Monopoly - economics Essay Example for Free

Monopoly economics Essay Monopoly means a market where there is only one seller of a particular good or service. In economics, a monopoly (from the Latin word monopolium – Greek language monos, one + polein, to sell) is defined as a persistent market situation where there is only one provider of a product or service. Monopolies are characterized by a lack of economic competition for the good or service that they provide and a lack of viable substitute goods. Monopoly should be distinguished from monopsony, in which there is only one buyer of the product or service; it should also, strictly, be distinguished from the (similar) phenomenon of a cartel. In a monopoly a single firm is the sole provider of a product or service; in a cartel a centralized institution is set up to partially coordinate the actions of several independent providers (which is a form of oligopoly). Characteristics Only one single seller in the market. There is no competition. There are many buyers in the market. The firm enjoys abnormal profits. The seller controls the prices in that particular product or service and is the price maker. Consumers don’t have perfect information. There are barriers to entry. These barriers many be natural or artificial. The product does not have close substitutes. Advantages of monopoly Monopoly avoids duplication and hence wastage of resources. A monopoly enjoys economics of scale as it is the only supplier of product or service in the market. The benefits can be passed on to the consumers. Due to the fact that monopolies make lot of profits, it can be used for research and development and to maintain their status as a monopoly. Monopolies may use price discrimination which benefits the economically weaker sections of the society. For example, Indian railways provide discounts to students travelling through its network. Monopolies can afford to invest in latest technology and machinery in order to be efficient and to avoid competition. Disadvantages of monopoly Poor level of service. No consumer sovereignty. Consumers may be charged high prices for low quality of goods and services. Lack of competition may lead to low quality and out dated goods and services. Advantages Disadvantages of Monopolies A monopoly is a market structure having only one producer or seller of a product or service. Some of the negative aspects of a monopoly include the single business being able to control pricing and charge relatively high prices, exceptional power over the market and a lack of new products being introduced into the market. Monopolies are created by economic, social or political factors. When one entity has control over a natural resource, a monopoly market for that resource is created. An example would be Saudi Arabia where the government has complete control over the oil industry. Monopolies are also formed when companies have copyright or patent rights to a product.

3-Methylglutaconic Aciduria Research

3-Methylglutaconic Aciduria Research A distinct type of 3-methylglutaconic aciduria due to a mutation in the Translocase of Inner Mitochondrial Membrane 50 (TIMM50) gene Abstract BACKGROUND: 3-methylglutaconic aciduria biochemically characterized by increased urinary excretion of 3-methylglutaconic acid result from defective leucine metabolism and disorders affecting mitochondrial function though in many cases the cause remains unknown. Recently mutations in mitochondrial TIMM50 gene has been reported in four patients from two unrelated families. We report additional mutations in TIMM50 gene in 6 individuals from two unrelated consanguineous families with a distinctive type of 3-methylglutaconic aciduria. METHODS:Â  We report on three patients of South Asian ancestry with intractable epilepsy, microcephaly, developmental delay, visual deficit spastic quadriplegia and three Caucasian patients of eastern European origin with intellectual disability with or without seizure. Metabolic testing revealed mild lactic acidosis and excretion of large amount of 3-methylglutaconic acid in urine in all patients. Full exome sequencing was performed using genomic DNA isolated from one surviving patient, two healthy siblings and both parents of South Asian family. Exome sequencing was also performed for Caucasian patients of eastern European origin. RESULTS:Â  Exome sequencing identified two homozygous mutation Gly372Ser and Iso392Thr mutations in the gene TIMM50. There were no other candidate alterations in exome that could explain the phenotype in the proband. The mutations are located in the conserved C-terminal domain of the Tim50 protein that interacts with the N-terminal domain of the Tim23 protein in the intermembrane space and regulates mitochondrial protein import of presequence-containing polypeptides Both parents are heterozygous. CONCLUSION: Given the phenotypic similarilty of the patients from two unrelated families and an earlier report of mutations in additional family, we conclude that TIMM50 gene mutation results in a novel mitochondrial disorder with 3-methyl glutaconic aciduria. INTRODUCTION 3-methylglutaconic aciduria (MGCA), an increase in urinary 3-methylglutaconic acid or 3-methylglutaric acid, can be a nonspecific finding in mitochondrial disorders, organic aciduria, urea cycles disease, neuromuscular disorders. but is a consistent abnormality of 3-methylglutaconyl-CoA hydratase deficiency and patients with mutations in TAZ, SERAC1, OPA3, DNAJC19 and TMEM70 gene1. These genes all encode mitochondrial membrane or membrane related proteins. In 3-methylglutaconyl-CoA hydratase deficiency due to mutation in AUH gene , 3-methylglutaconic acid derives from 3-methylglutaconyl CoA (3MG CoA), an intermediate in leucine catabolism1. It has been proposed that in other disorders, 3-methylglutaconic acid derives from aberrant isoprenoid shunting from cytosol to mitochondria via mevalonate pathway or redirection of mitochondrial acetyl CoA toward production of 3MGA due to an increase in the intra-mitochondrial NADH/NAD+ ratio resulting from mutation induced impairment in electron transport chain or Kreb cycle function 2. Examples of mitochondrial include Barth syndrome, a cardioskeletal myopathy with neutropenia, abnormal mitochondria and MGCA. Barth syndrome is caused by X-linked recessive mutations in the TAZ gene which encodes the mitochondrial membrane localized transacylase involved in the maturation of cardiolipin. Autosomal recessive mutations in the OPA3 gene (OMIM: 606580), the mouse ortholog of which encodes a mitochondrial inner membrane protein of unknown function, cause MGCA3 (OMIM: 258501), a neuroopthalmologic syndrome characterized by early-onset bilateral optic atrophy and later-onset spasticity, extrapyramidal dysfunction and cognitive deficit. MGCA5 (OMIM: 610198) is yet another form of MGCA caused by autosomal recessive mutations in the DNAJC19 gene (OMIM: 608977) and in addition to increased urinary excretion of 3-methylglutaconic acid, patients present with infancy or childhood onset dilated cardiomyopathy, microcytic anemia, mild muscle weakness and ataxia. Many patients die of cardiac failure. The DNAJC19 gene encodes the human homolog of the yeast Tim14 which is a part of the Tim23 mitochondrial protein import machinery and hasbeen shown to interact with the mtHsp70 in an ATP-dependent manner to regulate Tim23 function (Davey, 2006). WE report a distinct type of 3-methylglutaconic aciduria resulting from a mutation in mitochondrial TIMM50 gene in 3 sibs from a consanguineous family. We initially reported these xases in abstract form. Recently two different mutations in mitochondrial TIMM50 gene have been reported in four patients with 3 methylglutaconic aciduria, epilepsy, severe intellectual disability and lactic acidosis. Subjects Family 1 Family 1 has three affected sibs of South Asian ancestry with intractable epilepsy, microcephaly, developmental delay, visual deficit spastic quadriplegia. Two affected sibs died unexpectedly when they were visiting families in a remote area of a South Asian country. Metabolic testing had revealed large amount of 3-methylglutaconic acid in urine in all three affected sibs. The patients have a healthy brother and a healthy sister. Mother and father are first cousins. Detailed clinical history, imaging, EEG and metabolic testing were obtained for all affected persons. Full exome sequencing was performed using genomic DNA isolated from one surviving patient, two healthy siblings and both parents. Patient IV-1. Patient IV-1 was the first born child of the parents and was born at 36 weeks gestation after a normal pregnancy and delivery. Her weight at birth was 1.99 kg. Her weight, height and head circumference were always below 5th centile. She also had asthma and frequent episodes of pneumonia presumably due to aspiration, but the family refused G-tube placement. She was severely delayed. She never sat, stand or spoke. She has poor head control, truncal hypotonia but very brisk tendon jerks and sustained clonus. Funduscopy revealed bilateral optic atrophy. She developed seizures at 1 year of age. EEG revealed multifocal spikes arising from both hemispheres. She was treated with phenobarbital and Zonegran but family was noncompliant with medications. She continued to have daily myoclonic jerks. MRI at 2.5 and 5 years of age showed increased T2 signal in basal ganglia and periventricular white matter, brain atrophy, prominent ventricle, increased extraxial fluid. Normal liver en zymes and blood count, normal blood and CSF glucose and a serum ammonia of 21. Several serum lactate levels were mildly elevated. Lactate 2.8, 4.5 (Pyruvate 0.23), 5.4 (normal 0.7 to 2.1) Lactate to pyruvate ratio 20:1. Urine organic acid analysis revealed very high lactic acid, 3-methylglutaconic acid, and 3-methylglutaric acid. Muscle biopsy revealed only scattered atrophic muscle fibers on electron microscopy. Respiratory chain enzyme activities were within normal limits. She died at 7.5 years of age apparently due to complications from an infection while she was visiting families in a remote area of a South Asian country. Patient IV-4 was twin A born at 36 weeks gestation after an uncomplicated twin pregnancy. Her weight, height and head circumference were always below 5th centile. She was severely delayed. She never sat, stand or spoke. She has poor head control, truncal hypotonia but very increased reflexes and spasticity in the limbs. At nine-month-of age, she started to experience several episodes of eye fluttering and body jerking. Her EEG reved slow background, poor sleep architecture and frequent multifocal spike and sharp wave activities coming from both the left and right hemispheres. Her seizures were treated with Zonegran and was poorly controlled but parents refused more aggressive treatment of seizures. Metabolic testing revealed mild elevation of lactate and moderate increase of 3 methylglutaconic, 3 methylglutaric acids in urine. A brain MRI at 11-month-of age revealed diffuse volume loss supratentorially with prominent sulci and extraaxial fluid spaces, mild enlargement of the ventricl es and patchy signal abnormalities in the basal ganglia bilaterally, especially involving the caudate nuclei and putamen. On spectroscopy with voxel placed in the right basal ganglia with short and long TE, there was a lactate peak which inverted on long TE spectrum. Also, the NAA peak was low with NAA to creatinine being 1.15 on short echo and 1.29 on long echo spectrum. Also, the choline was elevated with choline/creatine ratio being 1.00 on short echo and 1.41 on long echo images. She died at 1.5 years of age apparently due to complications of an infection while she was visiting families in a remote area of a South Asian country. Patient IV-5 is a 13 year old female of South Asian ancestry, with 3-methylglutaconic aciduria intractable epilepsy, microcephaly, developmental delay, visual deficit and spastic quadriplegia. She was born at 36 weeks gestation after an uncomplicated twin pregnancy. She was twin B and stayed in NICU for 18 days for feeding issues. Her weight was 1.4 kg and she was not intubated. Patient first presented with seizures at 3 months of age with eyelid fluter and jerking of extremities. Her initial EEG revealed multifoal spikes. Initial biochemical evaluation revealed normal serum and CSF glucose, normal ammonia and liver enzymes. Serum lactate and CSF lactate 4.24 mmol were mildly elevated . Lactate was 2.7. Ammonia 25. Serum amino increased alanine 43.6 micromol/dl (9.9-34.5). Csf lactate 4.24 mmol. CSF alanine 7 micromol/dl (0.6 -4.7). There were also mild elevations of serum and CSF valine, leucine, isoleucine and alanine and lysine. Urine organic analysis revealed moderate increase of 3 methylglutaconic, 3 methylglutaric, glutaric, adipic, suberic, and sebacic acids. MRI of brain at 11 months of age revealed severe atrophic changes involving gray and white matter, predominantly of the cerebrum. Grossly abnormal signal is seen in the basal ganglia, particularly the caudate nucleus and the putamen with relative sparing of the globus pallidus and thalamus. A recent MRI (at age 13 years) reveals severe but stable atrophic changes of the gray and white matter of the supra and infratentorial brain, stable white matter changes of the putamen, caudate nucleus and periventricular white matter, Scattered diffusion restriction in the retrotrigonal white matter, compatible with active demyelination and atrophic changes of the optic nerves. Her seizures were treated with with Keppra, Lamictal, Zonegran and Onfi. She also receives carnitine. She continues to have brief episodes of whole body stiffening each week, but the family was also not very compliant with medications. He r current EEG shows slow background for age, poorly formed sleep spindles indicatvie of diffuse neuronal dysfunction, frequent multifocal interictal spike and wave suggests increased risk of seizures arising from multiple foci and hypsarrhythmia in sleep . She has failure to thrive despite G-tube feeding. At 12 years of age, G-tube was placed due to history of aspirations. Height, weight and head circumference below 5th centile. She is severely delayed. She is nonverbal and never learned to sit independently, stand or walk. She recognizes family members, responds to their voice and looks and smiles at them. Her fundoscopy shows mild optic atrophy. She has bilateral esotropia and dysconjugate gaze. She has poor head control and truncal hypotonia, but her limbs are spastic and her tendon reflexes are very brisk. Family 2 Patient V:1 was the first son of Caucasian consanguineous parents (IV:4 and IV:5) of Eastern European origin. Within the context of an organic acid and amino acid study in young and adult subjects with non-syndromic developmental delay and intellectual disability, he was investigated at the age of 17 years and presented with a developmental language disorder (involving semantic, syntactic, and pragmatic components of the linguistic system), emotional and communicative problems (fearful, aggressive, and loner), and hyperactivity. On neuropsychological testing he showed a short attention span. The child was born at term after an uneventful pregnancy and his birth weight was 2.9 kg. At 4 months of age he was affected by myoclonic jerks that were controlled by administration of valproic acid and lamotrigine. Developmental delay was observed starting from the middle of the first year of life, accompanied by decreased muscle tone. He could walk without support only at 6 years. At last medi cal exam, the patient showed a reduced muscle mass (height 148 cm, Z-score 3.43; weight 38 kg, Z-score 4.21; BMI 17.1 kg/m2, Z-score 2.02) and a head circumference of 51 cm (Z-score 2.76). Due to refusal of parents, no brain imaging studies could be performed. Fundoscopic examination was normal. Laboratory tests, including creatine phosphokinase (CPK), liver enzymes and plasma amino acids, were normal. The profile of urinary organic acids showed a large peak of 3-methylglutaconic acid (113 mmol/mol creatine) and a slightly increased level of 3-methylglutaric acid (17 mmol/mol creatinine). Patient V:3 was the younger brother of V:1, the third child of IV:4 and IV:5. He was investigated at the age of 11 years and presented with a clinical phenotype (developmental delay and intellectual and behavioral disorder) similar to that of his brother. The pregnancy and early postnatal course was unremarkable and birth weight was 3.1 kg. At 3 months he received valproic acid and lamotrigine to control tonic seizures with sudden stiffening movements of arms and legs. The boy walked independently at 4 years. When he was 9 years, his growing parameters were: height 119 cm (Z-score 2.47), weight 22 kg (Z-score 1.91), BMI 15.5 kg/m2 (Z-score 0.38), and head circumference 48 cm (Z-score 3.52). Neuropsychological exam revealed mental retardation and impaired communicative skills, including poor language abilities (few repetitive words with no sentences). Occasionally, the patient is aggressive. Ophthalmologic examination revealed left esotropia. High levels of 3-methylglutaconic acid (15 5 mmol/mol creatine) were identified in urine, together with smaller amounts of 3-methylglutaric acid (22 mmol/mol creatinine). Patient V:5 was the second son of consanguineous parents (IV:9 and IV:10) related to those of patients V:1 and V:3. The girl was delivered by cesarean section because of growth arrest at 37 week. The neonate showed no external malformations. Birth weight was 2.1 kg. In the following years, the clinical phenotype was characterized by delayed developmental milestones, nocturnal enuresis, severe cognitive impairment, speech retardation, and lack of communicative skills. Results of the electroencephalogram were normal. No brain imaging data are available. On a few occasions, levels of ammonia and lactic acid were found to be slightly elevated, but these results could not be confirmed by repeated blood analyses. Plasma levels of amino acids are within normal range. Fundoscopic examination was normal up to 7 years, but since then there is evidence of mild bilateral optic atrophy. Urine levels of of 3-methylglutaconic acid and 3-methylglutaric acid were 176 mmol/mol creatine and 29 mmol/mol creatinine, respectively. DISCUSSION Deleterious Nature of the TIMM50 gene alteration: TIMM50 NM_001001563 c.1114G>A p.G372S The p.G372S variant (also known as c.1114G>A), located in coding exon 9 of the TIMM50 gene, results from a G to A substitution at nucleotide position 1114. The glycine at codon 372 is replaced by serine, an amino acid with somewhat similar properties. The alteration is not observed in healthy cohorts: Based on data from the NHLBI Exome Sequencing Project (ESP), the TIMM50 c.1114G>A alteration was not observed among 6,503 individuals tested. Allele frequency data for this nucleotide position are not currently available from the 1000 Genomes Project and the alteration is not currently listed in the Database of Single Nucleotide Polymorphisms (dbSNP). Though some variants may appear to be rare due to database-specific ethnic underrepresentation, rare missense alleles commonly exhibit a deleterious effect on protein function (Kryukov, 2007; Tennessen, 2012). The altered amino acid is conserved throughout evolution: The G372 amino acid position is completely conserved in eukaryotes all th e way from the yeast Saccharomyces cerevisiae to humans (Mokranjac, 2003). The alteration is predicted deleterious by in silico models: The p.G372S alteration is predicted to be probably damaging and deleterious by PolyPhen and SIFT in silico analyses, respectively. The amino acid is located in a functionally important protein domain: The p.G372S alteration is located in the conserved C-terminal domain of the Tim50 protein that interacts with the N-terminal domain of the Tim23 protein in the inter membrane space and regulates mitochondrial protein import of presequence-containing polypeptides (Geissler, 2002; Yamamoto, 2002; Guo, 2004). The alteration cosegregated with disease in the family herein: Co-segregation analysis revealed that this alteration is present in a heterozygous form in the mother, father and brother, and absent in the sister. Based on the available evidence, the TIMM50 c.1114G>A (p.G372S) alteration is classified as a likely pathogenic mutation. The TIMM50 gene is not currently known to underlie Mendelian disease (aka clinically novel). The TIMM50 gene function is consistent with the probands clinical presentation: The Translocase of Inner Mitochondrial Membrane 50 (TIMM50) gene (OMIM: 607381) is located on human chromosome 19q13.2 and consists of 11 exons. It encodes the Tim50 protein, a 353 amino acid 40 kDA homolog of the yeast Tim50 protein that functions as an integral part of the mitochondrial Tim23 protein import machinery by linking protein translocation across the outer and inner mitochondrial membranes. This interaction was confirmed by the coprecipitation of Tim50 with an antibody against Tim23 (Geissler, 2002; Yamamoto, 2002; Guo, 2004). The authors further confirmed that the C-terminal domain of Tim50 is located in the inter-membrane space (IMS) where it stably binds to the segment of Tim23 that spans the IMS and regulates its function. Nuclear encoded mitochondrial proteins are synthesized in the cytosol and subsequently imported into the mitochondria through the function of translocators, the TOM complex of the outer mitochondrial membrane (OMM), and the Tim23 and Tim22 complexes of the inner mitochondrial membrane (IMM) (Jensen, 2002). While the Tim22 complex is involved in the transport and insertion of proteins lacking the presequence into the inner membrane, the Tim23 complex is required to process and insert presequence-containing precursor proteins. The IMM generates a proton motive force that is critical for cellular energy synthesis (Stock, 2000) and the permeability barrier of the IMM needs to be maintained during the transport of proteins through the pore-forming Tim23 protein associated with other IMM proteins such as Tim14 (human DNAJC19), Tim17, Tim21, Tim44 and Tim50. Using various yeast IMM protein mutants, Meinecke et al. (2006) demonstrated that tim17 and tim21 mutant mitochondria displayed membra ne potential values that were comparable to wild type mitochondria, whereas tim50 mutant mitochondria showed a drastic reduction of the membrane potential. Further functional studies revealed that the Tim23 channel is tightly regulated by Tim50 in its inactive state to maintain the IMM permeability barrier and is opened only when presequence-containing polypeptide chains need to be translocated into the mitochondrial matrix or the inter membrane space (IMS). Loss of Tim50 function in yeast led to cellular growth arrest and reduced cell viability (Mokranjac, 2003). Knockdown to Tim50 expression in cultured human cells using RNA mediated interference resulted in an increase in the release of cytochrome c and apoptosis in response to cell death stimuli (Guo, 2004). A 50 kDa isoform of the human mitochondrial TIM50, TIM50a, consisting of 456 amino acids has been found to localize in nuclear speckles, specifically in the Cajal bodies, and interact with small nuclear ribonuclear proteins (snRNPs), the coilin protein and the Survival of Motor Neurons (SMN) protein (Xu, 2005) which has been implicated in Spinal Muscular Atrophy (SMA). The protein sequences of the mitochondrial TIM50 and the nuclear TIM50a are identical with the exception of additional 103 amino acids at the N-terminal of TIM50a that are the result of an alternative translational start sequence. This additional N-terminal sequence in TIM50a is thought to contain a putative nuclear localization sequence that allows the Tim50a isoform to display a nucleus specific localization. Based on their results, Xu et al. hypothesized that Tim50a might be involved in the regulation of snRNP biogenesis and possibly the function of the nuclear SMN protein encoded by the SMN1 gene. One of our patien ts had mulsle biopsy. Although there were atrophic changes, no neuropthic pattern was seen. Reference List (1) Wortmann SB, Kluijtmans LA, Rodenburg RJ et al. 3-Methylglutaconic acidurialessons from 50 genes and 977 patients. J Inherit Metab Dis 2013;36:913-921. (2) Ikon N, Ryan RO. On the origin of 3-methylglutaconic acid in disorders of mitochondrial energy metabolism. J Inherit Metab Dis 2016;39:749-756. Legends Legend to Figure 1 Five-generations pedigree of the family with mild 3-methylglutaconic aciduria in which the TIMM50 p.(Ile293Thr) was identified. Subjects V:1, V:3, and V:5 (filled symbols) are patients suffering from intellectual disability and increased urinary excretion of 3-methylglutaconic acid. They are born to consanguineous parents and homozygous for the TIMM50 c.1011T>C mutation predicting the replacement of isoleucine 293 with threonine in the encoded protein. The mutation was inherited by a common ancestor (either I:1 or I:2) and has been identified in the heterozygous state in the clinically and biochemically unaffected subjects III:3, III:4, III:9, IV:2, IV:4; IV:5; IV:9, IV:10, and V:2.

Theory of Multiple Intelligences

Theory of Multiple Intelligences The theory of multiple intelligences was proposed by psychologist Howard Gardner in the late 1970s. This theory attempted to disprove the intelligence quotient (IQ) by suggesting that individuals actually possess eight different and autonomous intelligences. Individuals combine and utilize these different types of intelligences to solve problems and make products valuable to society. The intelligences are linguistic, musical, logical-mathematical, naturalist, spatial, bodily-kinesthetic, intrapersonal, and interpersonal. Gardner believed that the intelligence quotient only tests for linguistic and logical-mathematical intelligence, and does not include the other equally important intelligence. This represents a departure from acknowledging only academic intelligence, but including other forms of intelligence as well. For example, musicians, quantum theorists, and professional sports players are the best at their field, but have different areas of intelligence that have variances that cannot be detected by taking the IQ test alone. With the accompanying work of Charles Spearman on the general intelligence, g, Alfred Binet designed the IQ test, or intelligence quotient. This was initially used in the early 1900s to test French schoolchildren for their levels of academic achievement in order to properly place them into classes. This theory still remains the primary conception and test of intelligence. But the multiple intelligence theory claims that individuals that excel in one area on intelligence may not necessarily do well in the other areas of intelligence. In another case of opposing beliefs, the general intelligence postulates that intelligence is an innate trait that the individual has no control over. Gardners theory of multiple intelligence asserts that intelligence is a product of both nature and nurture. Heritable traits give individuals high or low potentials in one area of intelligence, depending upon what skills and traits their parents had. In addition, the experiences and practice of the individu al can increase and hone one domain to its peak, or neglect can cause underachievement of potential. In Gardners seven areas of intelligence, linguists is the ability to analyze incoming information and utilizing or creating written and oral language, logical-mathematical intelligence is the ability to solve abstract problems and calculate effectively, and spatial intelligence is the ability to change images with the mind, musical intelligence is the ability to create and appreciate sound patterns, and naturalist intelligence is the ability to identify the natural elements of the world, including plants, animals, and weather. Bodily-kinesthetic intelligence is the ability to correctly place ones body in order to solve problems, interpersonal intelligence is the ability to recognize other individuals moods and intentions, and intrapersonal intelligence is the ability to recognize ones own moods and intentions. Some research that tests Gardners theory of multiple intelligences is informal questionnaires, written assessments, or multiple choice tests. These tests provide a sample of different domains of intelligences and identify each individuals relative and absolute strengths. This is because each domain has a certain score, and domains may be ranked from high to low intelligences for each person, with every individuals score unique and different from any other scores. These results correlate directly to an individuals performances on practical and immediate tasks. These multiple intelligence ideas were brought to the United States, and the first experiments were performed here. But over time, this theory has spread all over the world and has gained its place and importance in the world of psychology. This test of multiple intelligences allows individuals to have direct feedback of their strengths and weaknesses. In schools, teachers can use this to their advantage by nurturing the areas of strength and improving upon the weaker skills as well. The results of this test can provide a general direction for an individuals future success and the potential of a certain domain. In addition, different curriculums can be adjusted and modified in order to assist a student in learning to their fullest capacity. For example, The Gardner School of Arts and Sciences uses Howard Gardners theory of multiple intelligences as the framework for the schools teaching method. The school recognizes the different abilities and intelligences of their students, so teachers incorporate all eight domains to identify strength and weakness of each individual and develop each intelligence to the individuals full potential. When I took the written multiple intelligences test, I received individual scores for each domain of intelligence. My highest three intelligences are logical-mathematical, linguistic, and intrapersonal. These results allows me identify my areas of strengths and weaknesses as it relates directly to my actions and future success. My highest scoring domain is logical-mathematical intelligence. This means that I can understand logical concepts and mathematical problems well; I am able to reason out solutions and function at an abstract level. The jobs that would fit this category would be a physicist or computer programmer. I enjoy working with patterns, relationships, and the abstract. With this intelligence, I can solve difficult problems with reasoning and will tend to be more methodical to discern patterns between events and numbers. The second intelligence domain is linguistic intelligence. This means that I have a developed sense of oral and written communication and the different qualities of words and phrases. The careers consistent with high scores in linguistic intelligence are poets and writers. I am more attuned to the meaning, sound, and shapes of words, and am able to use this to my advantage in writing and in speeches in order to inform, persuade, or excite. I enjoy reading, writing, and puzzle solving. My third highest scoring intelligence domain is intrapersonal intelligence. This means that I have a highly developed sense of self-knowledge and an ability to act on that understanding. I learn best from working alone, having time to myself for reflection, and working on self-paced assignments where I have my own space.

Kurt Vonnegut :: essays research papers

  Ã‚  Ã‚  Ã‚  Ã‚  Kurt Vonnegut has always had a great awareness of the destructive social impact of science and technology. Contraptions that Vonnegut calls â€Å"social transplants† replace real relatives and friends with synthetic ones. Recordings, radio and television are just a few of these devices. They make it possible to bring synthetic relatives and friends right into your home and replace those friends and relatives who are not perfect, nor even consistent, with a better class of people. Vonnegut’s least favorite technology is the computer, because it is a nervous system outside of our own, and it has deprived humans of the experience of becoming. â€Å"All they have to do now is wait for the next program from Microsoft† (Pickering 24). Films, books and plays show us people talking much more entertainingly than people really talk. Singers and musicians show us humans making sounds far lovelier than humans really make (Skaw 568). All of these technological developments have decreased the amount of contact we have with other humans. The first of these â€Å"transplants† took place in the 4th century before Christ. Audiences accepted attractive people who memorized interesting things to say on stage as genuine relatives and friends (Vonnegut 266). We no longer have a need to make conversation with our dreadful real family and friends, not when we have all of these technological and entertaining transplanted friends and family. Vonnegut believes contemporary society is lonely because we have alienated ourselves from each other because of all of the technology in our world. Throughout his many writings Vonnegut shows his fascination with the way technology changes the social environment (Lundquist 88).   Ã‚  Ã‚  Ã‚  Ã‚   He never abandons his theme of hatred for science and technology and its social impact on society. Vonnegut also believes that we no longer have developed imaginations because of destructive technological developments. We are not born with an imagination; teachers and parents help us to develop it. Imagination was once very important because it was your major source of entertainment. The imagination circuit is built in your head. People can read a book and envision it in their mind. However, this is no longer necessary. Now there are shows, actors, and movies that show us the story instead of letting us use our imagination to envision it. We do not need imagination just like we do not need to know how to ride horses in our society. We have cars that can go much faster than horses so why learn how to ride one? This question can be applied to imagination. Why unleash your imagination to envision an unknown world in a book

Shakespeares Julius Caesar :: Plays William Shakespeare Caesar Essays

Shakespeare's Julius Caesar "A talent for drama is not a talent for writing, but is an ability to articulate human relationships"- Gore Vida. This is certainly true for William Shakespeare, on of the greatest writers of all time. He wrote such dramas like Romeo and Juliet, Macbeth, Hamlet and Othello. Julius Caesar is no different. His ability to relate to human nature by using drama accurately distinguishes Julius Caesar from the rest by creating suspense, eagerness and tension. Act III Scene II is an especially important part to the play. Brutus I explaining got the crowd why Caesar was slain "as he was valiant, I honor him; but, as he was ambitious, I slew him" (ll. 30-31) and "Not that I loved Caesar less, but that I loved Rome more" (ll. 21-22). This quote proves and summarizes Brutus' point in his speech. To achieve his goals, Brutus' oratory techniques were simple, logical, and rational. Brutus' speech is very formal, controlled and it seems that all of the sentences are perfectly balanced. Although he did a very good job at explaining to the confused crowd that murdering Caesar was for the good of Rome, he still had not won them over yet. After he explained himself and his purpose, the people were reluctant to believe him, yet there were convinced for only a short while. Antony has sworn not to attack the conspirators, although he intends to. This creates more tension within the plot by adding layers of opposition. In Antony's speech, he paints a different picture of Caesar "HE hath brought many captives home to Rome/ Whose ransoms did the general coffers fill/ Did this in Caesar seem ambitious?" (ll.80-82). Antony continues by stating, "I thrice presented him a kingly crown/ Which he did thrice refuse. Was this ambition?" (ll. 87-89). He asks the people if they consider this ambitious, obviously implying it was not, because Caesar's deeds were for the good of Rome, not for Caesar himself. This art of persuasion is able to move the mob. All at once, they discard "noble Brutus" and listen to Antony who is a "plain blunt man". Clearly wooed by his impressive oration, the mob alters the fate of the conspirators, adding more suspense and drama to the plot. During the whole scene, it teases us leaving us on the edge waiting for the conclusion. The introduction of two characters adds suspense in Act II. Calphurnia, Caesar's wife, tries to convince him to stay at home. Being persistent she is able to convince him "Do not go forth today: call it my fear/ That keeps you in the house, and not your own" (Scene

Kate Chopins The Storm and The Story of an Hour Essay -- Papers Chopi

Kate Chopin's "The Storm" and "The Story of an Hour" 'The Storm' and 'The Story of an Hour' expresses the attitudes of two women's rebirth and liberation. These two stories are alike in several ways. Natures plays a major role in both of these women's lives. Calixta and Mrs. Louise Mallard struggle to find their independence and in doing so the endings are triumphant and tragic. 'The Storm' begins on a stormy spring day, with the protagonist Calixta at her sewing machine. She is alone, her husband Bobinot and son Bibi have gone to the store. Calixta seems to be a bored woman, confined to her duties as a housewife and mother. As the distant storm approaches she is unaware of what the storm brings, her former lover Alcee. Calixta allows Alcee into her home and opens her whole world to him. There is a connection between the storm that is going on outside and the storm of emotions going on in Calixta and Alcee. The weather sends Calixta into Alcee?s arms, he wraps his arms around her, and they can no longer hide their feelings for one another. They gave into their raging emotions and made love. Outside the weather was subsiding and Calixta and Alcee?s bodies felt relaxed and calmed. ?The rain was over; and the sun was turning the glistening green world into a palace of gems.? (1614) His face beamed with light like the sun. The storm inside of her was satisfied and for a brief instant Calixta felt liberated from her ordinary dull life. Unlike Calixta, Louise Mallard is a fragile woman afflicted with heart trouble. It comes to her attention through a trustworthy friend that her husband, Brently Mallard has been killed in a railroad disaster. She is overcome with intense grief and instantly weeps o... ... she has. Mrs. Mallard?s freedom did not last but a few moments. Her reaction to the news of the death of her husband was not the way most people would have reacted. We do not know much about Mr. And Mrs. Mallards relationship. We gather from the text that her freedom must have been limited in some way for her to be feeling this way. Years ago women were expected to act a certain way and not to deviate from that. Mrs. Mallard could have been very young when she and Brently were married. She may not have had the opportunity to see the world through a liberated woman?s eyes and she thought now was her chance. Bibliography: Chopin, Kate. ?The Story of an Hour.? Literature For Composition. Ed. Sylvan Barnet, et al. New York: 1996. 12-13 Chopin, Kate. ?The Storm.? The Norton Anthology. Ed. Nina Baym, et al. New York: 1999. 1612-1615

Friend Classification

Friend Classification Having friends is an important part of life. It is friends that I share everything with. There are many types of people in the world and many types of friends. Knowing that, it becomes all the more important to select the right people so that I might have the correct friends. A friend is somebody that will always be there for me. I always have a great bunch of friends but sometimes some people are more of a friend then others. I have my general acquaintance friends and then I have my best friends. What is the difference between a best friend and a general acquaintances friend? A best friend is a person that I know well and regard with affection and trust. My best friend knows me better than anyone, definitely better than my parents, and sometimes better than I know myself. For best friends there is a feeling, and an emotion for every event shared together: a feeling of love, a feeling of happiness and a feeling of remorse; a feeling of laughter, and a feeling of tears. My best friend has seen me at my worst, and helped me be my best. My best friend will always tell me that I look good, even on my worst days. My best friend is someone with whom I've shared my most intimate secrets with, and laughed the loudest. I've already made plans to name one of my children after her, in hopes that my next of one is a girl. And although we may grow apart and not talk to each other as much, it is safe to say that true best friends are the ones you have for life. My best friend always understands me, or at least pretends to, and she is always willing to listen to my opinions and never criticizes them, even if they are a little weird. We have a secret language with special codes that no one would ever be able to crack. She was with me and held my hand when I got my belly button pierced and she was there with me when my dad threatened to rip it out. She comes to all my family functions like Christmas, Thanksgiving, and Easter and makes fun of my strange great-aunts with me. When we go through these emotions together, we learn and grow from them and become closer than ever before. A general acquaintance friend is just simply an acquaintance. This means that I basically only know their name. I might not even remember what they look like if I go away for a short vacation. Usually, I meet these types of friends in school, at work, on the bus, in the gym, or anywhere else I might be. I normally would not mind having a cup of coffee with them, but if anything else came up, I usually would have no problem parting company. I normally don’t miss them when they are elsewhere. It is also this type of friends who give me the most amount of aggravation. Since most of the time I am placed in a position where you have to act friendly, such as school or work, I would not normally tell an acquaintance when he or she is doing something aggravating, such as tapping the fingers a table or chewing gum loudly. This is why I call them â€Å"pest friends. A general acquaintance friend is not someone I would ever really consider hanging out with a lot or getting to know more than I have to. Human survival is based on some kind of friendship. From the highest authority to the lowest bums living on the streets all of us have experienced in some way or the other one of these different kinds of friendships. I take this friendship for granted because it is something that exists naturally in society and I never really have to actually go out into the world looking for a friend. My personal realization came when I had to start life in a new city, in different surroundings. The feeling of loneliness I had was enough to drive a person to near madness. So in conclusion what I’m trying to say is that we cannot thrive successfully as individuals or as a society without having some form of friendship with other individuals rather it be general acquaintance friends or best friends.