Abortion In The United States Essay Example | Topics and Well Written Essays - 1000 words

Abortion In The United States - Essay Example Statistics suggest that 50 percent of all women opting for abortion, in the United States, fall in the age group of below twenty-five years of age and 66 percent of all abortions are performed on women who have been never-married. Women under the age of twenty-five or even younger are far less likely to have sufficient means to sustain themselves much less, have the resources to look after their yet unborn child. Giving birth further increases the burden on the mother to provide for the child and in the absence of adequate financial and social means, the life and well-being of both - the mother and the child could be threatened thus causing more harm than good in the long run. The debate on abortion is subject to a range of philosophical as well as constitutional deficiencies, which often threaten to push the subject into a potential gray market of even more complex choices. The advocates of equal rights for both the genders suggest that equal rights include the right to choose and m ake decisions concerning their own health and safety, which in case of women includes abortion. Graber suggests that preventing women from making such choices that may directly affect their well-being amounts to preventing them access to basic civil rights. It is similar to preventing a section of society from accessing education, or a certain type of food of their choice. For some, relinquishing the food of their choice may be an easier alternative than having to debate over choices that directly affect their own health.

Augusta Nationals Two Female Members Essay Example | Topics and Well Written Essays - 750 words

Augusta Nationals Two Female Members - Essay Example The Augusta National Golf Club has shown gender discrimination throughout its history by allowing none of its almost 300 members to be a woman until recently, when the Cub took an action long overdue on it by announcing Condoleezza Rice, the former US Secretary of State, and Darla Moore, the South Carolina financier to be its members. The Club was also publicly pressured by Martha Burk, the women’s rights activist in the year 2001 to allow membership to women, but Hootie Johnson, the chairman of the Club at that time said in response that the Club might alter its policy one day â€Å"but not at the point of a bayonet† (Johnson cited in Tyler). When Bubba Watson joined the Augusta National Golf Club’s tradition of wearing the green jacket upon winning the Masters Golf Tournament, the celebrations were tarnished by the exclusive discrimination displayed by the Club towards the women. One of the lawyers said that the implications of this discrimination could be broader and extend to all working women. The Augusta National Golf Club has been disreputable for a long time in history because of its disallowance for women to become its members. â€Å"The fathers and sons of Augusta know full well that they have built for themselves not just a golf course but one of the great corridors of power in America, and with chests fully puffed, have fiercely and proudly denied women access to those corridors† (Brennan).... In addition to that, all of the past IBM CEOs had served as the Club’s members. The only factor that differed this time was that the CEO was a woman unlike the past CEO members who were all men. Payne retreated the discussion and Rometty did not wear the green jacket to symbolize the club’s membership over the weekend. David Scher, the Employment Law Group’s attorney expected the effects of the exclusive policy of the Augusta National Golf Club to reach all working women. He said, â€Å"This is not the only place that this is happening. Free association allows all kinds of clubs, but there are lots of men's organizations that keep women out of the workforce and it is really time for that to change† (Scher cited in Mielach). 21st century is the time for the discrimination to recede, be that against races or genders. Discriminatory policies do not help any organization holding it, but just serves to complicate things for certain members of the society. †Å"Playing golf and other pastimes is integral to the business world, and outright discrimination against women in the private golf world, although technically legal, can have a severe and lasting illegal impact in the workplace† (Scher cited in Mielach). Grant of the Augusta National Golf Club’s membership to two women in this year is a very big milestone in the way of realization of the equality of genders and will have far-reaching effects for all women in the society and bring a positive revolutionary change in the acceptability of women in the business world in general and the sports in particular. Something like selection of women members for the first time since the establishment of a prestigious club will have an effect on the policies of similar

Religious Dissent, Discord, Settlement and Religious Essay Example for Free

Religious Dissent, Discord, Settlement and Religious Essay This section of the paper introduces the topic and the thesis. In support of the formation of the thesis, the introduction discusses a brief history of the Tudor reign, and how prior monarchies have created religious divisions within the English society. The introduction enumerates the main concerns surrounding the topics of religious dissent, discord, settlement and religious atmosphere that took place before and during the reign of Elizabeth I. The introduction also establishes the argument as to whether Elizabeth I’s solution to the religious conflict, the creation of a united church, was an important and feasible move considering the politics surrounding her reign and the pressing influence of Rome on the religious affairs of many countries, particularly in Europe. Although this would eventually lead to the formation of the Church of England and the English Reformation, it is important to examine the historical impact of Elizabeth I’s decision in terms of implementing a defined and united English church. II. The Religious Atmosphere Prior to Elizabeth II Overview Elizabeth I’s impact on the religious life in England can be attributed to the problems which she inherited; this section discusses these factors, briefly touching on the religious atmosphere during the reigns of Henry VIII, Edward VII and Mary I. As religion played an important role in England at that time, especially with the influence of the Roman Catholics pertaining to England’s foreign relations with Rome and other parts of Europe, the religious atmosphere prior to Elizabeth I’s reign can be observed to represent deep divisions as some groups wanted to have a different interpretation and practice of the sacred Christian texts and rituals, whereas some wanted to follow the Roman Catholic way. Although this may seem like a small problem, religion’s role in the societies of those times was critical. At that time, the Church had a strong influence on the State, and this was something upheld by previous monarchs before Elizabeth I took the throne. Certain wars sprung out because of religious conflict, and it became a pressing problem especially as before Elizabeth I had to address the re-installation of Catholicism in England under Mary I’s period. II. a Religious Atmosphere Under Henry VIII II. b Religious Atmosphere Under Mary I III. Elizabethan Reign: Dissent, Discord and Religious Settlement and Atmosphere Overview This section provides a more detailed historical approach in Elizabeth I’s religious settlement. This takes from Elizabeth I’s decision to re-establish the Church of England and break ties with Rome. This section also touches on the different acts or laws implemented at that time which would serve as steps in the implementation of the Church of England and address religious divisions in the society. This section also provides a concise but substantive background on Elizabeth I’s installation as Queen in supplement to her religious settlement. This is an important aspect of the paper as Elizabeth I’s background provides the motivation and the decision of the queen, especially in terms of her religious settlement. IV. Elizabethan England: Religion and Renaissance This section touches on the English society during the Elizabethan era. This provides a background of the religious atmosphere in the country and how, during Elizabeth I’s reign, the English society started to change. This also gives a background on how and why Elizabeth I’s period has been considered as the Golden Age of English history in which this era became a point of significant accomplishments of literature and art, in addition to the prevalence of the Protestant Reformation mindset of the people. What is interesting is that although Elizabeth I would stabilise Protestantism in England, and she would be recognised for it, this did not prevent the emergence of the English Renaissance where the Elizabethan society would adopt a more open mind towards the arts and the sciences. V. Conclusion This paper concludes with an analysis of Elizabeth I’s religious settlement and how this would serve as an important seed to the formation of the English society especially in the religious and political context. This section also summarises the aspects of religious dissent and discord, especially as to whether Elizabeth I successfully addressed the deep religious divisions in the English society; this is an important point of discussion as her religious settlement was not just aimed to address religious conflict within the country but also as a means for her to install her legitimacy and rule an era of renaissance instead of religiosity.

Puc18 Plasmid Engineering

Puc18 Plasmid Engineering Abstract The objective of the experiment was to engineer a pUC18 plasmid so that it contained a kanomycin resistance gene in its multiple cloning site and to transform it into cells. The kanomycin resistance gene was obtained from a pKAN plasmid. The desired plasmid was constructed by digesting pUC18 and pKAN with the same restriction enzymes,(BamHI and HindIII) and religating the products to give the engineered pUC18. The created plasmid was then transformed into E.coli strains DH5ÃŽ ±. The strains that contained the engineered plasmid were selected using two methods of selection. According to the indirect method of selection the percentage of competent cells transformed with the plasmids was 0.063% which is a low number. According to the direct method of selection on the other hand no cells were transformed. In conclusion even though some colonies with the engineered plasmids were obtained the percentage of cells transformed was very low. Also, the indirect method of selection gives better results for selection of desired strains. Introduction Bacteria can carry antibiotic resistance genes either in their chromosomes or extrachromosomally in phage or a plasmid(Hausner and de Jong 2010). B-galactosidase is an enzyme involved into the cleavage of lactose into glucose and galactose and is encoded by the lac Z gene of the lac operon.(Glick et al 2010) The lac operon is prevented from being transcribed through repression of the lac promoter. Activation of this promoter can be done by the addition of lactose or isopropyl-ÃŽ ²-D-thiogalactopyranoside(IPTG) to the medium. Lactose and IPTG simply prevent binding of the lac repressor(the product of the Lac I gene) to the promoter. (Glick et al 2010) In the following experiment plasmids pUC18 and pKAN are used to provide the genes to be transformed into bacteria. pUC18 is 2686 base pairs(bp) long and contains a bacterial origin of replication, an ampicillin resistance gene, a lacI gene, a segment of the lac Z gene encoding part of B-galactosidase(which breaks down X-gal) and a multiple cloning sequence(MCS) that is within the lac Z gene.(Glick et al 2010) The lac Z gene encoded by the plasmid is part of the B-galactosidase protein which complements a gene carried by the Escheria. coli chromosomally thus forming a functional B-galactosidase.(Glick et al 2010) If a DNA segment is cloned in the MCS then the lacZ gene will be interrupted and will not give rise to a functional protein. If that occurs then the Bacteria transformed with the plasmid will not break down5-bromo-4-chloro-3-indolyl-ÃŽ ²-D-ÃŽ ²-galactosidase( X-gal) present in the plates. When X-gal is broken down by ÃŽ ²-galactosidase it turns blue whereas when it is not bro ken down it stays white. This color differentiation is a way to tell if there has been any DNA incorporated in the MCS of pUC18. Finally in order for the ÃŽ ²-galactosidase in pUC18 to be transcribed, IPTG has to be present in the medium so that the lac operon can be induced.(Glick et al 2010) pKAN plasmids can serve as sources for the kanomycin resistance gene. In the following experiment the kanaomycin resistance gene will be inserted in the MCS of pUC18. pKAN contains an origin of replication, a kanomycin resistance gene and multiple restriction sites.(Hausner and de Jong 2010) More importantly it contains only one BamHI and HindIII recognition sites in the whole plasmid which flank the kanomycin resistance gene.(Hausner and de Jong) This allows researchers to cut out the antibiotic resistance gene by simply using BamHI and HindIII producing only two fragments of DNA: the gene and the rest of the plasmid. Once experimenters have inserted the pKAN gene into the MCS of pUC18 and transformed the E.coli strains they need a way to select for the desired plasmid. There are two methods to select for the desired those colonies: the direct method and the indirect method. The direct selection method involves spread plating transformed strains into plates containing both the antibiotic ampicillin and kanomycin. (Hausner and de Jong 2010) Since the pUC18 plasmid confers amplicillin resistance(Glick et al 2010) and the kan gene confers kanomycin resistance (Hausner and de Jong 2010) then only the cells that contain Puc18 with the kanomycin resistance gene should be able to grow in these plates. The indirect method on the other hand is a two step selection process. In the first step the transformed strains are plated onto LB plates containing ampicillin and X-gal.(Hausner and de Jong 2010) Only the cells that have up-taken pUC18 will grow since they will be resistant to ampicillin. Furthermore cell s that contain pUC18 with inserted DNA in the MCS will produce white colonies since they cant produce a functional ÃŽ ²-galactosidase. Cells that give rise to blue colonies will have up-taken pUC18 without any DNA inserted in their MCS since they are able to break down X-Gal. (Glick et al 2010) To select the cells with pUC18 containing the kanomycin resistance gene the white colonies are plated in plates containing kanomycin. Only the cells that have the kanomycin resistance gene in their pUC18 will grow.(Hausner and de Jong 2010) The objectives of the following experiment include the construction of a pUC18 plasmid containing the kanomycin resistance gene in the MCS, the transformation of that plasmid into the E.coli DH5ÃŽ ± cells and the selection of the cells containing the engineered plasmid. If both pUC18 and pKAN plasmids are digested with BamHI and HindIII and the digests are ligated then a plasmid which contains both kanomycin and ampicillin resistance genes should be produced; consequently cells transformed with the engineered plasmid should be resistant to both antibiotics. Materials and Methods Plasmid extraction and plasmid engineering pUC18 and pKAN plasmids were extracted from the DH5ÃŽ ± and MM294 E.coli strains respectively using a DNA isolation kit as described by (Hausner and de Jong 2010). Confirmation for proper extraction was done through agarose gel electrophoresis by running the extracted DNA in a 0.7% gel at 100V for 1 hour. The gene containing kanomycin resistance from pKAN was cloned into pUC18. The restriction digests to do the cloning were prepared as described in Table 2 in (Hausner and de Jong 2010). After plasmid digestion the kanomycin resistance gene was inserted into the multiple cloning sequence of pUC18 in a ligation reaction using the enzyme ligase and the reaction was allowed to go to completion for 24 hours at room temperature. The ligation reactions were set up according to table 3 in (Hausner and de Jong 2010) E.coli transformation and strain selection E.coli strain DH5ÃŽ ± was sub-cultured for 1 hour at 37Â °C. The cells were then made competent by washing them in 10mM CaCl. Next cells were transformed with three different combinations of plasmids. The set of cells in tube 1 was transformed with uncut pUC18 DNA. The set of cells in tube 2 was transformed with cut pUC18. Cells in tube 3 were transformed with pUC18 containing the cloned pKAN resistance and finally cells in tube 4 were transformed with just water as a negative control. The transformation procedure has been described in (Hausner and de Jong 2010). Transformed cells from all tubes were spread plated onto LB+carb+X-gal plates for indirect selection. Furthermore cells from tube 3 were plated onto LB+carb+ kan plates for direct selection of cells containing pUC18 with the insert from pKAN. To determine the density of competent cells cells dilutions of , and were prepared. The two highest dilutions were plated onto LB plates. All the plates were incubated at 37Â °C and they were allowed to grow for ~24 hours. After the colonies had grown on plates plate they were counted and their numbers were recorded. White and blue colonies from the LB+carb+X-gal plates were then streaked onto LB + kan plates to obtain the colonies that had the kanomycin resistance gene incorporated in the MCS. For more information on the procedure refer to Experiments in Biotechnology Laboratory Manual (Hausner and de Jong 2010) Results Extraction of plasmids from E.coli strains Figure 1 contains the image of the 0.7% agarose gel in which the isolated plasmids Puc18 and pKAN were run to check for product. As it can be seen in lane 1 a lot of Puc18 was extracted from the DH5ÃŽ ± strain. Less plasmid DNA was collected for pKAN from the MM294 strain since the band in lane 2 is of much weaker intensity. There is more than one band in lane two. The additional bands represent additional plasmids isolated from the bacteria. Calculation of Competent cell density Table 1 shows the dilutions performed on the competent cells in order to calculate their cell density. It also shows the number of colonies on the plates that were spread plated with dilution 2 and dilution 3. The results for the dilution were not used for cell density calculation since less than 30 colonies grew on the plate. Dilution was used to calculate the cell density because the number of colonies was between 30 and 300. Indirect method of selection Cells plated from tubes 2 and 3 were used to calculate the % of transformed cells. Every colony represents a single transformed cell since it can be assumed the every colony has arisen from a single cell. Furthermore for tube 3 since five plates were spread plated the percentage of the transformed cells was obtained by using the average amount of colonies for all five plates. Calculation the percentage of transformed cells in tube 2: %of transformed cells= x 100 =0.0045% of cells transformed Calculation of transformed cells in tube 3 Average for blue colonies: = 58.6 ≈ 59 blue colonies Average for white colonies = 11.4 ≈ 11colonies Total number of colonies = 59 blue colonies + 11 blue colonies = 70 colonies in total Both blue and white colonies from tube 3 represent transformed cells since they both up-took plasmid DNA whether it was just pUC18 or pUC18+kanomycin resistance gene. Therefore since every colony came from a single cell there were 70 cells in total that were transformed from 100Â µl of media spread plated in each plate. % of transformed cells in tube 3: %of transformed cells= x 100 =0.063% of cells transformed Direct selection of clones containing the kanomycin gene: No colonies grew on LB + carb + kan plates. That means that there were no cells that were transformed with the engineered plasmid. Furthermore an accurate number for % of transformed cell could not have been calculated even if cells had grown in these plates. That is because this selection method takes into account only the cells that were trasformend with pUC18 which contained the kanomycin resistance gene and not the cells that were transformed with only pUC18. Discussion Isolation of plasmids from cells The optimal results for the gel would have been to see one strong band at ~2.7 kb representing pUC18 and one strong band at 4.2 kb which represents pKAN. For the pKAN lane there is more than one band seen. Those bands represent different sized plasmids that were also isolated from the cell. Since there was no DNA ladder on the gel it cannot be concluded what plasmid the lanes represent but the only thing that can be concluded is that there was plasmid DNA isolated from both the DH5ÃŽ ± and the MM294 strains which most likely was pUC18 and pKAN. In order to conclude whether pUC18 and pKAN plasmids were isolated from the bacteria the students should be provided next time with a DNA ladder in order to determine the sizes of the lanes. Indirect selection method The cells from tube 1 were transformed with un-digested pUC18. The cells from this tube represented a positive control for transformation. The colonies in the plates were all blue and they were too many to count. The reason for the high number of colonies was that these cells were transformed with undigested plasmids which are all stable and all allow bacteria to carry information extrachromosomally, making the transformation percentage of competent cells very high. All the cells from tube 1 produce blue colonies. That is because they all had a functional B-galactisidase since no genes were cloned into the multiple cloning site located within the lacZ gene. The cells from tube 2 were transformed with digested pUC18 plasmid. The cells from this tube represented a negative control for kanomycin resistance gene cloning. Tube 2 gave rise to very few colonies in comparison to tube 1 because the cells in tube 2 were transformed with unstable DNA. pUC18 had been previously digested with HinDIII and BamHI and a lot of plasmid did not re-ligate and for that reason the DNA was unstable. Since the DNA was unstable it was not able to maintain the ampicillin resistance gene in bacteria and consequently the strains were not able to grow in carbonicillin plates. As a result the number of percent transformed cells was as low as 0.0045%. The cells from tube 4 were transformed with sterile water i.e no DNA. These cells represented the negative control for transformation. Because no DNA was inserted in them none of the cells contained the ampicillin resistance gene and as expected none grew in the plates containing carbomicillin. The cells from tube 3 were transformed using pUC18 that contained insertion on the MCS as well as pUC18 that didnt. All five plates that were spread plated with E.coli from tube 3 contained blue colonies as well as white ones. The reason for the color difference is that the blue colonies contained a functional ÃŽ ²-galactosidase whereas the white ones didnt. The functional ÃŽ ²-galactosidase in the blue colonies was due to the fact that no DNA was inserted in the MCS to interrupt the lacZ gene. The white colonies on the other hand did not contain a functional ÃŽ ²-galactosidase since they had a DNA insertion in their multiple cloning site, which interrupted the lacZ gene. Consequently they could not break down X-gal. However just because they had a DNA insertion in their MCS it did not mean that they contained the kanomycin resistance gene. They might have contained the rest of the pKAN plasmid. As a result the white colonies needed to be streaked into plates that selected for kanomy cin resistance. If the cells then grew on LB + Kan plates and they also originated from white colonies on LB + Carb + X-gal plates then they contained a Puc19 plasmid with a kanomycin resistance gene inserted in the MCS. The percentage of transformed cells was also not very high: 0.063%. A way to improve this would be to maybe increase the molarity of the CaCl solution to make the cells more competent. Direct selection method According to the direct method of selection there were no cells that were transformed. This is contradictory to the results obtained from the indirect method of selection. This error could have been produced because of either improper spread plating of plates or because of improper transformation procedure. Also the conditions in the LB + carb + kan plates could have been too harsh(two antibiotics) for the bacteria to pick up growth even if they were resistant to both antibiotics. In following experiments it is better to use the indirect selection method since it seems more successful in selecting desired strains. Comparison of direct VS indirect selection methods The direct and indirect selection methods have both advantages as well as disadvantages. The main disadvantage of indirect selection is that it takes longer since it contains two steps and each step takes at least a day for completion. The main advantage is that if done correctly, the indirect selection methods gives very accurate selection for the desired cells. The reason for that is that first it selects for colonies that just have an insertion in the MCS and this tells the researcher that some type of cloning has occurred in plasmids. The second step then selects for the colonies that contain pUC18 with the kanomycin resistance gene inserted in the MCS. Thus the criterion of indirect selection is that cells have both pUC18 with an inserted DNA in MCS and also have kanomycin resistance. The colonies that grow in the second step fulfill both the criteria. The main advantage of the direct method is that it takes a shorter time to complete and it also uses up less equipment which can also save researchers some money. The main disadvantage with this selection is that it has a higher chance of giving false positives. Direct selection does not select for strains that have DNA inserted in the MCS of Puc18 but only selects for strains that have ampicillin and kanomycin resistance. Therefore the strains that grow in LB + carb + kan plates might have both pUC18 and pKAN plasmids but not the kanomycin resistance gene inserted in the pUC18 MCS. Those strains would still be able to grow since they still have both ampicillin and kanomycin resistance. However the genes would on different plasmids and not on the engineered one. Therefore even though the indirect selection method is longer it is more accurate in selecting the desired strains for this experiment. In conclusion, according to the indirect selection the desired plasmid was engineered by digesting both pUC18 and pKAN with HindIII and BamHI. Also when selecting for cells transformed with pUC18 it is better to employ the indirect method of selection because it gives more accurate results. Question 1: Although both lanes contain plasmid DNA, why doesnt the DNA appear to be in the same location in both lanes? The DNA does not appear in the same location in both lanes because pUC18 and pKAN are of different sizes. pUC18 is 2686 base pais long whereas pKAN is 4194 base pairs long.(Hausner and de Jong 2010) Because pUC18 is of smaller size it will travel farther from the wells than pKAN. Question 2: How would you verify that the transformed cells actually contain the carb/kan plasmid that was used for transformation? One accurate way would be to isolate the plasmid DNA from the transformad cells and run it on an agarose gel. If the kanomycin resistance gene was inserted into pUC18 then on the gel one will be able to see a band of the size 4548 base pairs which is different from both the pUC18 and the pKAN plasmids. The size of the created plasmid was calculated the following way by obtaining the information from (Hausner and de Jong 2010): To find the size of kanomycin resistance gene inserted in pUC18, the number of base pairs from the origin or replication of HindIII was subtracted to the number of base pairs from the origin of replication of BamHI. This was done because pKAN was digested with HindIII and BamHI to obtain the kanomycin resistance gene: 2095 233 = 1862 base pairs The size of the insert was then added to the size of Puc18: 2686 + 1862 = 4548 base pairs

Comparing Fitzgeralds Great Gatsby and Eliots The Love Song of J. Alf

Fitzgerald's Great Gatsby and Eliot's The Love Song of J. Alfred Prufrock   Ã‚   The Roaring Twenties bring to mind a generation of endless partying, which reflected very little of the morals of the generations preceding it. The world, for that generation, was fast-paced and thoroughly material, crowded with bizarre and colorful characters like David Belasco and Arnold Rothstein. Inspired by this era's "spiritually exhausted people" (Brians), F. Scott Fitzgerald's The Great Gatsby and T. S. Eliot's The Love Song of J. Alfred Prufrock address many of the same themes in attempting to restore the "lost generation." In developing these themes, both authors utilize weather, the concept of illusion versus reality and the direction of time as a mode of conveying the promise of their dream to the citizens of the Jazz Age. In both The Love Song of J. Alfred Prufrock and The Great Gatsby, weather and time of day play an important part in setting the tone and mood. Prufrock sets out in the evening, a time of uncertainty, neither day nor night, to confront his past. Likewise, the important events in the Great Gatsby occur at a significant time of day. Once, when Gatsby talked to Nick about his past, Nick describes it as "a time of confusion," (Fitzgerald 102) which the evening time has come to symbolize. Also, the time of final confession in the Great Gatsby was the night Daisy rejected Gatsby (148). Even the covering of the night was not enough to hide the disenchantment of his dream. At this time, Gatsby tells the whole truth about his past and his relationship with Daisy. This past was set in October, as was The Love Song of J. Alfred Prufrock. When Gatsby looks back through the mists of time, he sees a perfect ... ...both authors sought to communicate to their societies, the beauty of a dream uncorrupted by senseless illusions. In using the weather, the concept of illusion versus reality and the direction of time to convey the promise of their dream to the citizens of the Jazz Age, Fitzgerald and Eliot contrast the frustration and despair that was inherent in a spiritually bankrupt world with the fulfillment characteristic of a more grounded and less immoral lifestyle.    Works Cited:    Bewley, Marius. "Some Notes on The Great Gatsby." Mizener 70-76. Eliot, T.S.. "The Love Song of J. Alfred Prufrock." The Norton Anthology of English Literature. Ed. M.H. Abrams. New York: Norton, 1996. 2459-2463. Fitzgerald, F. Scott. The Great Gatsby. 1925. New York: Scribner Classic, 1986. Pinion, F. B. A T.S. Eliot Companion. Totowa: Barnes & Noble Books, 1986.

A Look at Humor, Laughter, Tickling, and the Brain Essay -- Neurology

A Look at Humor, Laughter, Tickling, and the Brain Everybody smiles and laughs at some time or another. The first laughter appears at about 3.5 to 4 months of age (8)., way before we are able to speak. The average adult laughs 17 times a day (4). Even monkeys and apes have some facial expressions that are similar to human smiles. But really, why do we laugh? Why are we not able to tickle ourselves? What part of the brain is responsible for laughter and humor? Why do we say some people have no sense of humor? We never go to the doctor because we feel good or because we think something is funny. Therefore, it is not a clinical problem; that is why there has not been much research done on the topic of laughter and the brain. Although there is considerable information on the neuronal representation of speech, little is known about brain mechanisms of laughter (2). While many researchers have tracked the brain mechanisms of depression, fear and anger, they have ignored positive emotions and have just begun to study humor. Their investigations are shedding some light on how the brain processes humor and prompts laughter. Take this joke for instance: How many Bryn Mawr college students does it take to change a lightbulb? Answer: None, they were all so busy studying that they didn't even notice the light was out. If you found this old joke funny, you will get some activity going on in the brain. Investigations into how humor and laughter influence the brain are leading to a clearer understanding of how positive emotions affect brain mechanisms. This in turn may lead to creative ideas for new therapies for emotion disorders and pain (1). The physiological study of laughter has its own name, "gelotology". Researc... ...Nature Journal http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v391/n6668/full/391650a0_fs.html 3)What is so Funny and Why: Laughter and the Brain http://faculty.washington.edu/chudler/laugh.html 4)How Laughter Works http://www.howstuffworks.com/laughter.htm 5)Humor on the Brain http://www.howstuffworks.com/framed.htm?parent=laughter.htm&url=http://abcnews.go.com/sections/science/DyeHard/dye990414.html 6)The Heart of Laughter http://www.howstuffworks.com/framed.htm?parent=laughter.htm&url=http://www.wm.edu/wmnews/research/laughter.htm 7)Brain may hinder sense of self-tickling http://seattletimes.nwsource.com/news/health-science/html98/tick_102098.html 8)A Big Mystery: Why do we Laugh? http://msnbc.msn.com/id/3077386/ 9)Scientists Locate Sense of Humor http://abcnews.go.com/sections/living/DailyNews/humor001128.html A Look at Humor, Laughter, Tickling, and the Brain Essay -- Neurology A Look at Humor, Laughter, Tickling, and the Brain Everybody smiles and laughs at some time or another. The first laughter appears at about 3.5 to 4 months of age (8)., way before we are able to speak. The average adult laughs 17 times a day (4). Even monkeys and apes have some facial expressions that are similar to human smiles. But really, why do we laugh? Why are we not able to tickle ourselves? What part of the brain is responsible for laughter and humor? Why do we say some people have no sense of humor? We never go to the doctor because we feel good or because we think something is funny. Therefore, it is not a clinical problem; that is why there has not been much research done on the topic of laughter and the brain. Although there is considerable information on the neuronal representation of speech, little is known about brain mechanisms of laughter (2). While many researchers have tracked the brain mechanisms of depression, fear and anger, they have ignored positive emotions and have just begun to study humor. Their investigations are shedding some light on how the brain processes humor and prompts laughter. Take this joke for instance: How many Bryn Mawr college students does it take to change a lightbulb? Answer: None, they were all so busy studying that they didn't even notice the light was out. If you found this old joke funny, you will get some activity going on in the brain. Investigations into how humor and laughter influence the brain are leading to a clearer understanding of how positive emotions affect brain mechanisms. This in turn may lead to creative ideas for new therapies for emotion disorders and pain (1). The physiological study of laughter has its own name, "gelotology". Researc... ...Nature Journal http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v391/n6668/full/391650a0_fs.html 3)What is so Funny and Why: Laughter and the Brain http://faculty.washington.edu/chudler/laugh.html 4)How Laughter Works http://www.howstuffworks.com/laughter.htm 5)Humor on the Brain http://www.howstuffworks.com/framed.htm?parent=laughter.htm&url=http://abcnews.go.com/sections/science/DyeHard/dye990414.html 6)The Heart of Laughter http://www.howstuffworks.com/framed.htm?parent=laughter.htm&url=http://www.wm.edu/wmnews/research/laughter.htm 7)Brain may hinder sense of self-tickling http://seattletimes.nwsource.com/news/health-science/html98/tick_102098.html 8)A Big Mystery: Why do we Laugh? http://msnbc.msn.com/id/3077386/ 9)Scientists Locate Sense of Humor http://abcnews.go.com/sections/living/DailyNews/humor001128.html

A very important life-lesson Essay

My friend David owned a motorcycle. It is not a big one, but it could reach a really dangerous speed. Just to remind those who like speeding, it is hazardous for you and other road users if you are speeding on the road. I learn this in a really painful lesson one night when I rode on the pillion on David’s motorcycle. We were on our way home one night after a movie in a cinema few kilometers away from my house, but the traffic on the road during our way back was badly congested. It was a benefit for us to ride on a motorcycle because we could pick our way through the cars and other motorcycles, but once we were on the main road, we cruised along freely. Maybe because the journey was too smooth while we were on the high way, I felt boring but David just don’t seem to feel in that way, so I decided to tease on him to make him speed up. He didn’t reply me in any words, but I could feel that the motorcycle starting to pick up speed. The cool breeze rushed through my face, the lamppost, the scenery and all the background passing by faster and faster makes me feel more and more excited! Just feeling curious, I placed my head over David’s shoulder and had a peep on the speedometer, and to my excite, the needle was shaking around 100km/h mark! This was the fastest experience that I ever had on a moving vehicle! I really felt excited riding on the pillion of David’s motorcycle!Suddenly, David stepped on the brakes and made a really hard left turn to get out from the highway and continue on our journey back. But during the turn, I heard a loud bang coming from the rear part of the motorcycle. David loose control of his bike and it drag both of us with it quite a distance away. The motorcycle was dragging me helplessly with my head scouring on the floor. It all happened in just a few seconds. I looked around desperately. Oh, my goodness! David was lying flat on his back and groaning softly. I managed to bring myself up and free David from the wrecked motorcycle. I had a glanced around to find out what just happened, but all I could see was a car with its right front light broken and its bumper dropped on the floor in a curved shape. David turned me around suddenly and had a good look on my left forehead, and then he said to me that I’m bleeding with a quite deep wound on my left forehead. I raised my left arm and try to wipe off the blood, and only then I found that my left arm was badly wounded and bleeding. I started felt very dizzy. All of a sudden, powerful lights blinded me. I heard voices talking anxiously and footsteps hurrying in our direction. Other road-users had arrived at the scene and they came to help us. The next half hour was daze, I vaguely remembered being carried into a van. I was too stunned to protest. I also heard that someone kept saying was all right, but before I could move my body, both of my leg suddenly paralyzed, I kneeled on my knees and blacked out. After I regain my consciousness, I’m sleeping on a bed with white pillowcase, white blanket and almost everything around me was white. It doesn’t take long for me to realize that I’m in a hospital bed. I looked around searching for David, but he is nowhere to be found. I starting to get worried but my parents came in and seem glad to see me awake. Surely the first thing came out from my mind was asking about David’s condition, and my mother replied that David’s condition was not as serious as mine, he just had some bruises and scratches around his body. I felt relieved. Eventually, we recovered from the painful accident in a month time. This incident made us aware of the speeding hazards and the terrible consequences that we have to bear for the mistake we have done. The price to pay was too much and too painful. I always thought that accidents only happen to other people, but it’s not true after this accident that I will never forget for the rest of my life. Remember that your life is very precious, and think of the people who cared for you.