14.Public Diplomacy has become increasingly important in recent years Assignment

14.Public Diplomacy has become increasingly important in recent years. Why Discuss and illustrate with empirical examples - Assignment Example Murrow’s Centre for Public Diplomacy, Edmund Gullion takes public diplomacy as â€Å"Through public diplomacy people understand the means by which private groups, governments, and individuals influence the opinions and attitudes of other people and governments in a manner to exercise impact on their foreign policy conclusions.† What stands out in these two definitions for Public diplomacy is that it has to involve mechanisms that will affect the attitudes as well as opinions of other people, countries and governments. This paper will examine the reasons that have led to the clamour for public diplomacy especially in recent times during the 21st century by looking at specific examples. Public diplomacy becomes the next frontier in the study and practice of diplomacy. The â€Å"ancient† diplomacy style has been supplanted with â€Å"fresh†, free American-style diplomacy (United States. (1987)Several states have advanced beyond upholding open diplomacy on the face of the world to using public to secure and promote their national interest overseas. Public diplomacy was a principally salient government quest during the Cold War era when ideologies contest, communism versus democracy, was at the peak. Bipolar quality of public diplomacy throughout the period of the cold war has been replaced by several nations involved in public diplomacy as central securities in soft power have risen. Wang (2011) outlines the theory of soft power as an international image, specifically highlighting the values underlying the interest of a particular government. For instance, United States soft power is the capacity to convince others through the acceptability of its actions. The connection with public diplomacy rests between the concept of theoretical international relations of several â€Å"forms† of power and the concrete elements of the manner in which states improve or expand the capacity of their soft power. In as much as public diplomacy has materialized to be

State's Rights v. Federal Supremacy Essay Example | Topics and Well Written Essays - 750 words

State's Rights v. Federal Supremacy - Essay Example Thus, the South Carolina Ordinance of Nullification was written and passed by the legislature of South Carolina in November 24, 1832. The South Carolina Ordinance of Nullification was enacted in response to the Tariff of 1828 passed by Congress with force and effect in all states. The Southern states felt that the law has favored the northern states which are basically into manufacturing industries over the southern states which are based on agriculture. The State of South Carolina led by Calhoun took the stand and actually passed the nullification ordinance which described the tariff laws as â€Å"acts, purporting to be acts laying duties and imposts on foreign imports, but in reality intended for the protection of domestic manufactures and the giving of bounties to classes and individuals engaged in particular employments, at the expense and to the injury and oppression of other classes and individuals†¦Ã¢â‚¬  The South Carolina ordinance thus declared the tariffs laws as un constitutional. It argued that the federal government has â€Å"exceeded its just powers under the constitution†¦ and hath violated the true meaning and intent of the constitution, which provides for equality in imposing the burdens of taxation upon the several States and portions of the confederacy.† Calhoun justified his theory of nullification using the arguments made by Jefferson when he wrote the Kentucky Resolution in 1798 which declared that, â€Å"the several states who formed that instrument, being sovereign and independent, have the unquestionable right to judge of its infraction; and that a nullification, by those sovereignties, of all unauthorized acts done under color of that instrument, is the rightful remedy.† In addition to the power of nullification, Calhoun also added that the state of South Carolina, or every other state for that matter, has the right to secede from the union if the federal government denies its power of nullification and uses m ilitary power to force its federal laws upon the dissenting state. In clear and very specific terms, Calhoun declared that the state of South Carolina and its people â€Å"will not submit to the application of force on the part of the federal government, to reduce this State to obedience.† He declared further that any attempt to coerce the state through military or economic means is â€Å"inconsistent with the longer continuance of South Carolina in the Union.† The South Carolina Ordinance may have borrowed some ideas from the Kentucky and Virginia resolutions. All three documents reminded the federal government as to where its powers come from and that these power-givers will never just sit in the sideline when these powers are abused and misused. Likewise, all three legislations strongly promote the individual state’s power to nullify an act of the federal government that are not in accord with the spirit and purpose of the constitution. However, Calhounâ€⠄¢s ordinance differs from Madison and Jefferson’s resolutions because the former did not just stop at declaring an act of Congress as null and void. It went on to declare that if the federal government does not recognize its nullification ordinance and uses force to coerce them into obedience, then the state has the concomitant power to secede from the Union â€Å"and will forthwith proceed to organize a separate government, and do

Creative Photography Essay Example for Free

Creative Photography Essay This paper would seek to provide a comparative analysis between some of the most talented and creative photographers ever introduced to this genre of arts by examining their individual creative sense and sensibilities. Annie Leibovitz, Diane Arbus and lastly Richard Avedon. All three had three equally different styles and were truly exceptional in their own styles. Annie Leibovitz established herself as a photographer who was truly experimental as was indicated by her images and hence, was widely recognized as someone who was not afraid to portray what she truly believed in. In fact her sudden rise to fame and popularity at the tender age of 20 resulted in her being one of the most revered photographers of the modern times. One of her most famous photos was that of John Lennon as it highlighted Lennon as he was; an unpretentious image who was unfazed by all the popularity and success and hence, this image showcased Leibovitz’s ability to capture the â€Å"inner† sense of people-to go beyond the mere public image. Her bold and modern images such as that of John Lennon and his wife were an indicator of Leibovitz’s ability to capture the essence of emotions and relationships; a highly intriguing concept for this photographer. This image represented the strong connected between the pair and was a landmark in the sense that it allowed the viewer to connect with John Lennon and his wife’s emotions. Throughout her career, Leibovitz has always been considering something of a controversy as a result of her ability to capture images under a theme of subtle nudity. This very ability allow this artist to portray an image of honesty and over time, this same creative talent has been inconsistent as she moved across different forums and themes but there has always been a need to capture the inner honestly and emotion. In comparison to this, Richard Avedon was a photographer who was more interested in the way images could be used to highlight the soul and the personality of the person in question. His main source for taking cameras was his 8 by 10 camera which became sinuous with his name and he was widely recognized for his ability to take large images of famous faces. He focused more on people who made up the list of commoners and hence, his work titled the American West was criticized for showing a negative imagery of American cultural system. Audrey Hepburn was his muse and this signifies the extent to which Avedon’s talent was appreciated by his peers and other people alike and he himself however, felt that he could not translate Hepburn’s personality on camera due to its immense height. The last photographer who would be analyzed and compared would be Diane Arbus, who represented a totally different creative sense from the other two; one who believed in capturing the emotions while the other wanted to capture the inner soul. The mediums used by both were quite different as were their focuses as while Annie focused more on the capturing the famous faces, Richard showed an extensive interest in the commoners. Diane Arbus however, showed an entirely different creative sense as she focused more on capturing the relationships between specific people and a bond was highlighted which was not considered to be in tune with the normal bonds. She has been perceived as one of the most influential members of the photography genre as a result of her unfailing ability to capture a side of her subjects which seemed to want a sense of understanding on the behalf of the viewer. John Szarkowski ‘s exhibition of her works made Diane Arbus one of the most recognizable faces of photograph and her eventual suicide portrayed the tragedy of a woman who seemed incline to capture the more tragic aspect of her characters unlike the aforementioned artists who were in touch with other aspects of their subjects. Works Cited Farley, Christopher John. â€Å"Shooting to Thrill. † Retrieved from Dow Jones Company. 27 Apr 2009. http://s. wsj. net/article/SB122670139623729593. html. Leibovitz, Annie. â€Å"John Lennon. † Retrieved from RealNetworks, Inc. 27 Apr 2009. http://www. rollingstone. com/news/coverstory/10247676/1/John_Lennon. Bosworth, Patricia. 2005. Diane Arbus: A Biography. W. W. Norton, 2005. Diane Arbus: Revelations. Random House, 2003. PBS American Masters, Richard Avedon: Darkness and Light, Directed by Helen Whitney, 1995

Human Resources Culture Makes for Top Employer

Human Resources Culture Makes for Top Employer Vincent M. Mendez In 1966 at the North Carolina State University (NCSU), individuals from eight other universities where brought together by the National Institute of Health (NIH). The purpose of this group of individuals was to develop software to analyze data being developed by the United States Department of Agriculture (USDA). The original product was identified as Statistical Analysis System (SAS). This gave way to both the name and corporate beginnings. In 1972 NIH ended funding for the project. When funding ended the members of the team decided to each contribute $5,000.00 a year to continue the project at NCSU. Over the next few years SAS software was licensed to various companies across the business spectrum. As more business requested the software it was determined in 1976 by the original developers to privatize their efforts. SAS Institute Inc. originated at 2806 Hillsborough Street, Raleigh, North Carolina (NC), building located across the street from NCSU. In the beginning the small business relied on everyone in the business to know and do everyone elses job. When a shipment of users manuals arrived, everyone stopped what they were doing and formed a human chain to hoist each box, person to person, to storage space on the second floor. (SAS Institute Inc., 2016). Throughout the rest of the seventies SAS continued to grow and add employees. SAS also expanded into the global market opening subsidiary office overseas. In 1980 SAS moved to its current Headquarters location in Cary, NC. What makes SAS Institute Inc. a great place to work. CEO James Goodnight put it best in interview by Angus Loten for CIO Journal by The Wall Street Journal. The culture is the heart of the company and started in the beginning. The question and answer follows: SAS is often cited as a great place to work. Why is it important for you to keep workers happy? Because we are maintaining software for years and years, and constantly improving it and adding new features and capabilities, its very important to retain the people who originally wrote it. To do that, weve tried to create a culture where we have a great deal of respect for people and that rewards innovation. We have a weekly meeting every Tuesday where we have any number of people will come over and do demos of what theyre working on, for upper management, so we get a constant view of all the new things people are working on. (Loten, 2016). Culture is the key to SAS Institute Inc. success. Employee satisfaction along with showing their value to the company, was always at the beginning of the corporate culture of SAS. Early employees have related that in the beginning on Hillsborough street, James H. Goodnight (co-founder and current CEO) would take everyone in his car down the street to the pizza place. The company paid for everything during these outings. This was a regular occurrence when 100 customers where added. Flexible work schedules along with free MMs and breakfast goodies were present from the beginning. SAS posted its first company bulletin in 1978, which was type written on a single page of paper and posted on the bulletin board. Technology was not the only innovation SAS was a leader. In the year after moving to their new location in Cary, NC, SAS broke new ground opening the first employee child care center in the basement of the Headquarters building. This was decision by the company to keep employees (valuable programmers) considered not returning to work after pregnancy. At this point in time this was an idea not even considered by companies. This goes back to the interview Goodnight had with the Wall Street Journal in early 2016. These ideas began with the formation of the company and years before this type of information was identified as Strategic Human Resource Management (SHRM). This was the first of the ideas which made SAS a leading company to work for world wide. However, this was not the end. Following the opening of the daycare center, SAS took employee needs to a whole other level. At their headquarters campus, they open a recreation and fitness center. A health care center was open on the campus to support employees and families. This was followed by the opening of a gourmet cafà © to serve meals to employees. These additions garnered SAS awards to include Healthiest Company to Work For by Health and Living Magazine. The health care center has been a valuable to both SAS and their employees. Confirmation by a study conducted in conjunction with Duke Health. The finding was reported in a news release from SAS. Key point was the health care center lead to lower costs for both SAS and employees. For 30 years, analytics leader SAS has operated an on-site Health Care Center (HCC) for the convenience of employees and dependents. Now, a new study led by researchers at Duke Health finds those who use the HCC for primary care are less likely to need emergency department visits or hospitalizations than those who do not. (SAS Institute Inc., 2016). SAS highlights these benefits by providing them to all employees regardless of location. This type of culture is proof of success in that over the years has kept a turnover rate to around four percent. Employees, which are in 149 countries, are provided the same services as those at the Headquarters in North Carolina. Now it is not feasible to build and sustain medical clinics at all these location, the company has adapted ways to provide these services. For instance, in remote locations benefits such as childcare and medical are subsidized with local service providers. SAS does not hide it success in employee satisfaction. This is evident by visiting their website (http://www.sas.com/en_us/careers/life-at-sas.html). At this location, the company outlines what a career with SAS would be like. The headline here is this quote: By taking care of our employees, the rest takes care of itself (SAS Institute Inc., 2016). This location further discusses the culture and benefits. By separating these two areas the company can show its commitment to employees. Under the umbrella of culture there are eight areas discussed. These all relate to the company and how it manages work environment such as: open style of management to worker relationship, work conditions (college style campus at headquarters location), continuing employee growth, flexible work schedule allowing time during the day for fun and fitness, return investments (education and volunteer), and conservation. Benefits discusses four areas pertaining directly to the employee: money, career, health, and life. The founders of SAS had a vision and in that vison had the forethought that to succeed the company would not only have to provide a top line product but employ top line people. This has made for adjustments to business strategies, which requires changes to SHRM, easy and transparent. In other words: Organization development is a systematic approach to improving organizational capability, ie the capacity of an organization to function effectively in order to achieve desired results (Armstrong, 2016, p. 96). The company culture provides for change and growth. This type of corporate culture emulates SHRM. Much research has been carried out, which has shown that there is a correlation between good HRM practice and organizational performance. (Armstrong, 2016, p. 17). Being on the forefront of ideas which are now identified in discussions related to SHRM helps keep SAS as a leading place to work. The key to this is how to maintain and go forward into the future. SAS continues to be a leading place to work for many years. In 2016 Fortune ranked SAS the number two global company to work for. The reasons for the ranking came from Great Place to Work  ® reviews which related: At SAS Institute Inc., 94 percent of employees say their workplace is great (Great Place to Work, 2016). The survey provided a review of what employees think about the company and lists all the perks and programs SAS provides. What was discussed in this paper seems to be just the tip of the benefits. SAS by being far advanced in the idea of SHRM continues to adapt and change to new world and technological developments. In doing so has never forgotten to provide new and current customers great products and services requires those employees who got them in the first place. These practices has kept SAS a leader is analytical analysis and employee satisfaction. References Armstrong, M. (2016). Handbook of Strategic Human Resource Management. In M. Armstrong, Handbook of Strategic Human Resource Management (p. 17 p. 96). Philadelphia: Kogan Page Ltd. Great Place to Work. (2016, Aug 24). Great Place to Work SAS Institute Inc. Retrieved from Great Place to Work: http://reviews.greatplacetowork.com/sas Loten, A. (2016, Mar 08). SAS Institute CEO, the Godfather of Analytics, Sees Future in the Past. Retrieved from The Wall Street Journal, CIO Journal: http://blogs.wsj.com/cio/2016/03/08/sas-institute-ceo-the-godfather-of-analytics-sees-future-in-the-past/ SAS Institute Inc. (2016, Feb 03). Fewer ER, hospital visits for employer health center patients, per major academic medical center study. Cary, NC. Retrieved Dec 27, 2016, from http://www.sas.com/en_us/news/press-releases/2016/february/sas-duke-study-employer-health-care-centers.html SAS Institute Inc. (2016, May 10). Life at SAS. Retrieved 2016, from SAS, Careers, Life at SAS: http://www.sas.com/en_us/careers/life-at-sas.html SAS Institute Inc. (2016). SAS Institute Inc. Company Information. Retrieved Dec 27, 2016, from Company History 1976-1980: www.sas.com/en-us/company-infomation.html#1976-1980

What Genetic Factors Contribute to Obesity?

What Genetic Factors Contribute to Obesity? Obesity has increasingly become a challenging epidemic and is now a global concern which has shown no sign of lessening (McAllister et al, 2009, p. 868). While considerable efforts have been invested in stressing the importance of physical activity and the choice of food intake, studies have shown compelling evidence that genetic determinants brought by the inter-individual differences have high responsibility in obesity susceptibility (ORahilly Farooqi, 2006, p.1095). Substantive evidences about the molecular constituents of the major pathways involved in the balance of mammalian energy have only been recently deciphered. Therefore, this provides a gateway to a mechanistic understanding of obesity that will soon be a useful resource in the designing of effective drugs against obesity. Linkage studies and associations based on populations have identified specific loci where genetic variations occur among obese individuals. Efforts to indentifying and characterizing the monogenic obe sity syndromes have also shown considerable success (ORahilly Farooqi, 2006, p.1095). While a number of researchers have come into a consensus that genetic factors predispose individuals to obesity, some still slightly differ by appreciating the role of such factors like the influence on metabolic rate as well as the effect of selective partitioning of the excess energy in the human body into fats (ORahilly Farooqi, 2006, p.1095). This paper specifically identifies various genetic factors which contribute to obesity and provides recommendations for addressing the epidemic. To date, there are five main constituent genes known to be involved in food intake and energy expenditure pathways which ultimately contribute to obesity progression. These genes are leptin, leptin receptor, melanocortin-4 receptor, pro-opiomelanocortin as well as prohormone convertase genes (Bouchard, 2009, p.1499). The role of these genes in the occurrence of obesity and mutation consequences of such genes, wh ich are studied in different experiments, are elaborated and explained under different gene headings below. Leptin gene Efforts to perform leptin gene cloning in 1994 opened an avenue for rapid research in biomedicine and large scale genetic studies followed thereafter (Hinney, Vogel Heberbrand, 2010, p. 297). Finally, these efforts made success stories after effectively managing to treat leptin deficiency children using the recombinant leptin protein. The treatment of leptin deficiency children also provided other insights to biomedical researchers that single gene mutations could potentially lead to disorders such as obesity and hyperphagia (Hinney, Vogel Heberbrand, 2010, p. 297). Since its discovery, leptin has posed a potential possibility for the treatment of obesity. The development of obesity treatments has been centered in identifying main targets in leptin gene which was the first to be implicated for the genetic cause of obesity. The leptin hormone is mainly secreted depending on the body fat and is responsible for the regulation of appetite and energy metabolism mainly in the brain (Ahim a, 2002, p.196). Results obtained from linkage studies have deciphered that leptin is basically an assembly of 167 different amino acids that are produced by the leptin gene right from the adipose tissue. The protein encoded by the leptin gene displays a number of biological roles associated with obesity by binding with a defined receptor located in the hypothalamus. These biological roles of leptin include the control of food intake pathways, body weight regulation and homeostasis of energy (Wang et al, 2006, p.183). French studies and investigations into populations in Pennsylvania have associated leptin to cases of severe obesity. Among humans, the chromosomal locations of the genes for leptin receptor and leptin have been mapped to 1p31 and 7q31.3 respectively (Wang et al, 2006, p.183). Research had earlier shown that the variant G-2548A occurring in the LEP promoter was responsible for reductions in the BMI among overweight women. In addition, a few studies have shown correlati ons between obesity development and the presence of LEPR gene polymorphisms (Geller et al, 2004, p.572). According to Ioffe, Moon, Connolly and Friedman (1998, p.11852), subset of obese humans have considerably lower levels of leptin plasma. The findings imply that abnormal regulation of the gene in the adipose tissue could be the main cause of pathogenesis in obesity. Ioffe et al (1998, p.11852) carried out an experiment to test the propensity that decrease in the production of leptin could impact the bodys metabolism thus cause obesity. They performed their experiment by mating animal models that carried lowly expressed adipocyte specific aP2-human leptin transgene with mice that did not express any leptin gene. The leptin treatment of the mice that never expressed leptin resulted to a marked reduction in weight which resembled the results obtained after wild-type mice treatment. Usually, a subset of obese individuals expresses relatively low levels of leptin in plasma. The decreased rates of leptin production among obese individuals by the adipocytes have been implicated for the caus e of obesity (Ioffe et al, 1998, p.11854). Mutations in the leptin gene or the leptin receptor gene have been found to cause increased appetite, overeating, massive weight gain, impaired thermoregulation, insulin resistance and diabetes, immune dysfunction, sexual maturation failures and a number of neuroendocrine derangements in both human subjects and rats (Ahima, 2002, p.196). Melanocortin-4 receptor gene (MC4R) Mutations in the melanocortin 4 receptor have been said to be the most common genetic factors which contribute to obesity. While the gene coding for the protein, MC4R has been implicated for regulating the body weight of individuals and obesity, there are no convincing reports associating the gene with the increased binge eating among obese individuals. Contrary to what had been observed in the previous studies, the MC4R deficiency does not actually cause hyperinsulinemia. However, a frameshift mutation in the gene coding for the protein MC4R has been associated with dominant human obesity (Hinney, et al, 2003, p. 4258). The protein also acts as an antagonist for the agouti-related peptide (AgRP) gene that code for an endogenous antagonist for the receptor. The homologous of the MC4R gene, the MC3R gene has also been found to be a good candidate for causing genetic susceptibility to glucose intolerance in type II diabetes mellitus (Hinney, et al, 2003, p. 4258). In order to prove tha t MC4R is influential in causing obesity, researchers have sequenced the introns of the gene among the Pima Indians who among them, 300 were severely affected by obesity and 126 of them were neither obese nor diabetic. In their study, the researchers have addressed the assertion that substitution of G-A at codon 103 of the MC4R gene is responsible for influencing abdominal obesity and lipid, glucose and insulin metabolism. The substitution has also been implicated for its effect in inflecting the circulatory hormones such as the salivary cortisol (Hinney, et al, 2003, p. 4260). Genome wide association studies (GWAS) have been potential tools for identifying a number of candidate genes in specific regions of the chromosomes which harbor genes responsible and other phenotypes (Zlot et al, 2007, p.31). GWAS also provide critical tools for indentifying the common variants with reduces penetrance relevant as traits of interests or risk factors. Genes such as melanocortin-4 receptor gene occur in a coding region which also harbors other polygenic variants which regulate weight in healthy individuals apart from the mutations responsible for obesity (Yang et al, 2002, p.20328). These minor alleles that have been identified include various polymorphisms which code for isoleucine amino acid instead of valine at position 103 (103l) and the other that codes for leucine instead of isoleucine at 251L of the receptor protein. These polymorphisms are all negatively associated with the problem of obesity (Zlot et al, 2007, p.31). Homozygous carriers of such alleles have sli ghtly reduced basal metabolic rate (BMI) which is a risk factor for obesity. The biological mechanism of the MC4R gene has been suggested to involve the activation of the MC4R receptor which leads to a significant decrease in food intake. The MC4R has therefore been marked as the main therapeutic target for obesity treatment. The new regulatory biological mechanism has also been detected in cell lines which are derived from the murine hypothalamic neurons that express MC4R endogenously. This therefore points to the physiological importance of the endocytosis promoted by AgRP. In a study involving a number of obese children and adults, 6 percent of them were found to posses MC4R SNPs (Zlot et al, 2007, p.29). Following agonist stimulation, the MC4R usually signals via the intracellular adenylate cyclase pathway of signal transduction. Studies among the obese subjects have detected large quantities of MC4R mRNA in the membranes of the astrocytes contrary to the HEK-rMC4R cell membranes. Pro-opiomelanocortin (POMC) Feeding in humans follows habitually trained rhythms which are regulated by the hypothalamus. The amount of food one consumes happens as a response to the energy status in the body that depends on the hormones. Even though this is a complex process, there exists an integrated relationship between the energy needs of the body and the amount of food that is required by the body. As a result, the brain through the hypothalamus triggers the release of responsible hormones that regulate food intake. This happens through the release of pro-opiomelanocortin (POMC) (Millinvgton, 2007, p.4). The initial stage of the production of pro-opionmelanocortin starts with the production of the release of the POMC at the hypothalamus. Through a series of active enzymatic reaction steps, the pro-opiomelanocortin (POMC) plays an initial role in the production of corticotrophin (ACTH), melanocyte-stimulating hormones (MSH) and endorphin (Millinvgton, 2007, p.4). The MSH leads to the production of melanocortin peptides that plays a high role in the development of appetite. The melanocortin peptides also continue to have a role in body weight regulation. As the body continues to produce the necessary genes that regulate its development, some genes that develop in the central nervous system give rise to the production of the melanocortin peptides. According to Zemel and Shi (2000, p.179), melanocortin peptides work by coating the melanocortin-4 receptors through the formation of a layer around these receptors. This covering inhibits the food absorption and intake. The absence of this through the degeneration of the melanocortin peptide cover marks the onset of obesity. This means that melanocortin receptors POMC peptide s plays a significant role in the development of obesity. As seen earlier, feeding is a process that happens through responses of habitual rhythms such as circadian rhythms. These rhythms are controlled by the genes that are adapted to a given type of system. The lack of POMC in the body exhibits itself through adrenal failure, altered pigmentation and increment in height onset of obesity (Millington, 2007, p.8). The processing of POMC occurs partially in the pituitary cells and neurons of the hypothalamus. However, POMC derivatives can be discharged differently through varying hypothalamic sites. These are sites that are involved in feeding process. This process of release leads to slight variations in the amount of signal sent to the sites. From the above discussion, dietary related aspects especially obesity emanates from a complex combination of various genes that makes their significant contributions. Environmental factors are also known to have their equivalent contributions to the role of the genes in the dietary habits and their effects on the body. The melanocortin that is produced as a result of POMC stimulation plays a central role in the direct processes of food absorption. Additionally, the signals sent by the POMC maintain the hormonal levels that controls amount of food to be absorbed at any given moment. This is depending on the homeostatic energy requirement at any specific time. However, in the instance when the levels of POMC released by the hypothalamus get reduced to minimal levels, the immediate effect that follows is the reduced production of melanocortin peptides. This means that the body no longer has the ability to control the amount of food being taken up by the body. Obesity develops as a resul t of the body absorbing food at a higher level than required. Prohormone convertase 1 (PCSK1) Researchers have reported that common variants in the PCSK 1 gene could be a potential cause of obesity. The proprotein convertase subtilisin/kexin type 1(PCSK 1) has been suggested to play a critical role in proteolytic cleavage, a step which is also important in the maturation process of a number of hormones which are produced as precursors (Heni et al, 2010, p.86). The PCSK 1gene codes for the prohormone convertase 1 which is actively involved in peptide maturation. The protease is selectively expressed in the endocrine and neuronal tissues where its main substrates include the hormones which regulate energy metabolism such as proinsulin, proopiomelanocortin and proglucagon (Heni et al, 2010, p.86). Rare mutations in the PCSK 1 gene have been identified to be responsible for causing childhood obesity as well as the abnormal metabolism of glucose, proinsulin and insulin and the C-peptide. Common single nucleotide polymorphisms (SNPs) in the PCSK 1 gene, the rs6232 and rs6235 have b een associated with incidences of obesity (Heni et al, 2010, p.86). Various mutations of the PCSK1 gene cause monogenic obesity. The SNP rs6235 has a high correlation to the non-synonymous rs6234 which encodes the Q665E. This substitution occurs at the protein in the C-terminal region (Tuomas et al, 2009, 3499). This research found that there exist a significant correlation between age and crs6232 in the initiation and proliferation of obesity (Tuomas et al, 2009, 3499). Another research by Qibin et al (2010, p.456) found that the rs6234 has significant association with an increased risk of a combined obesity phenotype and an overall overweight condition. The PCSK 1 gene was also found to have a higher association to obesity among men as compared to women. The result of this gene is that it influences the increment in fat storage around the waist region. The study also found that there exist enough evidence that associates PCSK1 rs6234 with overweight and the level of body mass index in men. It was also revealed that PCSK1 rs6234 plays no role in the weight gain among women. There have been various recommendations in the use of several mechanisms in the management of obesity. This has been based on the knowledge of the fact that eating habits are part of acquired characteristics. However, studies have revealed that eating habits are controlled by genes. This has therefore called for more understanding on the gene make up of a person. The understanding of the role of PCSK1 gene in the control in insulin and consequent glucose synthesis is a breakthrough in the ongoing research in the search of the appropriate weight management measures. Studies conducted by Martin et al (2010, 9) have found that small amounts of alleles of PCSK1 and SNPs are associated in high levels of stimulation of glucose proinsulin levels. This gave an indication that the two are related in the reduction of proinsulin conversion with little effect on insulin itself. Under the normal conditions, prohormone convertase cleaves a substantial amount of proinsulin. The study further found that PCSK1 and SNPs alters the sequence of the amino acid sequence of the protein which makes up this hormone. The change that is initiated by the SNP rs6232 on asparagines is the reduction of the enzymatic activity. The similar change also occurs on the location of the protein thereby reducing its effectiveness in regulating insulin. The end result is the increment of body weight, a condition that is referred to as obesity. Fat Mass and Obesity Associated Gene (FTO) The FTO gene has also been identified, using the GWAS approach, to be associated with type II diabetes and obesity. The A-allele of the FTO variant rs9939609 in intron 1 has been shown to be associated with an increased risk to develop obesity complication by 31 percent (Hinney, Vogel Heberbrand, 2010, p. 302). The association of genes in obesity and overweight problems has been suggested to be high in both monogenic obesity and polygenic forms. The FTO gene is one of the best examples of the common variants which play a role in increasing the BMI and thus important among obesity individuals. The FTO gene is known to be found in chromosome 6 among humans and variants of the gene have closely been associated with human obesity. The gene is widely distributed in both adult tissues and fetal tissues but there is much expression in the pancreatic islets as well as in the hypothalamus. Transcribed amino acid sequence of the FTO gene has shown high homology with AlkB, an enzyme which demethylates DNA oxidatively. The FTO recombinant protein has the potential to catalyze 3-methylthymine demethylation in single-stranded DNA. Animal studies have shown that gene expression in FTO is usually upregulated in rats especially in the hypothalamus following food deprivation. The gene is also negatively correlated with the orexogenic galanin like peptide expression that is commonly involved in food intake stimulation. The increase in the expression of hypothalamic FTO is often associated with energy intake regulation but not the feeding reward. These consequences make the gene to be identified as a critical in causing obesity. An obesity risk allele of the FTO variant has been identified. Usually, the carriers with a single copy of the FTO allele are more susceptible to develop obesity than individuals without the copies. In another observation, the carriers of the two copies of the FTO gene weigh even more than those with a single copy of the gene. This implies that the gene causes an increased risk of obesity among the carriers compared to those without a copy of the gene. At the same time, researchers have identified the association of the single nucleotide polymorphisms (SNPs) in the similar region (rs14210850) of the FTO gene. The variation has been identified as the cause for some percentage of population variance in BMI and even a higher number of attributable obesity cases. The risk allele, according to the researchers, is found in cluster 10 SNP in intron 1 of the FTO gene known as the rs9939609. Morbid obesity has also been shown to be associated with both the INSIG2 SNPs and the FTO gene. Varian ts of the FTO have also found to be associated with the obesity condition using GWAS of BMI. In the study, individuals with AA and AT alleles at rs993909 have been found to consume more energy per day compared to the individuals having the protective genotype of TT. However, the similar studies have indicated no variation in energy expenditure based on polymorphisms. In other studies, the consequences of variations in the two different types of SNPs in the FTO gene have shown the possibility of the gene impacting the levels of circulating leptin as well as the energy expenditure. The SNPs that affect the energy expenditure and the circulating levels of leptin include the rs1421085 and rs17817449. Although the studies have not pointed on the biological mechanisms of the FTO gene in contributing to obesity and weight control, researchers have postulated that the gene could be responsible for regulating appetite through its influence in the hypothalamus. Discussion and Recommendations The pathogenesis of complex diseases such as obesity has always been associated with the interaction of environmental and genetic factors. This complexity has made it difficult for researchers to tease apart the accurate relationship between the genotype, phenotype and environmental factors by only using conventional experimental designs. Using genetic information maintained in databases, researchers have been able to identify critical molecular pathways responsible for obesity which are specifically brought by the interaction of the environmental factors and the genetic factors (Gohlke et al, 2009, p.46). Bioinformatics techniques and the Internet have offered critical tools for synthesizing data on the relationship between genes and diseases such as obesity. Methods such as genome-wide association scans have shown a number of genetic variants in the FTO gene which might be associated with phenotypes related to obesity (Scuteri et al, 2007, p.115). Researchers have identified the po tential benefits of genomic-wide association studies (GWAS) approaches in obesity intervention and prevention strategies such as the design of highly specific drugs targeting the identified molecular pathways (Zlot et al, 2007, p. 31). The role of epigenetics in obesity has been explored by a number of researchers including McAllister et al (2009, p. 892). Epigenetics encompasses the study of a number of inheritable variations mechanisms in gene expression which do not necessarily originate from alterations in the DNA sequence. These mechanisms are often established at the early stages of postnatal development and during the prenatal stages and they act to maintain a number of gene expression patterns throughout the life of an individual (McAllister et al, 2009, p. 892). Because of this, some environmental factors have become common in the recent past and have commensurately deranged the epigenetic mechanism establishment which results in the regulation of body weight (McAllister et al, 2009, p. 892). The roles of cytosine methylation within the CpG dinucleotides, the modification of histone proteins which package the DNA into the nucleus and the cell-dependent expression of a number of autoregulatory DNA binding p roteins have been investigated and shown to perpetuate the conformation of regional chromatic which dictates which type of gene will be competent transcriptionally in specific type of cells (McAllister et al, 2009, p. 892). This literally implies that apart from the genetic basis of obesity, the epigenetic studies shed light and provides extra information that is layered above the common understanding of gene sequences. Like the DNA sequence, epigenetic factors are also replicated at cell division during mitosis and meiosis thus bestowing transgenerational epigenetic inheritance (McAllister et al, 2009, p. 892). As reported by McAllister et al (2009, p. 896), the understanding of the environmental factors on the epigenetic processes has always remained elementary. Therefore, there has been little evidence to point out specific environmental exposures whose increasing levels might affect epigenetic mechanisms. Maternal obesity has however been identified as one of the main environmental exposure which results into obesity. It is accepted that the obesity epidemic affects even the childbearing women and feed-forward transgenerational obesity amplification has been proposed to result among children born of obese mothers. This is because the intrauterine environments of obese mothers are likely to induce developmental adaptations in the developing fetus which consequently predispose them to obesity. In an observation made to support this assertion, children born of obese mother after bariatric surgery were found to have reduced risks for obesity than the children born of the same mothers before bariatric surgery (McAllister et al, 2009, p. 893). Bariatric surgery is one of the medical procedures carried out with an objective of losing weight and has shown exciting evidence in reducing the chances of obesity among the born children. There are two types of disorders that have been identified to be caused by single-gene defects. The first class of these disorders is the Mendelian disorders which cause a variety of clinical features including obesity. The second class of single-gene defects is mainly characterized by disease conditions in which obesity is one of the main clinical features. 11 different genes have been reported to be closely associated with monogenic obesity and 52 genomic regions which harbor quantitative trait loci have also been indentified to have associations with human obesity. Five of the genes have been considered to be of clinical importance since they account up to 5 percent of the early obesity onset and severe cases of childhood obesity. These genes are leptin, leptin receptor, pro-opiomelanocortin, melanocortin 4 receptor as well as prohormone convertase genes. One of the most interesting observations is that all the five genes are associated with encoding receptors and peptides involve d in satiety and appetite regulation. Therefore, there is need to intensify research efforts in marking the five genes and developing molecular drug targets for critical receptors which control appetite and satiety. Apart from the five common genes that have been associated with obesity, other minor genes with smaller effects such as ACE, LDLR and VDR have also been implicated for causing obesity. These minor genes are more than 20 in number (Bouchard, 2009, p.1499). Conclusion and Recommendation The prevalence of obesity is increasing globally as biomedical researchers step up their efforts to indentify the specific genetic causes of the epidemic. A number of technological and conceptual advances have made it possible for a shift to an approach centered in single-gene search for interventions aimed at treating and preventing obesity. Before these advances, traditional approaches involved studying obesity from the polygenic approach which was very difficult to mark out the exact molecular processes that occur in at cellular level. A few complex segregation analyses maintained the assertion that obesity was mainly caused by more than a single segregating genes having large effects on the adiposity and body weight. Later studies supported the evidence that obesity could be caused by both polygenic and oligogenic determinants. With the improved technology and scanning of the entire genome, it has been possible to identify individual genes responsible for obesity using polymorphi c microsatellite markers. Among the enabling technologies in sequencing the human genomes involve SNP identification, bioinformatics and SNP genotyping technologies. At present, these technologies have made it possible to study the anatomy of the human genome with improved details and this is expected to yield newer insights into pointing out the exact genetic causes of obesity.

Essay --

Fear, suffering, danger, pain, and torture. These are all of the feelings that an abused animal feels. Only five states have had law officials directly take action against animal abuse. These states being: Idaho, Hawaii, Kentucky, Mississippi and North Dakota. Animals are abused to their deaths everyday. These owners or abusers have no appreciation for human or animal life at all. The abusers have been lucky enough to get away, with such a serious and cruel crime. And only facing the minimum punishment, or sometimes no punishment at all. Animals have just as much rights to live a happy abuse free life just like many of us do. Animal abusers need to face harsher consequences, before it begins a problem out of hand. In the following essay you will be able to comprehend and realize how bad these abused animals feel everyday. One of the first steps in saving animals and  ­creating effective laws is understanding what animal cruelty really is. There are two types of cruelty: Passive cruelty and Active cruelty. Passive cruelty is when the abuse happens as a result of neglect. It might s...

Sexism in Language Essay -- Language

Language refers to the method that humans use to communicate either through speech or written. It consists of the use of the word in a structured and conventional way. Language has been referred to as ‘our means of classifying and ordering the world; our means of manipulating reality. In structure and in its use we bring out the world into realisation and if it is inherently inaccurate, then we are misled. (Dale Spender, 1980).Language has power that allows us to make sense out of the reality we live in. Sexism is discrimination of a person based on their gender, especially on women. Sexism in language is the use of language which devalues members on one sex, almost always women, showing gender inequality. In the 1960/70’s there was a feminist campaign in Western Countries and a lot of research as conducted into gender inequality. The feminist campaign demanded that gender in equality should be eliminated from the educational system (Shi, 2001.) The existence of sexist l anguage is due to sexism in society and it is also related to social attitudes. There has been a movement amongst feminists to reduce sexual discrimination and it has led to a number of attempts to influence and change in language. Robert Hopper (2003) made a distinction between the terms ‘soft core’ and ‘hard core’ sexist language. He showed that ‘Soft core’ language was less obvious, subtle but still demeaning and patronizing to women. It was found to be more problematic because it was subtle and harder to spot. ‘Hard core’ sexism showed it to be easier to spot. Sexism in language takes many forms, though theses may be reduced to 3 types: language ignores, it defines and it deprecates women. Women and girls are hurt both physically and materially by it. Everyda... ... Language. Developmental Psychology. 20(4), 697-706. Lei, X. (2006). Sexism in Language. Journal of Language and Linguistics, 5 (1), 87-94. Mallett, R, Stangor, C, Swim, J.K. (2004). Understanding subtle sexism; Detection and Use of Sexist Language. Behavioural Science Sex Roles, 51(3/4) 117-128. Parks, J.B, Roberton, M.A. (2004). Attitudes Toward Women Mediate the Gender Effect on Attitudes Towards Sexist Language. Psychology of women Quarterly, 28(3), 233-239. Piercey, M. (2000), Sexism in the English Language. TESL Canada Journal, 17(2), 110-115. Turner-Bowker, M. (1996). Gender stereotyped descriptors in children's picture books: Does "Curious Jane" exist in the literature? Sex Roles, 35(7-8), 461-487. Ya-Lun, T. (2008). Child development (Research) Sex role (Portrayals) Children's literature (Educational aspects) Science & research, 45,(3), 310