2 page letter to the editor Assignment Example | Topics and Well Written Essays - 500 words

2 page letter to the editor - Assignment Example This involves an ability to clearly think through an issue, formulate opinion / policy, communicate it effectively and argue successfully the merits and demerits of the opinion and alternatives. In other words, a leader has to talk, listen and argue coherently to win over skeptics if any. Since we are all individuals from different socio-economic and political backgrounds, we manifest our leadership qualities in different styles. Some of us are authoritative, some are democratic and yet others are of please-all by nature. These styles appear appropriate in different situations e.g., military commanders are in general more authoritative, HR managers are more democratic etc. Authoritative leaders impose their will on the subordinates or even colleagues by the force of their personality and the power of their hierarchical status. Persuasive leaders opt for a more democratic approach Since the topic of healthcare reform is with the political leaders, I wish to draw a parallel with the council member of our neighborhood and the successful way he practices his leadership skills. On the one hand, this council member has to listen to the suggestions and grievances of his constituency (voters), prioritize them and do his best to get them executed through the administration. On the other hand, he has to contend with similar (and sometimes, opposing) demands from the other council members who have obligations to their own voters. There are political careers involved here and the contest is, as in the National Congress, among local leaders. Our council member is a soft spoken Republican. His priorities are dictated by public opinion and national policy. His interactions with the other council members can be seen as the flip side of his interactions with his own voters. Skillfully, he persuades the other council members to support his priorities within reasonable limits and extends similar support to them. By this way, he has

US History Essay Example for Free

US History Essay 4. Describe how prokaryotes carry out photosynthesis and cellular respiration when they lack compartmentalized organelles such as chloroplasts and mitochondria. The area of cellular respiration in prokaryotes is the respiratory membrane. For aerobic prokaryote the infoldings of the plasma membrane are similar to the cristae of mitochondria, whose purpose in eukaryotic cells is cellular respiration. In photosynthetic prokaryotes, the area responsible for cellular respiration is the thylakoid membrane. It functions are similar in manner to chloroplasts in eukaryotic cells. 5. Explain why prokaryotes are unable to grow in very salty or sugary foods, such as cured meats or jam. Prokaryotes have the ability to live harsh environments. Prokaryotes however are unable to live in very salty or sugary foods like cured meats or jams because they lack the essential nutrients that water etc provide. In response to these harsh conditions endospores are formed. In essence, endospores are a touch wall surrounding a set of chromosomes. Eventually as water is removed from the cell its metabolism halts and the rest of the cell disintegrates. In this manner prokaryotes die out in harsh conditions like sugary or salty foods. 6. State the function(s) of each of the following prokaryotic features: a. Capsule i. A capsule is a sticky layer that surrounds the cell wall of some prokaryotes, protecting the cell surface and sometimes helping to glue the cell to surfaces. b. fimbriae ii. A short, hairlike appendage of a prokaryotic cell that helps it adhere to the substrate or to other cells; also known as an attachment pilus. c. sex pilus iii. In bacteria, a structure that links one cell to another at the start of conjugation; also know as a conjugation pilus d. Nucleoid iv. A dense region of DNA in a prokaryotic cell. e. Plasmid v. A small, circular, double stranded DNA molecule that carries accessory genes separate from those of a bacterial chromosome. Plasmids are also found in some eukaryotes, such as yeasts. f. Endospores vi. A thick-coated, resistant cell produced by a bacterial cell exposed to harsh conditions. 7. List three factors that give rise to high levels of genetic diversity in prokaryotes. Rapid Reproduction- Rapid reproduction is comparable to a prokaryote reproducing by binary fission repeatedly. After rounds of division most of the offspring cells are identical Mutation- Genetic Recombination- 8. Describe three processes that produce recombinant DNA in prokaryotes.

Neurobiological Mechanisms that Cause Aggression

Neurobiological Mechanisms that Cause Aggression Review of the Neurobiological Mechanisms Which Underpin Reactive Aggression in Humans: a Closer Look at Monoamine Oxidase A (MAOA) Module 1: Prosocial and antisocial behaviours across the lifespan Violent acts have a significant toll on human societies: annually over 1.6 million deaths worldwide occur due to human violence (Viding Frith, 2006). Although acts of aggression have an important adaptive purpose, when overexpressed, they may result in destructive consequences. Conventionally, aggression has been defined as an intentional action with a purpose to inflict physical damage on another individual (Nelson Trainor, 2007). Currently two forms of aggression have been recognized in humans: controlled aggression instrumental subtype, and reactive aggression impulsive subtype (Vatiello Stoff, 1997). Instrumental aggression, also referred to as premeditated and predatory, is generally planned and goal-oriented and has often been linked to psychopathy (Blair, 2001). This kind of aggression is thought to be regulated primarily by higher cortical systems and is characterized by diminished amygdala response (Nelson Trainor, 2007). Reactive aggression on the other hand, is depen dent on the limbic and hypothalamic systems, and is characterized by high autonomic arousal (Siever, 2008). Impulsive aggression generally represents a direct response to stimuli and accounts for the majority of violent acts. Individuals with borderline personality disorder, intermittent explosive disorder, or ADHD are particularly prone to reactive aggression and impulsivity. Previous research on the neurobiology of aggression pointed out that for such individuals, repetitive acts of aggression are often influenced by the underlying neurobiological susceptibility (Nelson Trainor, 2007). Indeed, one remarkable feature of aggression is its apparent heritability. Twin and adoption studies suggest that genetic factors account for between 40% and 50% of population variance in risk of antisocial aggression (Buckholtz Meyer-Lindenberg, 2008). However, the relationship between aggression and the underlying neurobiology is far from being simple (Nelson Trainor, 2007; Siever, 2008). Previous research in individuals prone to impulsivity and reactive aggression as well as a number of studies based on animal models identified numerous genetic loci and neurotransmitters associated with reactive violence, including, but not limited to, Dopaminergic genes (DRD4, DRD5, and DAT1), Serotonergic genes (5HTT, HTR1B), and genes responsible for encoding enzymes involved in regulating the levels of these neurotransmitters, particularly catechol-O-methyltransferase (COMT), and Monoamine Oxidase A (MAOA), often referred to as â€Å"the warrior gene†. However, the association between genotype and phenotype of aggression is only beginning to be properly understood (Caspi, McClay, Moffitt, Mill, Martin, Craig, Taylor, Poulton, 2002; Nelson Trainor, 2007; Siever, 2008). While there have been many studies showing the association between different genes and aggression, results were often mixed and inconclusive. Currently, the best candidate gene with the most supportive evid ence appears to be Monoamine Oxidase A (see: Brunner, Nelen, Breakefield, Ropers, van Oost, 1993; Byrd Manuck, 2014; Cases, Seif, Grimsby, Gaspar, Chen, Pournin, Muller, et al.,1995; Caspi, et al., 2002). The MAOA gene, located on the X chromosome, is a functional polymorphism with high activity (MAOA-H) and low activity (MAOA-L) variants, which encodes the MAOA enzyme, responsible for breaking-down neurotransmitters such as serotonin, dopamine, and norepinephrine (Shih, Chen, Ridd, 1999; Viding Frith, 2006). Previous research using animal models as well as humans demonstrated an association between aggression and genetic deficiency in MAOA activity (Rowe, 2001). Transgenic mice without the gene encoding MAOA had higher amounts of brain serotonin (5-HT), dopamine (DA), and norepinephrine (NE), and displayed increased aggression (Cases, et al., 1995). After restoring MAOA activity, mice aggression was stabilized (Shih Thompson, 1999). In humans, point mutation in the MAOA gene led to MAOA deficiency and was found to be associated with reactive aggression in several men from the Dutch family. Moreover, across generations, these men with MAOA knockout also showed frequent violent outb ursts, particularly in response to mild provocation, and impulsive antisocial behaviour such as assault, rape, and attempted murder. (Brunner, et al., 1993). This condition, however, is quite uncommon and is unlikely to explain much variation in human violence and aggression. Findings of the studies that only looked at levels of MAOA activity and antisocial outcomes in adulthood have been mixed and thus problematic to interpret since both MAOA-H and MAOA-L were linked to reactive aggression (Ficks Waldman, 2014; Nelson Trainor, 2007; Siever, 2008). The study that produced very robust findings in that area and has later proven seminal was conducted by Caspi and colleagues (2002). This study was the first to look at the effects of MAOA activity in combination with childhood maltreatment on reactive aggression in adulthood. Indeed, adverse childhood experiences were found to affect the development and functioning of neural pathways involving the neurotransmitters metabolised by MAOA which can potentially result in increased aggression (Caspi, et al., 2002). Thus, Caspi and colleagues (2002) hypothesised that childhood maltreatment can predict reactive aggression in adulthood, and that this relationship is moderated by levels of MAOA expression. Results of this study demonstrated the dose-response effect of childhood maltreatment on the aggressive behaviour in adulthood, which was consistent with prior findings. However, this effect was much smaller in participants with the high-activity version of the MAOA gene as compared to men with low MAOA activity, suggesting the protective property of MAOA-H (Caspi et al, 2002). Moreover, as levels of maltreatment increased, so did the protective effect of the MAOA-H variant. A low-activity MAOA gene combined with a history of childhood maltreatment increased the risk of aggressive behaviour in adulthood sevenfold. These results supported the predicted hypothesis that MAOA activity would act as a moderator of the effects of childhood maltreatment on antisocial outcomes in adulthood. This study paved the way to a number of subsequent studies looking at gene and environment interaction. A recently published meta-analysis, which looked at 27 peer-reviewed studies on adverse childhood experiences, MAOA genotype, and aggressive and antisocial behaviour showed that results across 20 male cohorts (11064 participants) were largely consistent with findings from the original study by Caspi and colleagues (2002) (Byrd Manuck, 2014). These findings remained robust even after removing each study individually. However, the question remains, how does low activity MAOA gene in combination with childhood stressors translate to antisocial behaviours in adulthood? Several theories have been proposed to answer this question. On one hand, the association between low activity MAOA gene and aggression appears paradoxical, since MAOA-L leads to increased levels of serotonin, which has been found to be positively correlated with impulse control and negatively correlated with aggression (Manuch, Flory, Ferrell, Mann, Muldoon, 2000; Siever, 2008). However, MAOA also plays a role in regulating dopamine and norepinephrine, which were shown to lower thresholds for violent response to perceived threat (Manuch, et al., 2000). High levels of DA and NE, resulting from MAOA dysfunction, would activate a fight or flight response, and indirectly enhance aggression (Volavka, Bilder, Nolan, 2004). Indeed, previous studies showed a similar association between COMT gene (also responsible for breakdown of NE and DA ) and aggression (Siever, 2007; Volavka, et al., 2004). Therefore the elevated levels of NE and DA, due to low expression of MAOA, would be consistent with the results of previous studies, showing an association between low activity MAOA gene and aggression. Nevertheless, this theory does not account for the role of childhood maltreatment on aggression, and as it was mentioned previously, results of studies looking solely at MAOA activity and aggression are mixed and inconclusive, showing both high and low activity MAOA gene being associated with impulsive aggression (Ficks Waldman, 2014; Nelson Trainor, 2007; Siever, 2008). Another theory that sheds more light on the mechanism through which MAOA deficiency in combination with childhood maltreatment influences aggression in adulthood relies on the findings that high concentrations of intracellular serotonin have been associated with increased reactivity to stress and elevated anxiety (Seif De Maeyer, 1999, Viding Frith, 2006). Therefore, it is possible that MAOA deficiency might predispose individuals to neural hyper-reactivity to a threat (maltreatment). While genetic predisposition alone rarely results in adverse outcomes in adulthood, when combined with childhood stressors, it might potentially have consequences on brain function (Meyer-Lindenberg, Buckholtz, Kolachana, Hariri, Pezawas, Blasi, Wabnitz, et al., 2006). Previous findings in populations prone to impulsive violence demonstrated functional and structural abnormalities in brain areas associated with perception and regulation of emotions, particularly in the amygdala, orbitofrontal cortex, and the interconnected regions (Davidson, Putnam, Larson, 2000). Neuropsychological functions associated with these brain regions were also compromised in the aforementioned populations (Blair, Peschardt, Budhani, Mitchell, Pine, 2006). Previous work using animal models and clinic samples seems to suggest that maltreatment negatively affects the functioning of the neural structures involved during an individual’s reaction to threat (i.e., pariaquaductal gray and amygdala) and the regulation of the triggered threat response (i.e., orbitofrontal cortex and anterior cingulate). Therefore, the genetic risk (MAOA-L) along with childhood maltreatment may result in changes to brain function, and subsequently increases the risk of impulsive aggression (Viding Frith, 2006). These speculations imply that there is no one clear explanation for the findings we currently have regarding genetic variation and its effect on aggression. The human brain and the effects of genetic and environmental factors on its development are too complex to assume that one specific gene, or neurotransmitter levels are responsible for aggression. More likely, it is the gradual change in neural pathways that regulate aggression. As of this moment, it still remains unclear if aggression in adulthood that is observed in many of the aforementioned studies is due to developmental change in neural circuits or to a change in neurotransmitter function. Moreover, the effects of these changes for adults are very different than for children. Therefore, it is possible that low MAOA activity resulted in compensatory changes which transformed the organisation of the nervous system in children during the sensitive period of brain development, and was later reflected in antisocial outcomes in a dulthood (Lesch Merschdorf, 2000). Attempts to replicate Caspi et. al. (2002) findings in female populations yielded significantly different results. Recent meta-analysis that looked at 11 studies with female samples produced inconclusive results: even though MAOA activity had a significant association with adverse childhood events, high, as opposed to low, MAOA activity in combination with childhood maltreatment was associated with antisocial behaviour in adulthood. Moreover, this interaction was weaker, and after removing a few individual studies, it lost its significance (Byrd Manuck, 2014). Replicating Caspi and colleagues’ study using female cohorts has proven to be significantly more complicated for two main reasons. First of all, dividing females into two groups based on MAOA activity is challenging due to uncertain inactivation of heterozygous alleles. Secondly, severe personality disorders and antisocial outcomes are quite rare in women, thus it is difficult to get a large enough sample to demonstrate dose-response relationships. In sum, taking into account findings from previous studies it is unclear what relationship MAOA activity plays in antisocial outcomes in women, and calls for further investigation (Caspi, et al., 2002; Byrd Manuck, 2014). In attempts to understand the relationship between genes, environment, and aggression, the study by Caspi and colleagues (2002), as well as numerous studies that came out afterward, certainly advanced our understanding in the field. However, it is important to point out the limitations that characterise many of the research studies investigating the relationship between gene-environment interaction and adult antisocial behaviour. First of all, lack of published articles reporting null findings due to publication bias still remains a big problem in the field. As a result, published findings seem more robust than they actually are (Duncane Keller, 2011). Secondly, the samples of many studies, primarily those with female subjects, are often too small resulting in inadequate statistical power (Byrk Manuck, 2014). Indeed, negative findings had larger sample sizes compared to positive ones. These limitations make it difficult to correct for potential false-positive results (Duncan Kelle r, 2011). This is especially the case in replication attempts using female populations, and in neuroimaging studies. Finally, due to the difficulty recruiting participants for these studies, samples are often not easily comparable and consist of individuals with many comorbid psychiatric conditions, making it difficult to tease apart effects of certain genetic variations and maltreatment on specific psychopathology (McCrory, DeBrito, Viding, 2010). While there is strong evidence to suggest that genotype, particularly variants of the Monoamine Oxidase A gene, in combination with childhood maltreatment, plays an important role in reactive aggression in human adulthood, the exact underlying mechanism remains unclear. The aforementioned controversies call for caution when making any strong conclusions regarding the effects of genetic variation on antisocial outcomes. Further research, including longitudinal studies, genome-wide association studies, gene-environment-sex and gene-gene interaction studies, and neuroimaging studies, is necessary to better understand the underlying neurobiological mechanisms which underpin reactive aggression in humans. References: Blair, R. J. (2001). Neurocognitive models of aggression, the antisocial personality disorders, and psychopathy. Journal of Neurology, Neurosurgery and Psychiatry, 71, 727-731. Blair, R. J. R., Peschardt, K. S., Budhani, S., Mitchell, D. G., Pine, D. S. J. (2006). The development of psychopathy. Journal of Chid. Psychology and Psychiatry and allied disciplines, 47(3-4), 262-276. Brunner, H. G., Nelen, M., Breakefield, X. O., Ropers, H. H., van Oost, B. A. (1993). Abnormal behaviour associated with point mutation in the structural gene for monoamine oxidase A. Science, 262(5133), 578-580. Buckholtz J. W. Meyer-Lindenberg, A. (2008). MAO and the neurogenetic architecture of human aggression. Trends in Neuroscience, 31(3), 120-129. Byrd, A. L. Manuck, S. B. (2014). MAOA, Childhood Maltreatment, and Antisocial Behavior: Meta-analysis of a gene-Environment Interaction. Biological Psychiatry, 75(1), 9-17. Cases, O., Seif, I., Grimsby, J., Gaspar, P., Chen, K., Pournin, S., Muller, U., et al. (1995). Aggressive behaviour and altered amounts of brain serotonin and norepinephrine in mice macking MAOA. Science, 268(5218), 1763-1766. Caspi, A., McClay, J. Moffitt, T. E., Mill, J., Martin, J., Craig, I. W., Taylor, A., Poulton, R. (2002). Role of Genotype in the Cycle of Violence in Maltreated Children. Science, 297(2), 851-853. Davidson, R. J., Putnam, K. M., Larson, C. L. (2000). Dysfunction in the neural circuitry of emotion regulation- a possible prelude to violence. Science, 289(5479), 591-594. Duncan, L. Keller, M. (2011). A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry. The American Journal of Psychiatry, 168, 1041-1049. Ficks, C. Waldman, I. (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. Behavioral Genetics, 44(5), 427-444. Lesch, K. P. Merschdorf, U. (2000). Impulsivity, aggression, and serotonin: A molecular psychobiological perspective. Behavioral Sciences and the Law, 18, 581-604. Manuch, S. B., Flory, J. D., Ferrell, R. E., Mann, J. J., Muldoon, M. F. (2000). A regulatory polymorphism of the monoamine oxidase- A gene may be association with variability in aggression, impulsivity, and central nervous system serotonergic responsivity. Psychiatry Research, 95, 9-23. McCrory, E., De Brito, S. A., Viding, E. (2010). Research Review: The neurobiology and genetics of maltreatment and adversity. The Journal of Child Psychology and Psychiatry, 51(10), 1079-1095. Meyer-Lindenberg, A., Buckholtz, J. W., Kolachana, B., Hariri, A. R., Pezawas, L., Blasi, G., Wabnitz, A., Honea, R., Verchinski, B., Callicott, J., et al. (2006). Neural mechanisms of genetic risk for impulsivity and violence in humans. Proceedings of Natlional Academy of Sciences of the United States of America, 103(16), 6269-6274. Nelson, R. J., Trainor, B. C. (2007). Neural mechanisms of aggression. Nature, 8, 536-546. Shih J. C. Thompson, R. F. (1999). Monoamine oxidase in neuropsychiatry and behaviour. American Journal of Human Genetics, 65(3), 593-598. Seif, I. De Maeyer, E. (1999). Knockout corner: Knockout mice for monoamine oxidase A. International Journal of Neuropsychopharmacology, 12, 241-243. Shih, J. C., Chen, K., Ridd, M. J. (1999). Monoamine Oxidase: from genes to behaviour. Annual Review of Neuroscience, 11, 197-217. Siever, L. J. (2008). Neurobiology of Aggression and Violence. American Journal of Psychiatry, 165, 429-442. Vatiello, B., Stoff, D. M. (1997). Subtypes of aggression and their relevance to child psychiatry. Journal of American Academy of Child and Adolescent Psychiatry, 36, 307-315. Viding, E. Frith, U. (2006). Genes for susceptibility to violence lurk in the brain. Proceedings of the National Academy of Sciences of the United States, 103(16), 6085-6086. Volavka, J., Bilder, R. J., Nolan, K. (2004). Catecholamines and aggression: The role of COMT and MAO polymorphism. Annals of the New York Academy of Sciences, 1036, 393-398.

Warren G. Harding :: essays research papers

Before his nomination, Warren G. Harding declared, "America's present need is not heroics, but healing; not nostrums, but normalcy; not revolution, but restoration; not agitation, but adjustment; not surgery, but serenity; not the dramatic, but the dispassionate; not experiment, but equipoise; not submergence in internationality, but sustainment in triumphant nationality...." A Democratic leader, William Gibbs McAdoo, called Harding's speeches "an army of pompous phrases moving across the landscape in search of an idea." Their very murkiness was effective, since Harding's pronouncements remained unclear on the League of Nations, in contrast to the impassioned crusade of the Democratic candidates, Governor James M. Cox of Ohio and Franklin D. Roosevelt. Thirty-one distinguished Republicans had signed a manifesto assuring voters that a vote for Harding was a vote for the League. But Harding interpreted his election as a mandate to stay out of the League of Nations. Harding, born near Marion, Ohio, in 1865, became the publisher of a newspaper. He married a divorce, Mrs. Florence Kling De Wolfe. He was a trustee of the Trinity Baptist Church, a director of almost every important business, and a leader in fraternal organizations and charitable enterprises. He organized the Citizen's Cornet Band, available for both Republican and Democratic rallies; "I played every instrument but the slide trombone and the E-flat cornet," he once remarked. Harding's undeviating Republicanism and vibrant speaking voice, plus his willingness to let the machine bosses set policies, led him far in Ohio politics. He served in the state Senate and as Lieutenant Governor, and successfully ran for Governor. He delivered the nominating address for President Taft at the 1912 Republican Convention. In 1914 he was elected to the Senate, which he found "a very pleasant place." An Ohio admirer, Harry Daugherty, began to promote Harding for the 1920 Republican nomination because, he later explained, "He looked like a President." Thus a group of Senators, taking control of the 1920 Republican Convention when the principal candidates deadlocked, turned to Harding. He won the Presidential election by an unprecedented landslide of 60 percent of the popular vote. Republicans in Congress easily got the President's signature on their bills. They eliminated wartime controls and slashed taxes, established a Federal budget system, restored the high protective tariff, and imposed tight limitations upon immigration. By 1923 the postwar depression seemed to be giving way to a new surge of prosperity, and newspapers hailed Harding as a wise statesman carrying out his campaign promise--"Less government in business and more business in government.

Great expectation Novel vs Film

In 2012, Mike Newell created a film replicating one of Charles Dickens's famous novels Great Expectations. Both novel and film both are set in Kent, England and recount us through the life of a young commoner named Pip. Pip eventually moves to London and has wealth bestowed upon him by an anonymous benefactor. With the money he receives, Pip is able to become a gentleman.The film was not an effective representation of the novel because the omission of certain characters, the haracters are presented differently than they are In the book and the story Is told through dialogue instead of narration. Due to the film being so fast and compressed, some of the Characters are left out. For example, the character that was missing In the film was a menacing, broad-shouldered, loose-limbed (15. 35) cruel man named Orllck. Dickens uses these types of characters In his novel to set a cruel nature and to give an unpleasant feeling of threat.The omission of Orllck Is significant because it does not allow the audience to see PIP's final repentance. This is important because it is when pip realizes his guilt and disloyalty towards his loved ones, Joe and Biddy. Another instance is when Orlick is interested in Biddy, as a result she becomes frightened, and this leads to his hatred and disgust towards Pip. Orlick began to bully Pip. Without Orlick, viewers are unable to see the characteristics of his cruelty, and the unpleasant feeling, atmosphere that he gives towards people and the protagonist.Another difference between the novel and the film was that some characters are represented differently. Dickens portrays Estella as a cold hearted, unloving and one whose goal is to break others men's hearts in the novel. She shows no feelings of love towards men and especially not towards Pip. In the film, Holliday Grainger, the one who played Estella poorly presented Estella. For example, when Pip comes back to see Estella and Miss. Havisham, She speaks to him with care and love, showing her feelings and affections towards Pip.Another character that was poorly presented in the film was Wemmick. In the novel, Dickens howed his dual personality between his â€Å"Office â€Å"and â€Å"Walworth† personality. Although his â€Å"Walworth† personality was shown in the film, his office personality was not. At the offce, he seems to have his loving and kind personality towards others and especially to Pip. These changes make the viewers view Estella and Wemmlcka completely dfferent way, not the way that Charles Dickens's intended. In the film of Great Expectations, there was no narration.Dickens wrote the novel from the point of view of the protagonist Pip. Throughout the novel, Pip usually spends most of his time expressing his feelings and thoughts through narration. In fact, Newell did not portray fully the details of PIP's love for Estella. In the novel, through the narrations, Pip expresses his feelings and love for Estella and his love for her was the reason why he wanted to become a gentleman, wanting to Impress her. In the film, It seems that Pip only lust over Estella and makes It seems that he Is only attracted to her because of her appearance.Jeremy Irvine, the actor of PIP uses dialogue and ctions to portray Pip's feelings and emotions. Although the dialogue and actions help the audience know about Pip's character, viewers are unable to identify the true similar in comparison to Dicken's novel. However the omission of certain characters, the way characters are presented, and the narration make the film different enough to illicit a different response from the viewer as opposed to the reader. This difference in response indicates that the film is not an adequate representation of the novel.

The Cell Cycle

The cell cycle is a sequence of events in the life of a cell, including cell division. Cell division distributes identical sets of chromosomes to daughter cells. This process is used for reproduction, growth, and repair in the body. The cell cycle can be broken down into two parts: interphase and the mitotic (M) phase. Interphase, a growth period, alternates with mitosis and accounts for 90 percent of the cell cycle. During interphase, the cell grows, duplicates its DNA, and prepares for mitosis. This phase can be broken down into 3 sub phases: G1, S, and G2. During the G1 or first gap phase, the cell grows and performs normal metabolic roles, including producing proteins and organelles. During the S phase, which stands for synthesis of DNA, the cell’s chromosomes are copied. Lastly, in the G2 phase, the cell continues to grow and prepares for cell division. This phase of the cell cycle is regulated by stop and go signals called checkpoints, which are located between G1 and S, G2 and M, and M and G1. These make sure that the cell cycle can proceed and is being performed correctly. The hallmark of this phase is that the DNA appears as loosely packed chromatin and the centrioles are together. Centrioles play an important role in animal cell division. They are composed of microtubules which become spindle fibers that guide the movement of chromosomes in mitosis. Mitosis is the division of the nucleus, which accounts for only 10 percent of the cell cycle. Mitosis can be broken down into five sub phases: prophase, prometaphase, metaphase, anaphase, and telophase; cytokinesis takes place last. In prophase, the chromatin condenses to chromosomes and the two sister chromatid are joined at the centromere. As the centrioles begin to separate, the mitotic spindle, made of microtubules, begins to form and the nucleolus disappears. In prometaphase, the nuclear membrane dissolves, which allows the spindle to interact with the chromosomes, although the spindle isn’t fully formed yet. The sister chromatids of the chromosomes develop proteins within the centromeres called kinetochores. These allow the chromosomes to attach to the microtubules of the spindle, which are called kinetochore microtubules. Nonkinetochore microtubules aren’t connected to chromosomes, but they interact with other microtubules rom the other pole of the cell. By metaphase, the centrioles are at the opposite poles of the cell and the spindle is fully formed. The chromosomes, attached to the spindle, move to the middle of the cell and line up at the imaginary metaphase plate. Anaphase begins when the centromeres of the chromosomes split and the chromatid is now a chromosome. The chromosomes begin to move to ward the opposite poles of the cell and the poles move farther apart. In telophase, two daughter nuclei form at the poles of the cell, the nucleolus and nuclear membrane reappears, and the chromosomes unravel. Cytokinesis, the splitting of the cytoplasm, occurs simultaneously as telophase. Two daughter cells appear by the creation of a cleavage furrow, which pinches the cell in two. After mitosis, the cell can grow and mature to divide again like epithelial, blood, and stem cells, or grow and mature to never divide again like brain, nerve, and muscle cells. These cells go to the G0 phase, a non-dividing resting period. Liver cells can be called back from the G0 phase to divide again, which makes the liver the only organ to regenerate. This demonstrates the importance of the cell cycle.