The Alhambras Structure Buildings and Gardens

The Importance of Being Earnest Review

'The Importance of Being Earnest' Review ​​The Importance of Being Earnest is Oscar Wildes most well-known and best-loved play, as well as being an enormous success in his lifetime. For many people, it is the apogee of Wildes work. Like Wilde, the play is the very embodiment of fin de sieclà © British dandyism. However, this seemingly frivolous play has a much darker side. Its critique of Victorian societythough delivered in a velvet gloveis every inch an iron fist. The play is a satire both of the hypocrisies of the society in which Wilde lived, and the damaging effect that these hypocrisies can have on the souls of those live under their rule. Wilde was to become one of those souls shortly after the first performance of the play when he initiated a libel trial that was to lead to his imprisonment for being a homosexual.​ Overview ofThe Importance of Being Earnest The play is based around two young men, one of whom is an upright young man called Jack who lives in the country. However, in order to escape the drudgery of his highly conservative lifestyle, he has created an alter-ego, Ernest, who has all kinds of reprobate fun in London. Jack says he often has to visit his poor brother Ernest, which gives him his opportunity to escape his boring life and have fun with his good friend, Algernon. However, Algernon comes to suspect that Jack is leading a double life when he finds a personal message in one of Jack’s cigarette cases. Jack makes a clean breast of his life, including the fact that he has a young and attractive ward by the name of Cecily Cardew back on his estate in Gloucestershire. This piques Algernons interest and, uninvited, he turns up on the estate pretending to be Jack’s brotherthe reprobate Ernestin order to woo Cecily. In the meantime, Jacks fiancà ©e, (and Algernons cousin) Gwendolen has also arrived, and Jack admits to her that he is, in fact, not called Ernest, but is called Jack. Algernon, despite his better judgment, also confesses to Cecily that his name is not Ernest either. This causes a good deal of trouble in our heroes love lives, as both women have a rather strange attachment to the name Ernest, and cannot consider marrying anyone who does not go by that name. There is another impediment to the marriages. Gwendolens mother, Lady Bracknell, will not countenance her daughter marrying someone of Jacks social status (he was an orphan who was found by his adoptive parents in a handbag at Kings Cross Station). As Jack is Cecilys guardian, he will not allow her to marry Algernon unless his aunt, Lady Bracknell changes her mind. This seemingly irresolvable conundrum becomes brilliantly solved when, on inspection of the handbag, Lady Bracknell reveals that Algernons brother had become lost in just such a handbag and that Jack must, in actuality, be that lost child. What’s more, the child had been christened Ernest. The play ends with a prospect of two very happy marriages. The Importance of Being Earnest combines a labyrinthine plot, the seemingly irresolvable narrative of a farce, and some of the most comic and wittiest lines ever written. It is, as can probably be surmised from its extraordinary to-ings and fro-ings and its incredibly unlikely resolution, is not to be taken as a serious drama. Indeed, the characters and the setting lack any real depth; they are, first and foremost, vessels for Wilde’s witticisms lampooning the shallow and roots-obsessed society in which he lived.   However, this is not to the plays detriment – the audience is treated to some of the most sparkling verbal wit ever seen. Whether luxuriating in paradox or simply in the ridiculousness created by the plot that Wilde has set in motion, the play is at its best when it is portraying supposedly serious things in an extremely trivial matter.   However, this seeming piece of fluff is enormously influential and is actually a destructive critique of the social mores of the times. The emphasis that is put in the play on surfacesnames, where and how people were brought up, the way that they dressbelies a yearning for something which is more substantial. Wilde can be credited, by producing a piece of polished decadence, with contributing to the destruction of a class-based, surface-obsessed society. Wildes play seems to say, look beneath the surface, try and find the real people stifled beneath social norms. Brilliant, inventive, witty andwhen performedabsolutely hilarious, Wildes The Importance of Being Earnest, is a landmark in the history of Western theater, and probably that writer’s greatest achievement.

Statistical Mathematics Statistics Project Example | Topics and Well Written Essays - 1000 words

Statistical Mathematics - Statistics Project Example The peak is flat, which is characterized by kurtosis = -0.05. The peak is off centered; the distribution is slightly skewed to the right, which is marked by skewness = 0.06. Figure 2 illustrates histogram of daytime accidents. Visual inspection shows that the frequency distribution does not have a bell curve shape. The histogram does not have a peak and frequencies are not equally distributed. The peak is flat, which is characterized by kurtosis = -0.07. The peak is off centered; the distribution is moderately skewed to the right, which is marked by skewness = 0.42. Figure 3 illustrates histogram of total vehicles on the street. Visual inspection shows that the frequency distribution does not have a bell curve shape. The histogram resembles the back of a two-humped camel; it is close to a bimodal distribution. The histogram does not have a peak and frequencies are not equally distributed. The peak is flat, which is characterized by kurtosis = -0.88. The peak is off centered; the distribution is moderately skewed to the left, which is marked by skewness = -0.14. The assignment is using a data set that has three variables: daytime car accidents, nighttime car accidents and total observed cars in evaluating number of accidents (Table 1). . The distribution characters of the variable in statistics are measured through the calculation and analysis of central tendency and dispersion of the data set. The following section provides the analysis mentioned above. Each variable has twelve values. The assignment uses mean, mode, median, and midrange to study the central tendency of the data set. Table 2 describes the central tendency. The mean and median tell us about data those are on the right and left sides of theses values. For example, total cars mean is 450. In ascending orders, the set shows that five values are on the left, and seven values are on the right side of the average. When we compare the same set with the median value of

Humor and madness Essay Example | Topics and Well Written Essays - 500 words

Humor and madness - Essay Example Seriously, what are the odds of someone who faked insanity to escape his punishment suddenly taking on messianic attributes en route to â€Å"liberating† a group of mentally ill patients? In a fictional setting of course its viable. This happenstance borders on the fantastic, and it is highly remote that people could just walk into asylums on the pretext of chicanery and â€Å"heal† the insane with the power of laughter. The novel shows us the great divide between humor and madness as a form of symbolism in connoting sanity vis-à  -vis insanity. In the dour, oppressive wards of the asylum people are so rooted in madness that they have completely forgotten how it is to legitimately feel happiness and appreciate humor. And then comes McMurphy, whose witty, cheery approach enlivens up a ward which hadn’t heard true laughter in years. The novel highlights the fact that those embroiled in madness no longer have the capability to experience real joy. Thus, humor serves as a virtual shield for the protagonist, lest he fall into the same trap that the patients have found themselves in. He utilizes humor so that it would serve as insulation from the madness around him, but in the process he inspires the rest of the occupants of the ward. The relationship between humor and madness go hand in hand as the story unfolds, with humor standing as a unique symbol for free-thinking, fully functional human bei ngs and the absence thereof showing a descent into the recesses of madness. Once Mcmurphy has gradually empowered the patients with his own brand of rebellious humor, the reader would get a distinct notion that the patients had actually improved and that they were slowly entering the realm of reason again. This was clearly manifested in the scene where Harding, Scanlon, Sefelt and Doctor Spivey all could truly laugh at the end of their bending-the-rules fishing expedition. It is quite obvious that a reasonable understanding of the

Etiology of Parkinsons Disease

Etiology of Parkinsons Disease Parkinson’s Disease is the second most common neurodegenerative disease, after Alzheimer’s. Onset typically occurs late in life, affecting approximately 1% of 65 year olds, with the prevalence increasing to 4-5% by age 85 (Dawson Dawson 2003). There are also rare cases of early-onset Parkinson’s, which are usually familial. Research into the gene mutations discovered in such hereditary cases has also contributed to the understanding of the aetiology of the spontaneous, late onset form of the disease. Parkinson’s Disease (PD) is characterized clinically by tremors at rest, bradykinesia (slowness of voluntary movement), muscle rigidity, decrease in postural reflex and facial expression and an altered gait (Kumar et al. 2005). A subset of patients (10-15%) also develop dementia. Symptoms are progressive and result in decreased mobility and eventually severe disability. The symptomatic motor disturbances arise from the progressive loss of dopaminergic neurons in the substantia nigra of the brain. This results in a decrease in the dopaminergic content of the striatum. These areas play an important role in modulating feedback from the thalamus to the motor cortex. AIMS AND OBJECTIVES This report aims to investigate the current knowledge of the aetiology of PD, by examining evidence in the literature. It is crucial to understand the pathological mechanisms underlying the selective destruction of dopaminergic neurons in PD so that effective treatments and prophylaxis can be developed. PROPOSED STRATEGY Researchers have studied the molecular mechanisms of PD pathogenesis using a number of techniques: in vitro tissue cultures of human and animal neurons, post-mortem human brain tissue, mouse models of the disease, genetic studies and more novel techniques such as the use of ‘cybrids’. Evidence from all of these will be amalgamated and conclusions drawn. MOLECULAR PATHOGENESIS OF PD That PD is generally associated with old age must be considered an important clue when trying to elucidate the causal mechanism of PD. The same is also true of the most common neurodegenerative disease, Alzheimer’s Disease (AD). Both are also characterised by an accumulation of protein aggregates resulting in progressive neuronal loss, suggesting a common underlying pathology. Histological brain sections of PD patients shows characteristic, large inclusion bodies in the cytosol of surviving neurons of the substantia nigra, as well as locus ceruleus and surrounding brainstem nuclei, called Lewy bodies (Kumar et al. 2005). These are aggregates of à ¯Ã‚ Ã‚ ¡-synuclein (Spillantini et al. 1997), a protein whose gene (SYN, aka PARK 1) has been linked to familial PD (Athanassiadou et al. 1999), as well as other proteins such as ubiquitin and synphilin-1. It is unclear whether these aggregates contribute to the pathogenesis, are a simple by-product or even part of an attempted protective mechanism, described as the aggresome theory (McNaught et al. 2002). Some evidence has recently been produced by Setsuie and colleagues (2005), using a PD rat model in which proteasome inhibitors caused inclusion formation, which resulted in decreased dopaminergic neuronal death that normally follows 6-hydroxyl dopamine (6-OHDA) administration. Lewy bodies are also found in low numbers in normal aging and AD (Jellinger 2001). However, Lewy bodies are not found in some cases of juvenile onset PD, which suggests that the inclusions are not crucial for neuronal death in the substantia nigra (Fahn Salzer 2004). Animal models of the disease, created using neurotoxins such as rotenone or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), or transgenic mice that overexpress human SYN gene (for à ¯Ã‚ Ã‚ ¡-synuclein) mutations, do not faithfully replicate the structure and antigenicity of the Lewy bodies found in PD (Dickson 2001). This highlights the problems associated with designing and producing an accurate animal model of human disease, which can be valuable tools, despite some limitations. Role of the ubiquitin-proteasome system (UPS) Although the precise role of Lewy bodies in the pathogenesis of PD is still unclear, the accumulation and aggregation of proteins suggests that there is a deficit in the cellular systems that normally remove and degrade abnormal proteins. The ubiquitin-proteasome system (UPS) is one such pathway, and there is growing evidence that implicates this system in PD. In conjunction with the enzymes E1, E2 and E3, ubiquitin is activated and attaches to abnormal proteins to form a polyubiquitin chain. The proteasome recognises this complex and degrades the unwanted protein. The ubiquitin polymer is released from the targeted protein and digested by ubiquitin carboxy-terminal hydroxylases (UCHs), to release ubiquitin monomers back into the system (Alberts et al. 2002). Ubiquitination and recognition of proteins to be degraded are ATP-dependent processes. If the activity of this clearance pathway decreases, misfolded or oxidatively damaged proteins will accumulate rather than being recycled (Sherman Goldberg 2001). Studies of the rarer, familial cases of PD have revealed evidence that this system is involved in PD aetiology, which has aided the understanding of the pathogenesis of sporadic PD. Gene mutations for two proteins that are involved in the UPS are of particular significance. Kitada and colleagues (1998) demonstrated a link between mutations in the parkin gene (aka PARK 2) and familial incidence of autosomal recessive juvenile parkinsonism (AR-JP) in Japanese families. Parkin is an E3 ligase within the UPS, and has been shown to have a neuroprotective role (Petrucelli et al. 2002). Despite this, parkin null-mutant mice exhibited normal behaviour and brain morphology, with no loss of dopaminergic neurons. Dopamine levels were altered, suggesting a possible role in dopamine regulation (Goldberg et al. 2003). Drosophila parkin null-mutants showed a consistent pattern of pathology, with locomotor deficits, sterility and decreased lifespan (Greene et al. 2003). These were attributed to mito chondrial dysfunction, which is also a feature of PD (see below). Research into the potential toxic effects of accumulation of parkin substrates has been inconclusive (Betarbet et al. 2005). Evidence points to parkin involvement in the pathogenesis of PD, but mutations of this protein are not sufficient alone to cause the disease. A missense mutation for the gene encoding the protein UCH-L1 has been detected in autosomal dominant familial cases of PD in Germany (Leroy et al. 1998). In sporadic cases of PD, UCH-L1 is downregulated and oxidized in the cerebral cortex (Choi et al. 2004), the significance of this is unknown. UCH-L1 mutations in mice produce neuromotor signs that are not typical of PD, and are characterised as Gracile Axonal Dystrophy mice (GAD). As for parkin, the evidence confirms some involvement in PD pathogenesis of these elements of the UPS, but points to the need for further research to fully deduce their role. Other genetic mutations have been identified, such as LRRK2 (a kinase;Zimprich et al. 2004) and DJ-1 (aka PARK 7), which is involved in a similar protein degradation pathway (SUMO; Bonifati et al. 2003). It is tempting to attribute the accumulation of à ¯Ã‚ Ã‚ ¡-synuclein to a decrease in activity of the UPS, but evidence that à ¯Ã‚ Ã‚ ¡-synuclein is a substrate of this system is contradictory (Paxinou et al. 2001), with results differing between in vitro cell lines and conditions. Some studies suggest that à ¯Ã‚ Ã‚ ¡-synuclein accumulation may inhibit the UPS, resulting in further protein accumulation (Liu et al. 2005). Role of mitochondrial dysfunction and oxidative stress A significant amount of evidence supports the hypothesis of involvement of the UPS in PD aetiology. In familial cases genetic mutations have been discovered that account for a portion of the susceptibility to, and pathogenesis of PD; but other factors are obviously required for both early onset and sporadic cases to develop. UPS activity has been found to be lowered in sporadic PD patients, with impaired proteasomal activity and reduced expression of subunits in the substantia nigra (McNaught et al. 2003). Whether UPS impairment is a primary cause or secondary to another event is not yet clear. Some researchers believe that the mechanism underlying the dysfunctional UPS may involve mitochondrial dysfunction, which has also been implicated in other neurodegenerative diseases (Hashimoto et al. 2003). During energy production by respiration in the mitochondria, there is a continuous leakage of free radicals, such as reactive oxygen species (ROS), which are also released by inflammatory cells. Antioxidant mechanisms exist to mop these up before they can cause oxidative damage to surrounding molecules, such as proteins, lipids and DNA, but these are not 100% efficient. This results in a gradual increase in damaged cellular components with aging (Vigoroux et al. 2004). Higher levels of oxidization products have been found in brain tissue of patients with neurodegenerative diseases such as PD (Dexter et al. 1994) and suggest an important role for free radicals in its aetiology. Mitochondrial DNA (mtDNA) damage has been hypothesised to accumulate, leading eventually to mitochondrial dysfunction, which further increases free radical leakage. Mitochondrial complex I, in particular, has been implicated. Induced parkinsonism in animal models using the pesticide rotenone has been shown to inhibit mitochondrial complex I (Sherer et al. 2002). Administration of MPTP also induces PD symptoms and inclusion body formation, via the complex I inhibition of its metabolite MPP+ (Ram say et al. 1986). This has been recorded in human subjects following the use of illicitly manufactured narcotics, in which MPTP is produced as a contaminant, but has now been used to reliably induce disease in rodents to further knowledge of the pathogenesis of this disease. As well as providing valuable insights into the mechanisms underlying PD, the ability of chemicals to produce the symptoms and pathology of PD has also raised concerns about the role of environmental factors in the aetiology of the sporadic disease. Some epidemiological studies have linked pesticide exposure to an increased risk of developing PD (Park et al. 2005), as well as suggestions that increased coffee/caffeine consumption and smoking (Wirdefeldt et al. 2005) may have some protective benefits. Exposure to heavy metals, such as manganese has also shown a correlation with PD in some studies, but not all. Heavy metals are known to accelerate free radical formation and hence increase oxidative stress, so it w ould not be unexpected if higher levels were involved in PD aetiology. Results of epidemiological studies that claim to prove these positive and negative correlations with PD are contradictory, and further research is required, which could also take diet into account (particularly ingested antioxidant levels and lifestyle). Mitochondrial dysfunction may cause a decrease in UPS activity, either by reduced ATP production, which is essential for many processes of the pathway, and/or by increasing oxidative stress and damaging vital components of the system (Fahn Salzer 2004). The pivotal role of mitochondria has been elegantly demonstrated by the use of cytoplasmic hybrids. These ‘cybrids’ are formed by taking mtDNA from platelets of patients with PD and inserting it into cultured human neuroblastoma cells that have been depleted of their endogenous mtDNA. These neuronal cells faithfully recapitulate the structure and antigenicity of Lewy bodies (Trimmer et al. 2004), and similar studies have reported other pathogenic features consistent with a role for mitochondria and oxidative stress in PD. It is now widely accepted that oxidative stress is a contributory factor to PD aetiology, with markers of oxidative damage found to be higher than in non-PD controls. Antioxidants have been administered in a number of studies to further explore the impact of free radicals and therapeutic/prophylactic options. Transgenic mice that overexpress the endogenous antioxidant Cu,Zn-superoxide dismutase did not show any symptoms or DA neuron loss following exposure to paraquat (herbicide)-maneb (fungicide), compared to non-transgenic controls (Thiruchelvam et al. 2005). Studies involving exogenous antioxidants have produced inconclusive results, and more research is required in this area. The specificity of dopaminergic neuronal loss, mainly in the substantia nigra pars compacta, in PD is replicated in chemically induced animal models of disease. The reason for this consistent and specific pattern of neuropathology may be due to the oxidation properties of DA, with highly reactive DA-quinones being generated. These are able to form complexes with à ¯Ã‚ Ã‚ ¡-synuclein and may inhibit mitochondrial complex I (Asanuma et al. 2003). This has important implications for the commonly used L-DOPA therapy, which may also contribute to neurodegeneration. Some researchers also believe that inflammation may play a role in PD, as microglial cells proliferate in affected brain regions (McGeer McGeer 2004). CONCLUSION The aetiology of Parkinson’s Disease is multifactorial, with a combination of genetic, environmental and possibly immunological factors, many of which are still unknown or poorly understood. There is growing evidence from a variety of research techniques that oxidative stress, mitochondrial dysfunction and deficits in protein degradation pathways, such as the UPS are interlinked. The aetiological factors initiate a process that culminates in the accumulation and aggregation of proteins, mainly à ¯Ã‚ Ã‚ ¡-synuclein, in dopaminergic neurons of the nigrostriatal system, which leads to cell-death. Further research is required to fully elucidate the precise molecular mechanisms that underlie the neuropathology of PD, so that effective treatments or prophylactic advice can be established. REFERENCES Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., Walter, Molecular Biology of the Cell. 4th Ed. New York: Garland Publishing. pp.359-363. Asanuma, M., Miyazaki, I. Ogawa, N. 2003 Dopamine- or L-DOPA-induced neurotoxicity: the role of dopamine quinone formation and tyrosinase in a model of Parkinsons disease. Neurotox Res 5, 165-76. Athanassiadou, A., Voutsinas, G., Psiouri, L., Leroy, E., Polymeropoulos, M. H., Ilias, A., Maniatis, G. M. Papapetropoulos, T. 1999 Genetic analysis of families with Parkinson disease that carry the Ala53Thr mutation in the gene encoding alpha-synuclein. Am J Hum Genet 65, 555-8. Betarbet, R., Sherer, T. B. Greenamyre, J. T. 2005 Ubiquitin-proteasome system and Parkinsons diseases. Exp Neurol 191 Suppl 1, S17-27. Choi, J., Levey, A. I., Weintraub, S. T., Rees, H. D., Gearing, M., Chin, L. S. Li, L. 2004 Oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases. J Biol Chem 279, 13256-64. Dawson, T. M. Dawson, V. L. 2003 Rare genetic mutations shed light on the pathogenesis of Parkinson disease. J Clin Invest 111, 145-51. Dexter, D. T., Holley, A. E., Flitter, W. D., Slater, T. F., Wells, F. R., Daniel, S. E., Lees, A. J., Jenner, P. Marsden, C. D. 1994 Increased levels of lipid hydroperoxides in the parkinsonian substantia nigra: an HPLC and ESR study. Mov Disord 9, 92-7. Dickson, D. W. 2001 Alpha-synuclein and the Lewy body disorders. Curr Opin Neurol 14, 423-32. Fahn, S. Sulzer, D. 2004 Neurodegeneration and Neuroprotection in Parkinson Disease. Neurorx 1, 139-154. Goldberg, M. S., Fleming, S. M., Palacino, J. J., Cepeda, C., Lam, H. A., Bhatnagar, A., Meloni, E. G., Wu, N., Ackerson, L. C., Klapstein, G. J., Gajendiran, M., Roth, B. L., Chesselet, M. F., Maidment, N. T., Levine, M. S. Shen, J. 2003 Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons. J Biol Chem 278, 43628-35. Hashimoto, M., Rockenstein, E., Crews, L. Masliah, E. 2003 Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimers and Parkinsons diseases. Neuromolecular Med 4, 21-36. Jellinger, K. A. 2001 The pathology of Parkinsons disease. Adv Neurol 86, 55-72. 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R. 2002 Parkin protects against the toxicity associated with mutant alpha-synuclein: proteasome dysfunction selectively affects catecholaminergic neurons. Neuron 36, 1007-19. Ramsay, R. R., Dadgar, J., Trevor, A. Singer, T. P. 1986 Energy-driven uptake of N-methyl-4-phenylpyridine by brain mitochondria mediates the neurotoxicity of MPTP. Life Sci 39, 581-8. Setsuie, R., Kabuta, T. Wada, K. 2005 Does proteosome inhibition decrease or accelerate toxin-induced dopaminergic neurodegeneration? J Pharmacol Sci 97, 457-60. Sherer, T. B., Betarbet, R., Stout, A. K., Lund, S., Baptista, M., Panov, A. V., Cookson, M. R. Greenamyre, J. T. 2002 An in vitro model of Parkinsons disease: linking mitochondrial impairment to altered alpha-synuclein metabolism and oxidative damage. J Neurosci 22, 7006-15. Sherman, M. Y. Goldberg, A. L. 2001 Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases. Neuron 29, 15-32. Spillantini, M. G., Schmidt, M. L., Lee, V. M., Trojanowski, J. Q., Jakes, R. Goedert, M. 1997 Alpha-synuclein in Lewy bodies. Nature 388, 839-40. Thiruchelvam, M., Prokopenko, O., Cory-Slechta, D. A., Richfield, E. K., Buckley, B. Mirochnitchenko, O. 2005 Overexpression of superoxide dismutase or glutathione peroxidase protects against the paraquat+maneb-induced Parkinsons disease phenotype. J Biol Chem. Trimmer, P. A., Keeney, P. M., Borland, M. K., Simon, F. A., Almeida, J., Swerdlow, R. H., Parks, J. P., Parker, W. D., Jr. Bennett, J. P., Jr. 2004 Mitochondrial abnormalities in cybrid cell models of sporadic Alzheimers disease worsen with passage in culture. Neurobiol Dis 15, 29-39. Vigouroux, S., Briand, M. Briand, Y. 2004 Linkage between the proteasome pathway and neurodegenerative diseases and aging. Mol Neurobiol 30, 201-21. Wirdefeldt, K., Gatz, M., Pawitan, Y. Pedersen, N. L. 2005 Risk and protective factors for Parkinsons disease: a study in Swedish twins. Ann Neurol 57, 27-33. 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Micro and Macro Management Essay

Macro Management In a simple definition management is the person or persons who control or direct a business or other enterprise. However, management is much larger than just one person or small group of people. Management is also the practice of handling, supervision, direction, and control (www. dictionary. com). It is much larger than one person, or even a small group of people; management is everywhere. We use management in all aspects of our daily lives, whether it is organizing an event, or handling a purchase order. Management must be arranged through multiple levels in order to be successful, beginning with micro management, eventually its way up the ladder to macro management. Micro and macro components are the core make up of every business, each possessing different qualities and characteristics that form the overall building blocks to success. During the training of a new employee, most businesses use the micro-management process to provide the guidance and tools the employee needs to become successful with that business. Micro management is used my supervisors to observe and control the work of their employees. It involves giving employee smaller tasks, while they monitor and assess the work being done (www. dictionary. com). Micro management is often used in the beginning of any business or establishment; basically, you need to start somewhere. In the opening of a new business, guidance will always need to be offered from cooperate offices to ensure a clean transition in the opening process. Once a business is established, management will in turn micro manage their employees; guiding them through the procedures and responsibilities the company requires. Because micro managing involves supervisors overlooking the tasks their employees are undertaking, often times it is thought of as an unenthusiastic tactic. Through the eyes of an associate, micro managing can be de motivating, in turn creating doubt and lack of confidence in the workplace. Even though micro managing is used as an introductory tool, it can be drawn out for a longer duration of time. Distrust, skepticism, and uncertainty are typical feelings an employee may experience if their supervisor is abusing the method of micro managing. The role of manager is an important position of supervision in any organization. The supervisor/manager plays a key function, in the day to day needs of the organization, by finding a balance of work efficiency and managing personnel. This balance becomes even more prevalent when assigning projects or interacting with subordinates. This paper will analyze several aspects or pitfalls, managers could find themselves involved in; and will identify methods used to overcome these situations when supervising subordinates. The position of manager holds many responsibilities in an organization; those responsibilities range from dealing with requests from upper management and servicing employee’s needs, and while seeing to theses responsibilities, the manager still has to supervise the overall direction of his or her department. The multiple tasks a manager must operate within, requires the manager to be flexible and†¦Ã¢â‚¬ ¦

Difference Between Group and Team Diversity and Dynamics

The Difference between Group and Team Paper Difference between Group and Team Diversity and Dynamics Team The composition is planned and is set. People are recruited, groomed and trained or specific jobs that match their interest. People are recruited, groomed and trained or specific jobs that match their interests and the needs of the team. Each job has a specific set of skills. People with those skills or the ability to acquire them are recruited for the job. Teams have rookies and understudies who learn from those who are accomplished. They are preparing for the day they will lead. When people do not perform well, the team suffers. The team has ways of assisting the person or has systems for building their person's skills or moving him or her to another position. The planning by teams is called practice, run-throughs, or rehearsals. No matter how talented any individual team member, everyone plans. Teams have rituals, routines, and ceremonies that everyone learns and shares. Teams regularly review performance. Teams often prepare for the next piece of work based on the evaluation of the last piece of work. Teams know at most times how they are doing – if they are winning, scoring, or moving toward their stated goals. Teams often establish â€Å"Halls of Fame† retiring an honored jersey. Those who have performed well are held in high esteem. Members of teams are easily recognizable. There are usually colors, logos, T-shirts, and most important, common slang, songs, language, and history to link them to each other and the team. Time is important to teams. Most events have specific starting and ending times. Teams are often judged by what they can accomplish within a certain time frame (Klein, 2009, p. 77-80). Teams understand how important it is to consider the fans, the audience, everyone affected by the game. Teams know and respect the game's many stakeholders. Teams build team spirit into their plans and make sure to affirm and celebrate the work they accomplish together (Klein, 2009). Group The composition of the group changes from meeting to meeting – often without forethought. Members of groups are encouraged to take on jobs, positions, or tasks even if they are unprepared or not skilled in that area – and everyone knows it! People move in and out of jobs based on their inability to say no when asked. Little or no training or support is given by the group to individuals accepting jobs. . Leadership is often one-person deep, with the group highly dependent on a handful of people. When people either do not perform well or fail to perform at all, the group rarely acknowledges the failure. Groups often resist planning and use planning as corrective rather than proactive or preventive strategies. Planning is mostly done by a few people. Groups rarely create routine operations. Groups usually do not celebrate or debrief victories or defeats. Groups rarely assess their progress in achieving their stated goals or objectives in order to chart and measure their work. Groups rarely assess their progress in achieving their stated goals or objectives in order to chart and measure their work. Members of groups are often hard to identify. There’s rarely anything linking them to the group. Groups are often inconsistent in what time things start and end – especially meetings. Groups sometimes operate without thinking about their constituency (Klein, 2009, p. 77-80). Groups sometimes fail to develop a sense of team spirit. They assume everyone understands and works together. (Klein, 2009). Diversity and Dynamics Conclusion Reference Johnson, Heiman, & O'Neal. (2000). ProQuest. Journal of workplace learning, Vol_. (12),Iss_4, Laroche, Lionel. (2009). ProQuest. CMA Management. Vol. (75). Iss. 2; p. 22-26.