Mechanical Engineering at the University of Tulsa

Desmond Tutu essays

Desmond Tutu essays Archbishop Desmond Tutu was a well known and respected black church leader. He lived in South Africa. The government made it illegal for anyone to oppose it. So Archbishop Tutu called all the religious leaders in South Africa to his cathedral in Cape Town on February 29, 1988. There they linked arms and marched to government offices with the intent to deliver a letter to the Prime Minister. Met by armed riot police Archbishop Desmond Tutu was arrested and thrown in jail. Desmond Mpilo Tutu was born on October 7, 1931. He lived in Klerksdorp, a poor black township near Johannesburg. His home didnt have electricity, running water, or indoor toilets. This was a common place for black people to live in because black people were not allowed to live in the city unless they were servants. His father, Zachariah, was a respected school teacher but the Tutus still had to obey South Africas harsh unfair laws. His mother, Aletha, was a servant in a white home. Despite these conditions Desmonds home was a happy one. He was smart and did well in school which he rode to in a train where he played cards with other passengers, often cheating to get extra cash. When he was fourteen Desmond caught tuberculosis, almost died, and had to stay in the hospital for two years. While in the hospital Desmond met a white priest named Father Trevor Huddleston. Father Huddleston became very influential in Desmonds life. Father Huddleston brought many books for to the hospital for him to read. Desmond graduated from high school with honors and became one of the few blacks allowed to attend a university. Desmond Tutu wanted to be a doctor, but lacked the funds to pursue this goal. Instead, he studied to be a school teacher like his father. It was then that Tutu married his wife, Leah, who was a teacher in July 1955. Desmond became a teacher in a high school at Krugersdorp. He named his first son Trevor after father Huddleston. A ...

Making Sense of American Popular Songs Research Paper

Making Sense of American Popular Songs - Research Paper Example The American Popular Ballad of the Golden Era, 1924-1950. Princeton: Princeton University Press, 1995. In this work, much emphasis has been put on specific individuals that perform and work on popular music. In addition, the work has focused on a specific eras in which popular music were at its best in America. The book reveals what propelled people to start singing and performing popular music. These factors taken into consideration, the work is good enough to address the issues of American identity through popular music. Fuld, James J. The Book of World-Famous Music: Classical, Popular and Folk. Foreward by William Lichtenwanger. New York: Crown Publishers: 1966. This book looks at a wide range of music in America and their artists. The important information given about such music and their artists is imperative in the tracing of American identity through music. Among the cultures explored in this work are classic, popular and folk. As such, I found this book imperative in the writ ing of this paper. Grove Dictionary of American Music. Restricted database available online at through some schools and colleges. This source has a lot of information on the artists of popular music from the composers of songs to the performers. The information included is the bibliographic works for the artists. This makes the book significant in researching on the American identity through analysis of bibliographies of the composer and performers of pop music. Hamm, Charles. Yesterdays: Popular Song in America. New York and London: W.W. Norton & Company, 1983. Of significance about Charles’ work is that it concentrates on major works. Through the information found in this book, it is easy to establish the wave movement of Americans to the initiation of popular music. As... The paper tells that popular music in America took on a transformation in the second half of the 19th century to emphasize commercial expansion. This overlapped into the twentieth century and traces can still be seen in today’s popular music. As a result, the expansion of the music industry meant that more songs had to be composed, staged, produced and listened to in the entire country of the United States of America. In the first place, popular music was restricted to ethnic minorities or immigrant people to express their dissatisfaction in the manner in which the government was running social and economic matters in the country. However, commercialization expanded the market for such songs as well as thematic implications attached to the songs. On the other hand, Jewish artists incorporated segments from their tradition into the American music. This is well illustrated when Sophie Tucker performed her pop song â€Å"My Yiddishe Momme† which was staged in 12925. The so ng was performed in both Yiddish and English. Additionally, the Afro-American values resulted into a sequence of characteristic song style. This made most of the African American performers to be enthusiastic and confident with the themes central to pop culture. Nevertheless, there was a change in issues that were held true to popular music by 1950. These changes were in the contradictions over the period in which such songs were performed. In the first place, some songs remained stable from one period to another. The rise of other genres in music performed and composed in America like rock and roll, blues and soul music has an overriding impact on popular music.

Analzying group process Essay Example | Topics and Well Written Essays - 500 words

Analzying group process - Essay Example The group was trying to reach to a consensus which would be accepted by all the group members. At the beginning, all of them stated with their own desirousness. After a while, instead of thinking about one’s own choice, they shifted their focus to a particular solution which may serve or fulfill all members’ requirement. Ultimately the group was trying to come up with a particular solution as per the demand and requirement of the group. All the members did not perform at par. Few of them had excellent command over language and had guts to establish their view over other participants. From the beginning of the discussion, it has been noticed that Nelson and Kathrin had leadership quality. As both of them clearly stated their views and they also provided opportunities to Perez to give his verdict who did not properly participate because of shyness. Apart from these, three other participants were good as per the communication level but Megan and Allen always tried to suppress other to make their statement more prominent. This attitude brought in inconsistency with in the discussion. Regarding Davis, though he is not able to show the leadership attitude but he has followed all such techniques through which flow of the communication has not been affected. At the middle of the discussion, Megan added one topic which was a bit relevant with the topic. That is the education system of developing countries. But later on she began to emphasis on that topic only which made the discussion out of track and interrupted in the flow of the communication. Next, Kathrin takes the responsibility to get back to the actual track by avoiding that topic and gain the attention of the other members towards the actual topic. During the discussion Davis, Nelson and Kathrin addressed few of the past statistics related to the courses and the current education system which made the discussion more

Micronutrient deficiency Essay Example | Topics and Well Written Essays - 500 words

Micronutrient deficiency - Essay Example Still, much needs to be done, before a complete and conclusive success is achieved in this aspect of health care. Disorders Caused by Iodine Deficiency Iodine deficiency can impact human health much before the birth of a child. Iodine deficiency has the potential to jeopardize children’s mental health and in some instances could put to risk the very survival of a child (WHO: Online). Iodine deficiency leads to the impairment of the cognitive development in children (WHO: Online). Iodine deficiency has severe repercussions during pregnancy. It could lead to still births, abortions and may lead to congenital abnormalities like mental retardation that is grave and mostly irreversible, and cretinism (WHO: Online). Iodine deficiency also gives way to goiter (WHO: Online). These are some of the visible and easily discernable disorders caused by iodine deficiency. Of far greater significance is the less visible impact of iodine deficiency that most often gives way to mental impairmen t resulting in a compromise of the intellectual capacities in children and adults, in the day to day life (WHO: Online). Symptoms of Iodine Deficiency Some common symptoms of iodine deficiency include goiter or enlargement of the thyroid, weight gain, weakness, fatigue and depression (Mercer, 2006).

Analysis of NFL Injuries

Analysis of NFL Injuries INTRODUCTION Achilles tendon (AT) ruptures are increasing in incidence across all populations[1-9]. Recent large-scale analyses put the incidence as high as 7-40 ruptures per 100,000 person-years[3-5, 10]. A 33-year study from Finland discovered from 1979 to 2011 the injury rate increased from 2.1 to 21.5 ruptures per 100 person-years in all age groups and activities[6]. Even in the athlete population, the number of athletes suffering AT ruptures is increasing which poses a potentially career-altering and even ending injury[1, 6, 11-13]. Nearly a third (27.5-32%) of all National Football League (NFL) players who suffer an AT rupture are unable to return to competition[13, 14]. In the NFL from 1980-2001, around 4 AT ruptures that required surgical intervention occurred each year[11]. From 2009 to 2014 in the NFL, there was an average of 14.67 (Standard deviation: 4.13) AT ruptures each season[15]. These ruptures are seen most frequently in running, jumping and cutting movements[6, 12, 16]. Achilles tendon ruptures typically occur from a non-contact mechanism during explosive acceleration or a sudden change of direction with an eccentrically loaded foot[14]. The AT has elastic properties that are required for locomotion and is the strongest tendon in the human body[12, 17, 18]. This elastic nature and strength allows it to transmit high forces, up to 12 times ones body weight[17, 19, 20]. Durability requirements of the AT create a unique set of challenges in proper treatment decisions. Current reconstruction concepts differ behind the ideal treatment strategy[9, 21]. The recovery process from all surgical techniques is an arduous challenge involving significant physical therapy and medical treatment. Unfortunately a majority of patients, especially those in the general population are able to return to a pre-injury level, with the current exception being elite athletes[22]. Although several studies evaluate AT ruptures in multiple populations, including professional athletics, studies that assess trends in professional football are scarce. NFL athletes provide an interesting patient population due to the intricate details and variables reported for every game where data is archived and widely available. A recent NFL Injury Surveillance System (ISS) analysis by Mai HT et al., discovered only a 72.5% return to play rate for athletes who suffered an AT rupture. If the athlete was able to return, the average return was 375.1 days, similar to the recovery period for ACL reconstruction (378.1 days)[13]. Athletes fortunate enough to return to competitive action frequently experience a significant decline in performance, and their competitive athletic longevity may be shortened[13, 14, 23]. The potential devastating effect on high-level athletes has required the development of ideas to optimize treatment management and improve return to play rates[23]. Previously, anterior cruciate ligament (ACL) injuries have been scrutinized due to their high incidence, long rehabilitative process and potential career-threatening nature of the injury[24]. A recent review by Balazs et al. identified four studies that found an increased risk of ACL injury on artificial playing surfaces in football cohorts, although these findings are not consistent across all studies[24]. Current research evaluates multiple variables in efforts to find potential contributing risk factors, including playing surface, that may increase the risk and rate of these devastating injuries[24, 25]. Identifying and understanding risk factors from prior research has been used to develop and improve protocols and outcomes after ACL injuries[24]. With the growing incidence of AT injuries, research is necessary to improve management and prevention of AT ruptures, especially in football players where the current literature is limited. This study performed an extensive review of reported NFL injuries from public injury records and injury reports during the 2009-10 to 2016-17 seasons. This data was compiled to monitor the incidence and injury rates of AT injuries that occurred during the regular season to evaluate the influence of playing surface on rupture rate. Additionally, further analysis to identify potential effects of position and frequency of injury at different periods of the season on AT ruptures was performed to guide future studies. Our hypothesis is that playing surface has no impact on the incidence and injury rate of AT ruptures in professional football players despite a recent overall increase in AT ruptures. METHODS A thorough online review was conducted by three co-authors to document AT ruptures sustained in the NFL between the 2009-10 and 2016-17 seasons. Online search criteria consisted of information acquired from Rotoworld.com, NFL.com, ESPN.com, SBNation.com, SI.com and from each teams local sports reports and blogs covering the team. Open searches through Google.com utilized combinations of the words Achilles and tendon along with the player, team and year of injury. Published weekly injury reports and team injury reserve lists were utilized to identify players who suffered injuries to their lower extremity or leg. Their names were added to the open internet search key words in attempts to improve accuracy of documenting all AT ruptures of NFL athletes. Only injuries with corresponding reports that confirmed the injury were included. Additional information gathered through the online search and acquired reports included player-specific details including team, position, approximate date of injury, activity at time of injury and other injury specific details including mechanism and playing surface when available. Injury incidence was recorded for each season. A season was defined as the day after the prior Super Bowl until the day of the Super Bowl in each given season. Descriptive statistics characterizing the injuries by playing surface, time in the season (broken up in to four game segments specific to each team considering their bye week) and players participating on offense, defense or being a specialist (i.e. kicker, punter, long-snapper) were determined for analysis. As previously described by Lawrence et al., injury rates were calculated per 100 team-games (TG)[26]. A TG is defined as one team exposure to a game[26]. One regular season or post-season game is equal to two TG as there are two individual teams participating in each game[26]. Mid-P exact tests were calculated to evaluate differences in IRs with statistical significance established at p Team and schedule information was gathered through Pro Football Reference and official team websites. The yearly team schedules and location of games played was recorded to help determine the home team and playing surface for all injuries suffered in games. Adjustments were made when games did not take place at the stadium of the home team and corrected accordingly. An analysis of the number of AT injuries per game for each variable was calculated. An NFL game in this study included the participation of two teams. Injury rate ratios were used to compare the incidence of AT injuries on different playing surfaces (i.e. natural grass and artificial turf). RESULTS Between the 2009-10 and 2016-17 seasons, there were a total of 45 Achilles tendon ruptures reported in the NFL during games (Figure 1). There was a subtle increase in the number of ruptures suffered each year. The most Achilles tendon ruptures occurred during the 2013-14 and 2016-17 season (N = 9) and the incidence of ruptures on grass was 24 (IR: 1.00 per 100 TG) compared to 21 (IR: 1.13 per 100 TG) on artificial turf playing surfaces (Figure 2). The difference in rate was not statistically significant (p = .67). Of the 45 Achilles tendon ruptured over the eight years, 32 (71.1%) were suffered by defensive players.  Ãƒâ€šÃ‚   Offensive players only sustained 13 ruptures and specialists reported no ruptures over that time (Figure 3). Defensive players suffered the greatest number of Achilles tendon ruptures every season monitored except for 2015-16. Defensive players had a significantly increased IR (p = .005) compared to offensive players (Table 1). When factoring in the playing surface, offensive players suffered a higher percentage of their ruptures on turf (N = 8, 61.5%) compared to defensive players that sustained a great number of their ruptures on natural grass (N = 19, 59.4%). Achilles tendon ruptures were most likely to occur early in the season. The greatest incidence was reported in the 1st or 2nd 4 game segments of the regular season schedule (N = 17 and N = 14 respectively). These 31 ruptures in the first 8 games of the regular season made up 68.9% of all Achilles ruptures in games over eight seasons (Table 2). There was a significant rate difference between the first four games of the regular season with the last four games of the regular season (IRR: 3.40, p = .01). The second four games of the regular season also demonstrated a significant rate difference with the final four games of the regular season (IRR: 2.80, p = .04). DISCUSSION Previous studies have documented the increased incidence of acute Achilles tendon ruptures in the general population. After the NFL lockout, the increasing incidence of Achilles tendon ruptures in the NFL was noted and gained national attention[11]. The purpose of this study was to document the incidence and injury rates of Achilles tendon ruptures in games over eight NFL seasons. Using this data, we were able to evaluate the potential influence of playing surface on the rate of Achilles tendon ruptures between grass and artificial turf to improve our understanding of the growing injury. Game information provides playing surface details for each game for analysis. Since this injury compilation is from public records, the ability to accurately identify the playing surface for training and practice injuries is limited. Analysis of 4,272 regular season and playoff team-games reported 45 Achilles tendon ruptures. The overall game injury rate was 1.05 AT ruptures per 100 TG. As the current literature on AT rupture epidemiology in professional football is limited, this is one of the few studies in the past decade reporting IRs. The IR for artificial turf was 1.13 per 100 TG and 1.00 per 100 TG on natural grass. There was no demonstrated difference between rates on artificial turf and natural grass (p = .67). These early findings support that playing surface does not affect the rate of AT ruptures. Other studies evaluating injury patterns have confirmed that certain injuries are more likely during certain activities or periods of the season, like hamstring strains in the NFL preseason[27]. To further understand our findings, overall AT ruptures were broken down in to four game segments of the regular season and the post-season. The greatest IR was observed in the first and second four-game portions of the regular season (IR: 1.66 and 1.37 per 100 TG respectively). The only significant rate difference occurred between those two four-game segments with the final four games of the regular season (p = .01 and .04 respectively). These findings support the significantly increased rate of injury early in the season. A further analysis of all AT ruptures in practice and games is important to help understand the significance of these early findings. Previously between the 1997 and 2002 seasons, a total AT analysis reported that Achilles tendon ruptures sustained were evenly distributed[ 14]. Our game findings do not support this earlier analysis; however, the overall incidence has increased substantially since the previous study[14]. Further evaluation may confirm these findings and help identify risk factors that lead to an increased risk of AT rupture early in the season. Additionally, further evaluation should identify if this increase is only during the beginning of the regular season or is also distributed throughout pre-season training camps. Immediately following the NFL lockout in the 2011 season, there were 10 reported Achilles tendon ruptures in the first 12 days of training camp[11]. That off-season was unique for at least the last decade due to the elimination of rookie mini-camps and off-season training sessions (OTAs), but potentially highlighted the importance of adequate preparation for current physical demands of professional football players[11]. Ultrasound evaluation found that subjects who are less active have a thinner Achilles tendon compared to athletes[18, 28]. A recent meta-analysis of 27 studies identified that differences in the loading conditions affected the adaptive responses (tendon stiffness, Youngs modulus, and tendon cross-sectional area)[29]. Additionally, although shorter high intensity programs may induce adaptive tendon responses, intervention programs of longer duration appears to be more efficient and clearly demonstrated increased adaptive responses (greater than or equal to 12 weeks)[29 ].   The combination of findings after an NFL Lockout off-season preventing team-affiliated practice and the meta-analysis findings stress the significance of adequate player preparation[29]. An adequate player preparation programs involves sufficient high level intensity training of significant length that prepares the athlete and allows for tendon adaptations to prepare them for training camp exposures. Continued efforts to identify the best training protocols to prepare athletes for the demands of football training camp is crucial for optimal injury prevention. Additional analyses identify specific positions or position groups most likely to sustain specific injuries[14, 27]. We were interested if the reactive nature of defensive players increased their likelihood for injury. Of the 45 AT ruptures identified, a majority (N = 32, 71.1%) were sustained by defensive players that demonstrated a significantly increased rate in games compared to offensive players (p = .005). Eccentric movements increase the tendon length[29, 30]. The Achilles tendon functions as both a spring and a shock absorber[18]. Previously, athletes have been found to have a thicker Achilles tendon than subjects who are less active[18, 28]. Currently, ruptures are believed to be caused due to the overloading of the taut tendon, but other studies have also discovered degenerative changes within the ruptured tendon[8, 29, 30]. Although research demonstrates a genetic influence on the predisposition of a person towards an Achilles tendon injury[31], these findings clearly demonstrate an additional risk experienced by defensive players.   We suspect one factor that increased the incidence of AT injuries for defensive players is the reactive nature of the position and movements required of defensive players compared to the movements utilized by offensive and specialist players. A further analysis may be able to confirm this hypothesis and if practice injuries are included may be able to provide an adequate sample size to identify specific positions more susceptible to injuries. CONCLUSION Utilizing game data, there is no apparent correlation between playing surface and rate of AT ruptures. Our findings identify significant rate differences in AT ruptures in the first and second four game segments of the regular season compared to the final four games. Additionally, our findings are some of the most recent published game IRs for AT ruptures. Defensive players suffered a majority of ruptures compared to offensive or specialist players. Further analysis to identify an overall IR including practices and additional analysis of player position and time of the season of injury will improve our understanding of AT ruptures in professional football. LIMITATIONS This analysis of the NFL relies on publicly available data. We are aided in our analysis as the NFL requires all teams to report and publish injury reports each week of the season in addition to every game of the season televised. This allows the accuracy of game data to be of increased accuracy compared to practice information that is not as widely publicly available. Even with the precautions, there are possibilities for AT ruptures to not be documented. With the current attention to long-term injuries, there is potential bias from an increased attention and publication of athletes who sustained AT ruptures compared to the beginning of our study. REFERENCES [1] Fox G, Gabbe BJ, Richardson M, et al. Twelve-month outcomes following surgical repair of the Achilles tendon. Injury 2016; 47: 2370-2374. [2] Ganestam A, Kallemose T, Troelsen A, et al. Increasing incidence of acute Achilles tendon rupture and a noticeable decline in surgical treatment from 1994 to 2013. A nationwide registry study of 33,160 patients. Knee Surg Sports Traumatol Arthrosc 2016; 24: 3730-3737. [3] Huttunen TT, Kannus P, Rolf C, et al. Acute Achilles Tendon Ruptures: Incidence of Injury and Surgery in Sweden Between 2001 and 2012. Am J Sports Med 2014; 42: 2419-2423. [4] Mattila VM, Huttunen TT, Haapasalo H, et al. Declining incidence of surgery for Achilles tendon rupture follows publication of major RCTs: evidence-influenced change evident using the Finnish registry study. Br J Sports Med 2015; 49: 1084-1086. [5] Jacobsson J, Timpka T, Kowalski J, et al. Prevalence of Musculoskeletal Injuries in Swedish Elite Track and Field Athletes. Am J Sports Med 2012; 40: 163-169. [6] Lantto I, Heikkinen J, Flinkkilà ¤ T, et al. Epidemiology of Achilles tendon ruptures: Increasing incidence over a 33-year period: Clinical relevance level IV. Scand J Med Sci Sports 2015; 25: e133-e138. [7] Sheth U, Wasserstein D, Jenkinson R, et al. The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27 607 patients. Bone Jt J 2017; 99-B: 78-86. [8] Wertz J, Galli M, Borchers JR. Achilles Tendon Rupture: Risk Assessment for Aerial and Ground Athletes. Sports Health 2013; 5: 407-409. [9] Ververidis AN, kalifis KG, Touzopoulos P, et al. Percutaneous repair of the Achilles tendon rupture in athletic population. J Orthop 2016; 13: 57-61. [10] Raikin SM, Garras DN, Krapchev PV. Achilles Tendon Injuries in a United States Population. Foot Ankle Int 2013; 34: 475-480. [11] Myer GD, Faigenbaum AD, Cherny CE, et al. Did the NFL Lockout Expose the Achilles Heel of Competitive Sports? J Orthop Sports Phys Ther 2011; 41: 702-705. [12] Gajhede-Knudsen M, Ekstrand J, Magnusson H, et al. Recurrence of Achilles tendon injuries in elite male football players is more common after early return to play: an 11-year follow-up of the UEFA Champions League injury study. Br J Sports Med 2013; 47: 763-768. [13] Mai HT, Alvarez AP, Freshman RD, et al. The NFL Orthopaedic Surgery Outcomes Database (NO-SOD): The Effect of Common Orthopaedic Procedures on Football Careers. Am J Sports Med 2016; 44: 2255-2262. [14] Parekh SG, Wray WH, Brimmo O, et al. Epidemiology and Outcomes of Achilles Tendon Ruptures in the National Football League. Foot Ankle Spec 2009; 2: 283-286. [15] Hoffman J, Krill M, Hewett T. Anterior Cruciate Ligament And Achilles Tendon Injuries In The Nfl From 2009-10 To 2014-15 Seasons: 3075 Board #140 June 3, 3:30 PM-5:00 PM. Med Sci Sports Exerc; 48: 873. [16] Hess GW. Achilles Tendon Rupture: A Review of Etiology, Population, Anatomy, Risk Factors, and Injury Prevention. Foot Ankle Spec 2010; 3: 29-32. [17] Joseph MF, Lillie KR, Bergeron DJ, et al. Achilles Tendon Biomechanics in Response to Acute Intense Exercise: J Strength Cond Res 2014; 28: 1181-1186. [18] Malvankar S, Khan WS. Evolution of the Achilles tendon: The athletes Achilles heel? Foot Edinb Scotl 2011; 21: 193-197. [19] Lorimer AV, Hume PA. Achilles Tendon Injury Risk Factors Associated with Running. Sports Med 2014; 44: 1459-1472. [20] Oda H, Sano K, Kunimasa Y, et al. Neuromechanical Modulation of the Achilles Tendon During Bilateral Hopping in Patients with Unilateral Achilles Tendon Rupture, Over 1 Year After Surgical Repair. Sports Med. Epub ahead of print 3 October 2016. DOI: 10.1007/s40279-016-0629-3. [21] Gulati V. Management of achilles tendon injury: A current concepts systematic review. World J Orthop 2015; 6: 380. [22] Egger AC, Berkowitz MJ. Achilles tendon injuries. Curr Rev Musculoskelet Med. Epub ahead of print 13 February 2017. DOI: 10.1007/s12178-017-9386-7. [23] McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv 2014; 23: 179-183. [24] Balazs GC, Pavey GJ, Brelin AM, et al. Risk of Anterior Cruciate Ligament Injury in Athletes on Synthetic Playing Surfaces: A Systematic Review. Am J Sports Med 2015; 43: 1798-1804. [25] Hershman EB, Anderson R, Bergfeld JA, et al. An Analysis of Specific Lower Extremity Injury Rates on Grass and FieldTurf Playing Surfaces in National Football League Games: 2000-2009 Seasons. Am J Sports Med 2012; 40: 2200-2205. [26] Lawrence DW, Hutchison MG, Comper P. Descriptive Epidemiology of Musculoskeletal Injuries and Concussions in the National Football League, 2012-2014. Orthop J Sports Med 2015; 3: 232596711558365. [27] Elliott MCCW, Zarins B, Powell JW, et al. Hamstring Muscle Strains in Professional Football Players: A 10-Year Review. Am J Sports Med 2011; 39: 843-850. [28] Emerson C, Morrissey D, Perry M, et al. Ultrasonographically detected changes in Achilles tendons and self reported symptoms in elite gymnasts compared with controls An observational study. Man Ther 2010; 15: 37-42. [29] Bohm S, Mersmann F, Arampatzis A. Human tendon adaptation in response to mechanical loading: a systematic review and meta-analysis of exercise intervention studies on healthy adults. Sports Med Open 2015; 1: 7. [30] Pedowitz D, Kirwan G. Achilles tendon ruptures. Curr Rev Musculoskelet Med 2013; 6: 285-293. [31] Maffulli N, Margiotti K, Longo UG, et al. The genetics of sports injuries and athletic performance. Muscles Ligaments Tendons J 2013; 3: 173-189. FIGURES Figure 1. Figure 2. Figure 3. Table 1. IncidenceIRaIRRbp-value Defense320.752.46 (1.31-4.85).005 Offense130.30 a Injury rate based on 4,272 TG (4,096 regular season and 176 post-season TG) bInjury rate ratios with 95% confidence limits Table 2. IncidenceIRaIRRbp-value 1st 4 games171.66 1.21 (0.59-2.51)c.60 2.13 (0.93-5.21)d.08 3.4 (1.30-10.31)e.01 2.92 (0.53-61.68)f.29 2nd 4 games141.37 1.75 (0.74-4.40)d.21 2.80 (1.04-8.67)e.04 2.41 (0.43-51.37)f.42 3rd 4 games80.78 1.6 (0.52-5.38)e.42 1.38 (0.22-30.76)f.85 4th 4 games50.49 0.86 (0.12-20.45)f.83 Post-season10.57 aInjury rate based on 4,096 regular season (1,024 each 4-game period) or 176 post-season TG bInjury rate ratios with 95% confidence limits Compared with c2nd 4 games of the regular season, d3rd 4 games of the regular season, e4th 4 games of the regular season, or fpost-season

Hamlets Sanity Essay -- Shakespeare Hamlet

Hamlet's Sanity Throughout Shakespeare?s play, Hamlet, the main character, young Hamlet, is faced with the responsibility of attaining vengeance for his father?s murder. He decides to feign madness as part of his plan to gain the opportunity to kill Claudius. As the play progresses, his depiction of a madman becomes increasingly believable, and the characters around him react accordingly. However, through his inner thoughts and the apparent reasons for his actions, it is clear that he is not really mad and is simply an actor simulating insanity in order to fulfill his duty to his father. Hamlet only claims madness because it allows him to say and perform actions he otherwise would be prohibited from, while keeping people from taking his actions seriously. This seems to be part of his initial plan that is first mentioned when he asks Horatio and Marcellus not to make any remarks in relation to his ?antic disposition (1.5.192).? Hamlet?s madness allows him to talk to Claudius, Gertrude, Ophelia, and Polonius in a manner unsuitable for a prince. He is often disrespectful and insulting in his remarks. Although his acting backfires during his speech to Gertrude, Hamlet is able to severely criticize her for her actions because she thinks he is insane. During the play he also makes many sexual innuendos and even blatantly sexual remarks towards Ophelia such as ?That?s a fair thought to lie between maids? legs (3.2.125).? His convincing insanity act gives him the chance to vent his anger towards Ophelia for her abandonment. Similarly, in another scene, he is able to tell Polonius his true feelings through his guise. Upon Polonius deciding to ?take leave? of Hamlet, Hamlet replies, ?You cannot, take from me anything that I will more willingly part withal (2.2.233).? Furthermore, Hamlet uses his madness as almost an excuse, and definitely part of his apology, towards Laertes for his murdering of Polonious. Would a madman be able realize he was mad and call his actions uncontrollable? Were it not for his ?madness? he would have been reprimanded rather than feared, pitied, or ignored. Hamlet?s madness redirects attention away from what he is thinking about his father?s death, and puts it on why he has gone insane. This allows only himself to know what he is truly thinking, does not require him to answer any questions as to why he might be acting strange, a... ...th him in case he is biased. A madman would not have had the foresight, reason, or possibly even care, to think in this very organized fashion. Even when questioning whether ?to be or not to be (3.1.64)? Hamlet is sane in his thinking. He measures the ?pros and cons? of his situation, and although at this point he appears mad to most everyone, he is most definitely sane in thought. Hamlet can be considered no worse than an eccentric, determined, and possibly single-minded man, who was made so by his father?s murder and his request for revenge. His feigned madness is maintained because it allows him to continue with his plans. This madness is not, however, sustained when guard is unnecessary. Maybe Hamlet thought too much, but he thought as a sane man would. He commits no actions without reason, and he is far too astute and organized to be proclaimed mentally unstable. Hamlet?s portrayal of a madman is also very complex because it allows not only his points to be made, but in a believably insane way, which contrasts greatly with the expected ramblings of a truly insane person. Bibliography: Shakespeare, William. Hamlet. Ed. Cyrus Hoy. 2nd ed. New York: Norton, 1992.

Nb Assessment

Table 21-2 SUMMARY OF NEWBORN ASSESSMENT *MCH pages 479-473| NORMAL| ABNORMAL (POSSIBLE CAUSES)| NURSING CONSIDERATIONS| Initial AssessmentAssess for obvious problems first. If infant is stable and has no problems that require immediate attention, continue with complete assessment. | Vital Signs| TemperatureAxillary: 36. 5– 37. 5 °C (97. 7 – 99. 5 °F). Axilla is preferred site. | Decreased (cold environment, hypoglycemia, infection, CNS problem). Increased (infection, environment to warm). | Decreased: Institute warming measures and check in 30 minutes. Check blood glucose. Increased: the excessive clothing.Check for dehydration. Decreased or increased: look for signs of infection. Check radiant warmer or incubator temperature setting. Check thermometer for accuracy if skin is warm or cool to touch. Report abnormal temperature to physician. | PulsesHeart rate 120 – 160 BPM. (100 sleeping, 180 crying). Rhythm regular. PMI at 3rd-4th intercostal space lateral t o mid-clavicular line. Brachial, femoral, and pedal pulses present and equal bilaterally. | Tachycardia (respiratory problems, anemia, infection, cardiac conditions). Bradycardia (asphyxia, increased intracranial pressure).PMI to right (dextrocardia-heart situated to right of body, pneumothorax). Murmurs (normal or congenital heart defects). Dysrhythmias. Absent or unequal pulses (coarctation of the aorta). | Note location of murmurs. Refer abnormal rates, rhythms and sounds, pulses. | RespirationsRate 30 -60 (AVG 40 -49) BrPM. Respirations irregular, shallow, unlabored. Chest movements symmetric. Breath sounds present and clear bilaterally. | Tachypnea, especially after the first hour (respiratory distress). Slow respirations (maternal medications). Nasal flaring (respiratory distress). Grunting (respiratory distress syndrome).Gasping (respiratory depression). Periods of apnea more than 20 seconds or with change in heart rate or color (respiratory depression, sepsis, cold stress). Asymmetry or decreased chest expansion (pneumothorax). Intercostal, xiphoid, supraclavicular retractions or see-saw (paradoxical) respirations (respiratory distress). Moist, coarse breath sounds (crackles, rhonchi) (fluid in the lungs). Bowel sounds in chest (diaphragmatic hernia). | Mild variations require continued monitoring and usually clear early hours after birth. If persistent or more than mild, suction, give oxygen, call physician, and initiate more intensive care. Blood Pressure Varies with age, weight, activity, and gestational age. Average systolic 65-95 mm Hg, average diastolic 30-60 mm Hg. | Hypotension (hypovolemia, shock, sepsis). BP 20 mm Hg or higher in arms than legs (coarctation of the aorta). | Refer abnormal blood pressures. Prepare for intensive care and very low. | Measurements| Weight2500-4000 g (5 lbs. 8 oz. to 8 lbs. 13 oz. ). Weight loss up to 10% in early days. | High (low gestational age LGA, maternal diabetes). Low (small for gestational age SGA, preter m, multifetal pregnancy, medical conditions and mother that affected fetal growth).Weight loss above 10% (dehydration, feeding problems). | Determine causeMonitor for complications common to cause. | Length48-53 cm (19-21 inches)| Below normal (SGA, congenital dwarfism). Above normal (LGA, maternal diabetes). | Determine causeMonitor for complications common to cause. | Head Circumference32-38 cm (12. 5-15 inches). Head and neck are approximately ? of infants body surface. | Small (SGA, microcephaly, anencephaly-absence of large part of brain or skull). Large (LGA, hydrocephalus, increased intracranial pressure). | Determine causeMonitor for complications common to cause. | Chest Circumference30-36 cm (12-14 inches).Is 2 cm less than head circumference. | Large (LGA). Small (SGA). | Determine causeMonitor for complications common to cause. | Posture Flexed extremities move freely, resist extension, return quickly to flexed state. Hands usually clenched. Movements symmetric. Slight t remors on crying. Breech: extended, stiff legs. â€Å"Molds† body to caretaker’s body when held, responds by quieting when needs met. | Limp, flaccid, floppy, or rigid extremities (preterm, hypoxia, medications, CNS trauma). Hypertonic (neonatal abstinence syndrome, CNS injury). Jitteriness or tremors (low glucose for calcium level).Opisthotonos- extreme hyperextension of body, seizures, stiff when held (CNS injury). | Seek cause, refer abnormalities. | CryLusty, strong. | High-pitched (increased intracranial pressure). Week, absent, irritable, cat-like â€Å"mewing† (neurologic problems). Hoarse or crowing (laryngeal irritation). | Observe for changes in report abnormalities. | Skincolor pink or tan with acrocyanosis (cyanotic discoloration of extremities). Vernix caseosa in creases. Small amounts of lanugo (fine,soft downy hair) over shoulders, sides of face, forehead, upper back. Skin turgor good with quick recoil. Some cracking and peeling of skin.Normal var iations: Milia (tiny white bumps). Skin tags. Erythema toxicum (flea bite† rash). Puncture on scalp (from electrode). Mongolian spots. | Color: cyanosis of mouth and central areas (hypoxia). Facial bruising (nuchal cord). Pallor (anemia, hypoxia). Gray (hypoxia, hypotension). Red, sticky, transparent skin (very preterm). Greenish brown discoloration of skin, nails, cord (possible fetal compromise, postterm). Harlequin color (normal transient autonomic imbalance). Mottling (normal or cold stress, hypovolemia, sepsis). Jaundice (pathologic if first 24h). Yellow vernix (blood incompatibilities). Thick vernix (preterm).Delivery Marks: bruises on body (pressure), scalp (vacuum extractor), or face (cord around neck). Petechiae (pressure, low platelet count, infection). Forceps marks. Birthmarks: Mongolian spots. Nevus simplex (salmon patch,† stork bite†). Nevus flammeus (port-wine stain). Nevus vasculosus (strawberry hemangioma). Cafe au lait spots (6+) larger than 0. 5c m in size (neurofibromatosis). Other: excessive lanugo (preterm). Excessive peeling, cracking (postterm). Pustules or other rashes (infection). â€Å"Tenting† of skin (dehydration). | Differentiate patient bruising from cyanosis. Central cyanosis requires suction, oxygen and further treatment.Refer jaundice in first 24 hours or more extensive than expected for age. Watch for respiratory problems in infants with meconium staining. Look for signs and complications of preterm or postterm birth. Record location, size, shape, color, type of rashes and marks. Differentiate Mongolian spots from bruises. Check for facial movement with forceps marks. Watch for jaundice with bruising. Point out and explain normal skin variations to parents. | Head Sutures palpable with small separation between each. Anterior fontanel diamond shaped, 4-5 cm, soft and flat. Many bulge slightly with crying. Posterior fontanel triangular, 0. 5-1 cm.Hair silky and soft with individual hair strands. Normal v ariations: overriding sutures (molding). Caput succedaneum or cephalohematoma (pressure during birth). | Head large (hydrocephalus, increased intracranial pressure) or small (microcephaly). Widely separated sutures (hydrocephalus) or hard, ridged area at sutures (craniosynostosis- birth defect that causes one or more sutures on a baby's head to close earlier than normal). Anterior fontanel depressed (dehydration, molding), full or bulging at rest (increased intracranial pressure). Woolly, bunchy hair (preterm). Unusual hair growth (genetic abnormalities). | Seek cause of variations.Observe for signs of dehydration with depressed fontanel; increased intracranial pressure with bulging of fontanel and wide separation of sutures. Refer for treatment. Differentiate Caput succedaneum from cephalohematoma, and reassure parents of normal outcome. Observe for jaundice with cephalohematoma. | Ears Ears well-formed and complete. Area where upper ear meets head even with imaginary line drawn fr om outer canthus of eye. Startle response to loud noises. Alerts to high-pitched voices. | Low set ears (chromosomal disorders). Skin tags, pre-auricular sinuses, dimples (may be associated with kidney or other abnormalities).No response to sound (deafness). | Check voiding if ears abnormal Look for signs of chromosomal abnormality if position abnormal. Refer for evaluation if no response to sound. | FaceSymmetric and appearance and movement. Parts proportional and appropriately placed. | Asymmetry (pressure imposition in utero). Drooping of mouth or one side of face,† one-sided cry† (facial nerve injury). Abnormal appearance (chromosomal abnormalities). | Seek cause of variations. Check delivery history for possible cause of injury to facial nerve. | Eyes Symmetric. Eyes clear. Transient strabismus. Scant or absent tears.Pupils equal, react to light. Alerts to interesting sights. Doll’s eye sign- reflex movement of the eyes in the opposite direction to that which the head is moved, the eyes being lowered as the head is raised, and the reverse (Cantelli sign); an indication of functional integrity of the brainstem tegmental pathways and cranial nerves involved in eye movement. Red reflex present- reddish-orange reflection of light from the  eye's  retina. May have subconjunctival hemorrhage or edema of eyelids from pressure during birth. | Inflammation or drainage (chemical or infectious conjunctivitis). Constant tearing (plugged lacrimal duct).Unequal pupils. Failure to follow objects (blindness). White areas over pupils (cataracts). Setting sun sign- downward deviation of the eyes so that each iris appears to â€Å"set† beneath the lower lid, with white sclera exposed between it and the upper lid; indicative of increased intracranial pressure or irritation of the brain stem. (hydrocephalus). Yellow sclera (jaundice). Blue sclera (osteogenesis imperfecta- condition causing extremely fragile bones). | Clean and monitor any drainag e; seek cause. Reassure parents that subconjunctival hemorrhage and edema will clear. Refer other abnormalities. NoseBoth nostrils open to air flow. May have slight flattening from pressure during birth. | Blockage of one or both nasal passages (choanal atresia). Malformations (congenital conditions). Flaring, mucus (respiratory distress). | Observe for respiratory distress. Report malformations. | Mouth Mouth, gums, tongue pink. Tongue normal in size and movement. Lips and palate intact. Sucking pads. Sucking, rooting, swallowing, gag reflexes present. Normal variations: precocious teeth, Epstein’s pearls-Multiple small white epithelial inclusion cysts found in the midline of the palate in most newborns. Cyanosis (hypoxia). White patches on cheek or tongue (candidiasis). Protruding tongue (Down syndrome). Diminished movement of tongue, drooping mouth (facial nerve paralysis). Cleft lip, palate or both. Absent or weak reflexes (preterm, neurologic problem). Excessive drooling (tracheoesophageal atresia). | Oxygen for cyanosis. Expect loose teeth to be removed. Obtain order for antifungal medication for candidiasis. Check mother for vaginal or breast infection. Refer anomalies. | Feeding Good suck/swallow coordination. Retains feedings. | Poorly coordinated suck and swallow (prematurity).Duskiness or cyanosis during feeding (cardiac defects). Choking, gagging, excessive drooling (tracheoesophageal fistula, esophageal atresia). | Feed slowly. Stop frequently if difficulty occurs. Suction and stimulate if necessary. Refer infants with continued difficulty. | Neck/Clavicles Short neck turns head easily side to side. Infant raises head when prone. Clavicles intact. | Weakness, contractures, or ridgidity (muscle abnormalities). Webbing of neck, large fat pad at back of neck (chromosomal disorders). Crepitus, lump, or crying when clavicle or other bones palpated, diminished or absent arm movement (fractures). Fracture of clavicle more frequent in large infants with shoulder dystocia at birth. Immobilize arm. Look for other injuries. Refer abnormalities. | Chest Cylinder shape. Xiphoid process may be prominent. Symmetric. Nipples present and located properly. May have engorgement, white nipple discharge (maternal hormone withdrawal). | Asymmetry (diaphragmatic hernia, pneumothorax). Supernumerary nipples. Redness (infection). | Report abnormalities. | Abdomen Rounded, soft. Bowel sounds present within first hour after birth. Liver palpable 1-2cm below right costal margin. Skin intact. 3 vessels in cord. Clamp tight and cord drying.Meconium passed within 12-48hr. Urine generally passed within 12-24h. Normal variation: â€Å"Brick dust† staining of diaper (uric acid crystals). | Sunken abdomen (diaphragmatic hernia). Distended abdomen or loops of bowel visible (obstruction, infection, and large organs). Absent bowel sounds after first hour (paralytic ileus). Masses palpated (kidney tumors, distended bladder). Enlarged liver (infectio n, heart failure, hemolytic disease). Abdominal wall defects (umbilical or inguinal hernia, omphalocele, gastroschisis, exstrophy of bladder). Two vessels in cord (other anomalies). Bleeding (loose clamp). Redness, drainage from cord (infection).No passage of meconium (imperforate anus, obstruction). Lack of urinary output (kidney anomalies) or inadequate amounts (dehydration). | Refer abnormalities. Assess for other anomalies if only two vessels in cord. Tighten or replace loose cord clamp. If stool and urine output abnormal, look for missed recording, increase feedings, report. | Genitals| Female Labia majora dark, cover clitoris and labia minora. Small amount of white mucus vaginal discharge. Urinary meatus and vagina present. Normal variations: Vaginal bleeding (pseudomenstruation). Hymenal tags. | Clitoris and labia minora larger than labia majora (preterm).Large clitoris (ambiguous genitalia). Edematous labia (breech birth). | Check gestational age for immature genitalia. Refe r anomalies. | Male Testes within scrotal sac, rugae on scrotum, prepuce nonretractable. Meatus at tip of penis. | Testes in inguinal canal or abdomen (preterm, cryptorchidism). Lack of rugae on scrotum (preterm). Edema of scrotum (pressure in breech birth). Enlarged scrotal sac (hydrocele). Small penis, scrotum (preterm, ambiguous genitalia). Empty scrotal sac (cryptorchidism). Urinary meatus located on upper side of penis (epispadias), underside of penis (hypospadias, or perineum.Ventral curvature of the penis (chordee). | Check gestational age for immature genitalia. Refer anomalies. Explain to parents why no circumcision can be performed with abnormal placement of meatus. | Extremities| Upper and Lower ExtremitiesEqual and bilateral movement of extremities, Correct number and formation of fingers and toes. Nails to ends of digits or slightly beyond. Felxion, good muscle tone. | Crepitus, redness, lumps, swelling (fracture). Diminished or absent movement, especially during Moro r eflex (fracture, nerve injury, paralysis). Polydactyly (extra digits). Syndactyly (webbing) Fused or absent digits.Poor muscle tone (preterm, neurologic injury, hypoglycemia, and hypoxia). | Refer all anomalies, look for others. | Upper ExtremitiesTwo transverse palm creases. | Simian crease (normal or Down syndrome). Diminished movement (injury). Diminished movement of arm with extension and forearm prone (Erb-Duchenne paralysis). | Refer all anomalies, look for others. | Lower Extremities Legs equal in length, abduct equally, gluteal and thigh creases and knee height equal, no hip â€Å"clunk†. Normal position of feet. | Ortolani and Barlow tests abnormal, unequal leg length, unequal thigh or gluteal creases (developmental dysplasia of the hip).Malposition of feet (position in utero, talipes equinovarus). | Refer all anomalies, look for others. Check malpositioned feet to see if they can be gently manipulated back to normal position. | BackNo openings observed or felt in ve rtebral column. Anus patent. Sphincter tightly closed. | Failure of one or more vertebrae to close (spina bifida), with or without sac with spinal fluid and meninges (meningocele) or spinal fluid, meninges, and cord (myelomeningocele), enclosed. Tuft of hair over spina bifida occulta. Pilondial dimple or sinus. Imperforate anus. | Refer abnormalities.Observe for movement below level of defect. If sac, cover with sterile dressing wet with sterile saline. Protect from injury. | Reflexes See table 21-3. | Absent, asymmetric or weak reflexes. | Observe for signs of fractures, nerve injury, or injury to CNS. | TABLE 21-3 SUMMARY OF NEONATAL REFLEXES *MCH page 493| REFLEX| METHOD OF TESTING| EXPECTED RESPONSE| ABNORMAL RESPONSE/POSSIBLE CAUSE| TIME REFLEX DISAPPEARS| Babinski| Stroke lateral sole of foot from heel to across base of toes. | Toes flare with dorsiflexion of the big toe. | No response. Bilateral: CNS deficit. Unilateral; local nerve injury. 8-9 mos| Gallant (trunk incurvation )| With infant prone, lightly stroke along the side of the vertebral column. | Entire trunk flexes toward side stimulated. | No response: CNS deficit. | 4 mos| Grasp reflex (palmar and plantar)| Press finger against of infant’s fingers or toes. | Fingers curl tightly; toes curl forward. | Weak or absent: neurologic deficit or muscle injury. | Palmar grasp: 2-3 mos. Plantar grasp: 8-9 mos| Moro| Let infant’s head drop back approx. 30?. | Sharp extension and abduction of arms followed by flexion and adduction to â€Å"embrace† position. | Absent: CNS dysfunction.Assymetry: brachial plexus injury, paralysis, or fractured bone of extremity. Exaggerated: maternal drug use. | 5-6 mos| Rooting| Touch or stroke from side of mouth toward cheek. | Infant turns head to side touched. Difficult to illicit if infant is sleeping or just fed. | Weak or absent: prematurity, neurologic deficit, depression from maternal drug use. | 3-4 mos| Stepping| Hold infant so feet touch soli d surface. | Infant lifts alternate feet as if walking. | Asymmetry: fracture of extremity, neurologic deficit. | 3-4 mos| Sucking| Place nipple or gloved finger in mouth, rub against palate. | Infant begins to suck.May be weak if recently fed. | Weak or absent: prematurity, neurologic deficit, maternal drug use. | 1 yr| Swallowing| Place fluid on the back of the tongue. | Infant swallows fluid. Should be coordinated with sucking. | Coughing, gagging, choking, cyanosis: tracheoesophageal fistula, esophageal fistula, esophageal atresia, neurologic deficit. | Present throughout life. | Tonic neck reflex| Gently turn head to one side while infant is supine. | Infant extends extremities on side to which head is turned, with flexion on opposite side. | Prolonged period in position: neurologic deficit. | May be weak at birth; disappears at 4 mos|

Building a Movement for Constructive Commonwealth Essays

Building a Movement for Constructive Commonwealth Essays Building a Movement for Constructive Commonwealth Essay Building a Movement for Constructive Commonwealth Essay Building a Movement for a Constructive Commonwealth By: Lean Hall, Executive Director Alliance for a Just Society I have challenged people in diverse communities inner-city black folks from New Orleans and New York, immigrants in Idaho, and rural families in Montana to draw a picture of the community they want. Their pictures are strikingly similar: Their sky is blue and their air is clean; the schools are good and the kids are happy; there are parks, good food, and safe places to live and work, as well as artistic, cultural, and religious institutions that reflect the richness and diversity of our communities and society. The desire to create strong communities where families can thrive seems almost universal, and this is true despite the presence of conservative ideologies that promote rugged individualism. We all hold this kind of vision; this paper is offered as an early step in building the strategy for transformation toward the political and social economy that sustains this vision. The kind of society we want to build can be described by the phrase, Constructive Commonwealth. I use the words Constructive Commonwealth because it engenders our capacity to address hat is broken and rebuilding it, and the imperative for constructive, positive solutions to build a true commonwealth. Our Constructive Commonwealth is an innovative, equitable, and sustainable economy that measures its success on the well-being of people and communities across the globe. The notion of well-being of people and communities extends to the environment that we live in; the education of its members; the creation of shared wealth and prosperity; access to housing, health care, and healthy food; and a truly participatory democracy governing our public institutions, government and corporations. A participatory democracy requires a well-developed civil society with people coming together to build peoples organizations and institutions that advance local community-based leadership that can interact with public and private institutions from positions of power. The imperative to recreate and transform our economy comes from three fundamental dangers that we face today: the crisis of global inequity that thrives on racial bias, threats to democracy from increased implementation and corporate control, and the global environmental crisis. Ignoring the confluence of these crises is not an option; we need to lay claim to innovation, ingenuity, and inventiveness to advance new solutions and build the Constructive Commonwealth. Retreating this shift will not be easy it will require a cultural, power, and policy shiftto move in waves across our country and the world resulting in the reanimating and transformation of our economy and society. Many of us, myself included , think the economy is like the weather. We act like the economy is an abstract force that we have little control over. But that is not true; our decisions and actions shape the economy, which, in turn, shapes our lives. Every relations. And these influences often are Justified in te rms mammals and morality. For a constructive commonwealth, we want to bring a prevailing sense of morality into the political sphere and then shape the economy. For example, in the Bible, Jesus becomes outraged by the money-changers and their exorbitant credit rates and throws them out, declaring usury immoral. Congresss decision to lift the Glass- Steals Act allowed the financial sector to create new, highly speculative and risky investment products, becoming a critical factor in the recent and ongoing financial crisis. Campaigns to regulate the environmental impact of products and corporate practices have had a significant, although insufficient, impact on the quality of our lives. The movement during the Great Depression to put people to work and the post-war enactment of the 6. 1. Bill changed lives, shaped communities and had defining impacts on our economy. And while they didnt go far enough, these public investments greatly reduced inequality. The economy is not a separate sphere; the notion of a Constructive Commonwealth recognizes the social nature of the economy and holds it within the public sphere. Our actions stem from our beliefs. To spur action for change, we need to reflect on and assert deeply held beliefs and values into the mainstream culture and politics. 1. We all do better when we all do better. Inequity is a crisis in the U. S. And globally, with more than 56 percent of the world population living on $2. 50 a day. L While inequity is color-coded and international, it is also a universal crisis. As inequity grows in a society, people of color and low- income communities are hardest hit. It is also true that there are worse outcomes health, life expectancy, crime across the board. Addressing inequity will require that we understand our society from both a gender and racial Justice lens. 2. Race matters. Today our society is shaped by institutional and systemic racism. We will not achieve our aspirations unless we understand how racism functions and address it directly. Just look at the foreclosure crisis. As CNN reported in June, White Americans have 22 times more wealth than blacks a gap that nearly doubled during the Great Recession. The housing bubble and subsequent recession greatly exacerbated existing inequities. One need only look at the predatory lending 1 The Great Transition page 23 practices of the banks and the foreclosure crisis to get at the root of this wealth loss. As the market has become less regulated, we have seen skyrocketing inequity across the United States. These systems that undermine equity are embedded in our history of manifest destiny, slavery and the near genocide of native peoples. 3. Human beings, not corporations, have rights. As Franklin Delano Roosevelt in his Four Freedoms speech eloquently stated, human beings should be afforded the freedom from want, freedom of speech, freedom of religion and freedom from fear. Today that can be translated into access to basic needs: clean air and water, shelter, health, and food; a De-militaries society and a redirection away from a national budget dominated by military spending; an increase in availability to safe, dignified work with adequate compensation; and an end to the promotion of hate and the denomination of groups of people who are deemed to be the other. This kind of hate and denomination serves to divide us in ways that intensify inequity and diminish democracy, while weakening cross-cultural solidarity. It also advance our understanding of human rights, we must address the reality that report money and power have limited our democracy and freedom. 4. Global warming is a social and economic crisis. James Hanson, Annas director of the Goddard Institute for Space Studies, warns that if Canadas tar sands are exploited, dramatically increasing carbon dioxide levels will alone cause accelerated melting of ice sheets and rising in sea levels that would destroy coastal cities. He predicts that 20%-50% of the earths species would become extinct and our whole civilization would be at risk. I Just as our future will be shaped by the choices Canadians make, ours will also shape the rest of the world. It is time that we understand that our futures are deeply interconnected and interdependent. To date, corporations have not been required to internalize the costs of environmental degradation. It is time to assess the real cost of the production of goods by factoring in the future costs to society and to dramatically increase our investment in clean energy. 5. Corporate culture of consumption is not freedom and does not create happiness. Driven by marketing and advertising, we have been transformed from citizens into consumers. Collectively, we have forgotten that it is our family, community legislations, art, ideas, and spiritualism that fulfill us. As a society, we tend to value things over people and measure our worth based on what we have. The point about corporate-consumer culture should not be MIS-understood Economic insecurity, financial worries, and uncertainty undermine agglomerations and full participation in our democracy and the cultural life of our communities this, in turn, undermines happiness. 6. A healthy democracy is an essential part of our path forward. Our political democracy is awash with corporate dollars. The influence of this money is growing

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