  Ã‚   This hypothesis is based on research findings indicating that the use of cannabis during adolescence often predates the use of other illicit substances, including heroin, methamphetamines, and cocaine (Fergusson et al., 2006).   Though the causality of this link has been repeatedly questioned in the literature (e.g., Morral, McCaffrey, & Paddock, 2002; Van Gundy & Rebellon, 2010), many researchers have attempted to explain the mechanisms behind the early use of cannabis and the later use of other substances and/or development of a substance use disorder.   There are countless potential psychosocial explanations for this connection (e.g., peer pressure, propensity toward risk-taking behaviors, availability of substances, etc.); however, for the purposes of this paper, the potential neurobiological mechanisms behind the connection will be discussed. The major possible neurobiological mechanism behind the connection between early cannabis use and the later development of a substance use disorder has to do with the effect of cannabis on the brain’s opioidergic system.   A great deal of animal research has indicated that the endocannabinoid system and the opioidergic system are intricately linked.   For example, Pickel, Chan, Kash, Rodriguez, and Mackie (2004) and Rodriguez, Mackie, and Pickel (2001) found that CB1 receptors and  µ opioid receptors are found on the same neurons in both the striatum and the ventral tegmental area, and Cossu et al. (2001) and Ledent et al. (1999) found that animals without CB1 receptor genes do not self-administer opioids. Drawing upon this clear connection between the endocannabinoid and opioidergic brain systems, Ellgren, Spano, and Hurd (2007) investigated the hypothesis that cannabis exposure during adolescence changes opioid-related neural functions and leads to increased likelihood of later opioid use.   Findings of this research confirmed that rats exposed to THC during the adolescent period self-administered greater amounts of heroin compared to the control group.   Moreover, findings indicated that rats exposed to THC in adolescence showed a persistent disturbance in the activity of enkephalin, which is the endogenous opioid neuropeptide associated with reward behaviors and hedonic states.   Findings also indicated that THC exposure led to changes in the functions of  µ opioid receptors such that heroin use was more reinforcing (via dopamine release) for rats exposed to THC during adolescence as compared to the control group.   Taken together, these results indicate that cannabis use during adolescence leads to a greater vulnerability to the reinforcing effects of opioids during adulthood, potentially leading to a greater risk for dependence and likelihood of relapse of substance use disorders.   Conclusion Despite the increasing popularity of cannabis use, both for medicinal and recreational purposes (Hwang & Clarke, 2016; Leyton, 2016), it is important to consider the resulting increased availability of cannabis to individuals during the sensitive period of adolescence.   Given the profound changes occurring in the brain during adolescence (Arain et al., 2013; Dahl, 2003; Hart, 2007; Lubman et al., 2007), teenagers are particularly susceptible to the influence of substances, which may lead to lasting changes in the brain’s functioning.   Such changes are associated with poor outcomes in several areas, including deficits in performance on executive function tasks (Becker et al., 2010; Ehrenreich et al., 1999; Fontes et al., 2011; Gruber et al., 2014; Meier et al., 2012; Pope et al., 2003; Tapert et al., 2002), an increased risk for the development of anxiety and/or depressive symptoms (Brook et al., 2001; Degenhardt et al., 2013; Fairman, 2015; Hayatbakhsh et al., 2007; Patt on et al., 2002; van Laar, van Dorsselaer, Monshouwer, & de Graaf, 2007), an increased risk for the development of a psychotic disorder (Arseneault et al., 2002; Caspi et al., 2005; DiForti et al., 2012; Henquet et al., 2005; Moore et al., 2007; Rubino & Parolaro, 2014; Stefanis et al., 2004; van Os et al., 2002), and an increased risk for future substance use/dependence (Fergusson et al., 2006; Hall & Lynskey, 2005; Stuart & Green, 2008).   Such considerations may have important implications for policy development related to the legalization of cannabis.   References Arain, M., Haque, M., Johal, L., Mathur, P., Nel, W., Rais, A., Sandu, R., & Sharma, S. (2013). Maturation of the adolescent brain. Neuropsychiatric Disease and Treatment, 9, 13. Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search-proquest-com.proxyiub.uits.iu.edu/docview/1364721614?accountid=11620 Arseneault, L., Cannon, M., Poulton, R., Murray, R., Caspi, A., & Moffitt, T. E. (2002). Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study.  Bmj,  325(7374), 1212-1213. Retrieved from https://scholar.google.com/scholar?hl=en&as_sdt=0%2C15&q=Cannabis+use+in+adolescence+and+risk+for+adult+psychosis%3A+longitudinal+prospective+study&btnG= Becker, B., Wagner, D., Gouzoulis-Mayfrank, E., Spuentrup, E., & Daumann, J. (2010). The impact of early-onset cannabis use on functional brain correlates of working memory.  Progress in Neuro-Psychopharmacology & Biological Psychiatry,  34(6), 837-845. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1016/j.pnpbp.2010.03.032 Brook, J. S., Rosen, Z., & Brook, D. W. (2001). 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A., Dahlgren, M. K., Sagar, K. A., Gà ¶nenà §, A., & Lukas, S. E. (2014). Worth the wait: Effects of age of onset of marijuana use on white matter and impulsivity. Psychopharmacology, 231(8), 1455-1465. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1007/s00213-013-3326-z Hall, W. D., & Lynskey, M. (2005). Is cannabis a gateway drug? testing hypotheses about the relationship between cannabis use and the use of other illicit drugs.Drug and Alcohol Review,  24(1), 39-48. doi:http://dx.doi.org/10.1080/09595230500126698 Hart, H. (2007). Alcohol, drugs, and the adolescent brain.  Developmental Medicine and Child Neurology,  49(12), 883. Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search-proquest-com.proxyiub.uits.iu.edu/docview/195605999?accountid=11620 Hayatbakhsh, M. R., Najman, J. M., Jamrozik, K., Mamun, A. A., Alati, R., & Bor, W. (2007). Cannabis and anxiety and depression in young adults: A large prospective study.  Journal of the American Academy of Child & Adolescent Psychiatry,  46(3), 408-417. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1097/chi.0b013e31802dc54d Henquet, C., Krabbendam, L., Spauwen, J., Kaplan, C., Lieb, R., Wittchen, H., & Van Os, J. (2005). Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people.  BMJ: British Medical Journal,  330(7481), 11. doi:http://dx.doi.org/10.1136/bmj.38267.664086.63 Hill, M. N., Patel, S., Campolongo, P., Tasker, J. G., Wotjak, C. T., & Bains, J. S. (2010). Functional interactions between stress and the endocannabinoid system: From synaptic signaling to behavioral output.  The Journal of Neuroscience,  30(45), 14980-14986. doi:http://dx.doi.org/10.1523/JNEUROSCI.4283-10.2010 Hunt, G. E., Bergen, J., & Bashir, M. (2002). Medication compliance and comorbid substance abuse in schizophrenia: Impact on community survival 4 years after a relapse.  Schizophrenia Research,  54(3), 253-264. doi:http://dx.doi.org/10.1016/S0920-9964(01)00261-4 Hwang, J. K., & Clarke, H. (2016). Cannabis and pain: A review.  Journal of Pain Management,  9(4), 395-413. Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search.proquest.com/docview/1949290907?accountid=11620 Iversen, L. (2004). How cannabis works in the brain. In D. Castle, & R. Murray (Eds.),  Marijuana and madness: Psychiatry and neurobiology; marijuana and madness: Psychiatry and neurobiology  (pp. 19-40, Chapter xvi, 218 Pages) Cambridge University Press, New York, NY. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1017/CBO9780511543630.004 Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search-proquest-com.proxyiub.uits.iu.edu/docview/620584373?accountid=11620\ Jacobus, J., McQueeny, T., Bava, S., Schweinsburg, B. C., Frank, L. 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In  International review of neurobiology  (Vol. 125, pp. 49-84). Academic Press.   Retrieved from https://www-sciencedirect-com.proxyiub.uits.iu.edu/science/article/pii/S0074774215000987?_rdoc=1&_fmt=high&_origin=gateway&_docanchor=&md5=b8429449ccfc9c30159a5f9aeaa92ffb Levine, A., Clemenza, K., Rynn, M., & Lieberman, J. (2017). Evidence for the risks and consequences of adolescent cannabis exposure.  Journal of the American Academy of Child & Adolescent Psychiatry,  56(3), 214-225. http://dx.doi.org.proxyiub.uits.iu.edu/10.1016/j.jaac.2016.12.014 Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search-proquest-com.proxyiub.uits.iu.edu/docview/1875567972?accountid=11620 Lewis, S. W., Tarrier, N., & Drake, R. J. (2005). Integrating non-drug treatments in early schizophrenia.  The British Journal of Psychiatry,  187, s65-s71. doi:http://dx.doi.org/10.1192/bjp.187.48.s65 Leyton, M. (2016). Legalizing marijuana. Journal of Psychiatry & Neuroscience, 41(2), 75-76. http://dx.doi.org.proxyiub.uits.iu.edu/10.1503/jpn.160012 Retrieved from http://proxyiub.uits.iu.edu/login?url=https://search-proquest-com.proxyiub.uits.iu.edu/docview/1819128922?accountid=11620 Lovelace, J. W., Corches, A., Vieira, P. A., Hiroto, A. S., Mackie, K., & Korzus, E. (2015). An animal model of female adolescent cannabinoid exposure elicits a long-lasting deficit in presynaptic long-term plasticity.  Neuropharmacology,  99, 242-255. doi:http://dx.doi.org/10.1016/j.neuropharm.2015.04.034 Lu, A. T., Ogdie, M. N., Jà ¤rvelin, M., Moilanen, I. K., Loo, S. K., McCracken, J. T., McGough, J. J., Yang, M. H., Peltonen, L., Nelson, S. F., Cantor, R. M., & Smalley, S. L. (2008). Association of the cannabinoid receptor gene (CNR1) with ADHD and post-traumatic stress disorder.  American Journal of Medical Genetics Part B: Neuropsychiatric Genetics,  147b(8), 1488-1494. doi:http://dx.doi.org/10.1002/ajmg.b.30693 Lubman, D., Bonomo, Y., & Yucel, M. (2007).   Drug use in young people; short-term effects and long-term harms. In Gilvarry, E., & McArdle, P. (Eds.).   Alcohol, Drugs, and Young People: Clinical Approaches, Clinics in Developmental Medicine No. 172. London: Mac Keith Press, pp. 18-50.   Meier, M. H., Caspi, A., Ambler, A., Harrington, H., Houts, R., Keefe, R. S. E., MacDonald, K., Ward, A., Poulton, R., & Moffitt, T. E. (2012). Persistent cannabis users show neuropsychological decline from childhood to midlife.  PNAS Proceedings of the National Academy of Sciences of the United States of America,  109(40), E2657-E2664. doi:http://dx.doi.org/10.1073/pnas.1206820109 Moore, T. H. M., Zammit, S., Lingford-Hughes, A., Barnes, T. R. E., Jones, P. B., Burke, M., & Lewis, G. (2007). Cannabis use and risk of psychotic or affective mental heath outcomes: A systematic review.  The Lancet,  370(9584), 319-328. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1016/S0140-6736(07)61162-3 Morales-Muà ±oz, I., Jurado-Barba, R., Ponce, G., Martà ­nez-Gras, I., à ngel Jimà ©nez-Arriero, M., Moratti, S., & Rubio, G. (2014). Characterizing cannabis-induced psychosis: A study with prepulse inhibition of the startle reflex.  Psychiatry Research,  220(1-2), 535-540. doi:http://dx.doi.org/10.1016/j.psychres.2014.08.010 Moreira, F. A., & Lutz, B. (2008). The endocannabinoid system: Emotion, learning and addiction.  Addiction Biology,  13(2), 196-212. doi:http://dx.doi.org.proxyiub.uits.iu.edu/10.1111/j.1369-1600.2008.00104.x Morral, A. R., McCaffrey, D. F., & Paddock, S. M. (2002). Reassessing the marijuana gateway effect.  Addiction,  97(12), 1493-1504. doi:http://dx.doi.org/10.1046/j.1360-0443.2002.00280.x Patton, G. C., Coffey, C., Carlin, J. 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The Breakdown of Mental Health and Stability Essay -- Stress Stressing

The Breakdown of Mental Health and Stability Progress has always been an essential component in modern society. At times it is equivalent to success, learning, and overall growth. In the field of science, progress is measured by comparisons to what was known before, what is known now, and what can be known in the future. Therefore, one could say that much progress was made in the field of science in terms of understanding the functions of the human brain and some of its behavior. It seems that as each new day passes, something new is discovered about the brain, whether it be a new mental or physiological brain condition, or merely a link and clue to one of the vast number of questions the world has considering the human brain and behavior. These discoveries and answers are becoming more and more important and imperative due to the fact that the overall population seems to becoming more and more emotionally fragile and more subject to several cerebral ills such as depression, anxiety, hysteria, and clinical insanity. A good question to ask is whether or not the overall population seems to be suffering more mental and cerebral ills, or that it is merely a result of more cases being reported and more statistics calculated. But if it is true that the number of people suffering from conditions or types of behavior which hinder their ability to go on with their everyday lives, what is the cause? And when we find the cause, what is the cure? Or how will society as a whole handle it? A possible theory is to look at the correlation between the rate of growth and process in modern society and the stress level of the average individual. Another question to ask is what exactly is the role stress plays in an individ... ...raising the levels of anxiety and depression amongst the population. Perhaps evolution will take hold and those with brains and systems more well adapt to handling this relatively new level of stress will flourish, making our society stronger. Or it could have a reverse effect, making society weaker in the process. Hopefully stress and it's harmful effects will be brought to attention more by the scientific community and as a whole society will do something about it or risk suffering from the potential set backs. Sources Cited: 1)Physiological Effects of Stress http://tm.cme.edu/03.html 2)Holistic-online http://holistic-online.com/stress/stress_GAS.htm 3)http://www.brainsource.com/stress_&_health.htm 4)Neurobiology of Stress http://www.biopsychiatry.com/stress.htm 5)http://www.lifepositive.com/Mind/psychology/stress/symptoms-of-anxiety.asp The Breakdown of Mental Health and Stability Essay -- Stress Stressing The Breakdown of Mental Health and Stability Progress has always been an essential component in modern society. At times it is equivalent to success, learning, and overall growth. In the field of science, progress is measured by comparisons to what was known before, what is known now, and what can be known in the future. Therefore, one could say that much progress was made in the field of science in terms of understanding the functions of the human brain and some of its behavior. It seems that as each new day passes, something new is discovered about the brain, whether it be a new mental or physiological brain condition, or merely a link and clue to one of the vast number of questions the world has considering the human brain and behavior. These discoveries and answers are becoming more and more important and imperative due to the fact that the overall population seems to becoming more and more emotionally fragile and more subject to several cerebral ills such as depression, anxiety, hysteria, and clinical insanity. A good question to ask is whether or not the overall population seems to be suffering more mental and cerebral ills, or that it is merely a result of more cases being reported and more statistics calculated. But if it is true that the number of people suffering from conditions or types of behavior which hinder their ability to go on with their everyday lives, what is the cause? And when we find the cause, what is the cure? Or how will society as a whole handle it? A possible theory is to look at the correlation between the rate of growth and process in modern society and the stress level of the average individual. Another question to ask is what exactly is the role stress plays in an individ... ...raising the levels of anxiety and depression amongst the population. Perhaps evolution will take hold and those with brains and systems more well adapt to handling this relatively new level of stress will flourish, making our society stronger. Or it could have a reverse effect, making society weaker in the process. Hopefully stress and it's harmful effects will be brought to attention more by the scientific community and as a whole society will do something about it or risk suffering from the potential set backs. Sources Cited: 1)Physiological Effects of Stress http://tm.cme.edu/03.html 2)Holistic-online http://holistic-online.com/stress/stress_GAS.htm 3)http://www.brainsource.com/stress_&_health.htm 4)Neurobiology of Stress http://www.biopsychiatry.com/stress.htm 5)http://www.lifepositive.com/Mind/psychology/stress/symptoms-of-anxiety.asp