Strong versus weak advertising theory Essay Example | Topics and Well Written Essays - 2500 words

Strong versus weak advertising theory - Essay Example A case in point is Andrew Ehrenberg who advanced a controversial treatise in 1974 about how advertising works. He challenged the assumption that advertising has the capacity to change attitudes unaided, and suggested that it normally worked by strengthening beliefs shaped from what are usually high level of consumer experience and awareness (Heath 2006). The argument of Ehrenberg was concentrated on the prevalent theory that advertising was a strong kind of persuasion, and his assumption became widely accepted among advertising agencies (Agres, Edell & Dubitsky 1990). However, it is important to take into consideration the fact that it was a period when the sales impacts of advertising were viewed by many as lasting, difficult to determine even in observation and hard to predict (Agres et al. 1990). Ehrenberg had ascertained that there were 100% loyal customers in most markets, and majority of these buyers purchased more than one brand. He discovered that brand consumers had consistent stronger attitudes than non-consumers, but unable to adequately clarify how these attitudes occurred (Heath 2006). This encouraged him to challenge the central theory within the models of hierarchy of effects: that change in attitude comes first and forces change in behaviour (Shrum 2004). He believed that advertising can build, rekindle or reinforce brand awareness, and can be an aspect that enables trial purchase (Wells 1997). However, he also visualised a protective function for repetitive advertising as â€Å"reinforcing already developed repeat buying habits† (Weitz & Wensley 2002: 289). Afterwards, he expanded this to include split-loyal buyers, or those who habitually buy more than one brand, and identified a further function for advertising as ‘nudging’ or pushing spli t-loyals towards a larger buying percentage of one brand or another (Weitz & Wensley 2002). On the other hand, Jones disputed the influence of

RESEARCH AND THEORY METHODS Essay Example | Topics and Well Written Essays - 2000 words

RESEARCH AND THEORY METHODS - Essay Example In addition, the literature argues that the nature of gender bias changes as women and men mature from elementary school children through adolescence, to college undergraduate and graduate students (Kelley & Parsons, 2000) Given that men and women participate in gender bias behaviours, research provides limited qualitative insight to explain why men and women accept such behaviours in a classroom environment (Fritschner, 2000). This paper compares the perceptions of male and female graduate students regarding the influence of gender in the classroom. Once gender influences are better understood, women and men may also have the opportunity to improve their understanding of each other. Literature Review The Sex Discrimination Act 1975 outlawed discrimination based on several characteristics, including gender. However, long ­standing attitudes, traditions, and practices continued to subtly subjugate minority groups based on race, gender, ethnicity, age, and sexual orientation. As note d by Haslett and Lipman (1997), "As overt, visible discrimination was challenged in the 1960s and 1970s, it became replaced by subtle and covert discrimination" (p. 36). Beginning in the early 1980s, popular research by Sadker and Sadker (1985), Hall and Sandler (1982), and others explored subtle mechanisms that marginalised women in the classroom. As defined by Mary Rowe (1977), gender bias produces "micro inequities" reflecting "everyday interactions in which individuals are often treated differently because of their gender" (Sandler, Silverberg, and Hall, 1996, p.1 0). Haslett and Lipman (1997) observed: Micro inequities are particularly ubiquitous because in each instance the harm seems too small to bother with. In the aggregate, however, they constitute a serious barrier to productivity, advancement, and inclusion. Micro inequities are particularly difficult to respond to because of the face issues involved as well as the seeming "smallness" of each single instance. (p. 38) As summarised by Fassinger (1995), research efforts produce conflicting opinions. For example, Hall and Sandler's widely referenced 1982 report provided anecdotal documentation of gender bias in academia, concluding that gender bias created a "chilly climate" for women in colleges and universities. However, Howard and Henney (1998) dispute the existence of a chilly climate. While Young (2001) explores biases that have an adverse impact on boys, most gender bias research examines the marginalising behaviours committed by men against women. However, gender bias includes more than men marginalising women's efforts. Haslett and Lipman (1997) observed that "women may discriminate against other women through their reluctance to support other women. And women may discriminate against themselves through limiting their own aspirations or an unwillingness to take risks" (pp. 35-36). King (1998) found that women unconsciously favor academic papers based on the assumption that the paper was writte n by a man. Research on gender bias provides a rich assortment of quantitative and anecdotal investigations into the nature and impact of gender bias in academia. As examples, Karp and Yoels (1976) quantified classroom participation among undergraduate and graduate students. Hall and Sandler's chilly classroom reports (Hall & Sandler, 1982) were based primarily on anecdotal research. Jamison (1999) evaluated interviews with more than 340

Pregnancy Foetus Mother

Pregnancy Foetus Mother Pregnancy is a state whereby there is a symbiotic union between a mother and her foetus. During this period, all systems of the body change to accommodate the trophoblast, the immune system (a complex biological signalling system responsible for protecting us against infection, disease and foreign objects due to its ability to differentiate between self and non self) being one of these systems also undergoes a number of changes (Markert, 2005). The foetus is like a homograft attached to the uterine wall of the mother via the placenta, it inherits half its genetic makeup from its mother and the other half from its father. The paternal genes that it expresses are seen as antigens by the mothers immune system and are expected to cause the rejection of the foetus as a semi-allogenic tissue graft(2). Instead, the mothers immune system teaches itself to tolerate these genes and the development of the foetus is supported and regulated (Marker, 2005). The immunological puzzle that leads to t he sustainment of the foetus for the 9 months gestation period is known as the â€Å"immunological paradox of pregnancy† (Claman. 1993). A question that begets to be asked is how does the maternal body prevent rejection of the histoincompatible foetus and at the same time maintain enough maternal host defence mechanisms to fight disease and infection? To date it is not fully understood how this takes place, but it is known that in order to allow the foetus to escape rejection and immunological attacks by the maternal immune system, this symbiotic relationship must have distinctive immuno-regulatory actions. At the same time the mothers immune system must also provide protection against foreign antigens for her as well as her young. A number of explanations have been proposed during the last century as to why foetal rejection does not take place in healthy pregnancies. It is now agreed upon that the placenta plays an important role in this. The placenta is a very important organ because not only does it aid the transportation of nutrients and waste products and immunity between mother and foetus, it acts as an endocrine organ because it secretes growth factors and female hormones which helps maintain and support the pregnancy (Knobil and Neil, 1994) and finally the placental expression patterns of majorhistocompatibility complexes (MHC) is one of the vital factors that determine if a foetus is accepted or rejected, in humans these complexes are known as human leukocyte antigen (HLA) complexes (Claman. 1993). Although the mechanism for the maternal tolerance of the MHCs expressed by the fetus is still not fully known it is known that in humans, a number of HLA class I expressions have been detected in the placent a, these include HLA-C and HLA-G complexes. HLA-G is essential for the successful implantation of trophoblast and its protection from invasion. It does so by binding inhibitory receptors on T-lymphocytes and maternal uterine natural killer cells and thus protects the trophblast from maternal attacks caused by these cells. They also regulate cytokine secretion of cells, thus offering protection to the foetus (hla class 1 molecules reference). A recent study has also shown that HLA-G might inhibit the migration of NK cells across the placental endothelial cells. Till this day, no evidence has been brought forward to suggest that HLA-A, HLA-B and Class II MHCs are expressed in the placenta thus it is inferred that they are normally absent from the placenta during pregnancy (Bulmer and Johnson, 1985). Foetuses are protected not only from rejection during the gestation period but also from infections by the transmission of passive immunity from the mother.In 1892, Paul Erlich used mouse models to demonstrate that fetuses and neonates acquire protective immunity from their mothers both in utero and through breast milk. It has been shown that this involves the active transport of IgG from mother to her offspring. Passive immunity is transferred from the mother to her foetus through the placenta in the form of immunoglobulin G (IgG) and also via breast milk postnatally (Arvola et al 2000). IgG is the main defence against bacteria thus it accounts for 70-75% of antibodies found in human serum. Before birth the foetus is immunologically naà ¯ve because its synthesis of antibodies is very low. The immature immune system of the foetus is compensated for by the active transport of maternal IgG across the placenta into the foetal circulation. Before IgG reaches the foetal circulation, it h as to cross two cellular barriers, the barrier in contact with the maternal blood known as the syncythiotrophoblast and the capillary epithelium of the foetus. IgG antibodies are conveyed across the placenta and the intestinal epithelium via the human Fc receptor (add more). Although the ability of IgG to cross the placenta acts to convey passive immunity to the foetus there are instances where its ability to cross the placenta can have detrimental effects on the baby. An example of this is a condition called haemolytic disease of the new born (HDN). HDN is an alloimmune disease that develops in rhesus positive foetuses that have a rhesus negative mother. the mother produces IgG antibodies against the rhesus positive red blood cells which cross the placenta and attack red blood cells in the foetal circulation. It has been established that breast milk are rich in maternal cells including small proportions of epithelial cells, macrophages, leukocytes and T and B lymphocytes which make up a majority of cells found in milk on the other hand, 80% of the total cells found in the colostrum (first milk secreted after delivery) are mononuclear phagocytes. These cells aid the neonate by protecting the lumen of its gut and transferring immunity passively. Breast milk macrophages enter breast milk via the epithelium of the mammary gland, they are found to be highly phagocytic in breast milk and can easily be differentiated from other cells by the lipid rich inclusions found in their cytoplasm (breast milk macrophages reference). Milk and colostrum are also rich in the dimeric immunoglobin A. IgA antibodies are very important to the newborn because they are highly specific for pathogens found in the mucosae of the gut. This form of passive immunity from the mother thus conveys protection to the newborn until its immune response is mature enough to mount a good enough response (PDF2D). As well as transference of immunity, a mother can also convey infections to her foetus. The maternal transmission of an infection such as HIV, Hepatitis B and syphilis to foetus in utero, as a result of body fluid transmission during child birth and through breast milk is known as vertical transmission. During pregnancy, the maternal transmission of infection can result in a number of sequela. Infections found in mother have the potential of infecting the foetus or newborn. Side effects of infections include abortion or stillbirth, acute illnesses, congenital abnormalities, neonatal death and many more. The newborn can acquire infections in utero also known as intrauterine (congenital), during child birth (intrapartum) or after birth (postpartum). Different forms of infections can be vertically transmitted, these include viral and bacterial infections which are both covered in this essay. The most common examples of viral infections transferred from mother to her unborn child are cytomegalovirus, rubella both of which may cause severe neonatal disease or congenital defects, HIV and Hepatitis B. The human immunodeficiency virus (HIV) is a sexually transmitted virus that attacks the immune system by infecting CD4 cells thus leaving the host vulnerable to other infections. This virus can lead to the acquired immunodeficiency syndrome which is characterised by a very low CD4 cell count (less than 200/ml). The transmission of this virus from mother to child can occur in utero, during child birth and via breast milk. The most common mode of transmission of HIV occurs during labour or at child birth, about 50-80% of vertical transmission occurs via this route. The reason being that the fetus is in direct contact with infected blood and secretions, as a result of ruptured membranes and transmission of maternal blood to the foetus during labour (birth by caesarean section before the beginning of labour and membrane rupture is proven to reduce this risk of transmission of HIV) (www.aafp.org). HIV transmission can also occur in utero. The foetus can become infected if it comes in contact with infected maternal blood and secretions. This contact can be the result of placental haemorrhage or by the foetus swallowing some amniotic fluid (www. the-aids-pandemic.blogspot.com). The final mechanism by which vertical transmission if HIV can take place is through breast milk which occurs in 16-29% of cases (www. the-aids-pandemic.blogspot.com). Hepatitis B is a viral infection of the liver caused by the hepatitis B virus (a double stranded DNA virus which caused liver damage). In 2004, Zhang et al provided evidence that the main route of transmission of hepatitis from mother to foetus was via the placenta. Mothers that have the acute form of the virus and that are also infected in the first trimester of pregnancy have a 10% chance of passing the virus to their neonates. This percentage increases to a staggering 80-90% if the mothers were infected in the 3rd trimester. 90% of neonates on the other hand acquire the infection if the virus chronically infected the women (Hieber et al 1977). Transmission is also caused by the exposure of the foetus to infected blood and body fluids. A hepatitis positive mother has a 20% chance of passing the infection to her offspring during child birth, this risk increases to 90% if the mother is also positive for the hepatitis B e antigen (www.perinatology.com). According to Hill et al (2002), breast milk of infected individuals contains HBV DNA, but using appropriate immunoprophylaxis nullifies the transmission of HBV. Rubella (the German measles) is a condition caused by the rubella virus. This virus is moderately contagious. It can cross the placenta causing a condition known as congenital rubella syndrome (CRS) which leads to a number of side effects to the baby including low birth weight, deafness, mental retardation, congenital heart failure and death. The severity of the effect depends on the period that the fetus is infected; during the first two months of gestation the chances of foetal damage caused by infection is 65-0%, this chance decreases to 30-35% during the third month and finally to a mere 1-2% in the 20th week. There are two routes through which a newborn can acquire a bacterial infection, these routes include intraturerine (transplacental and assending infection) and intrapartum when the new born comes in contact with infected secretions and blood during delivery. Congenital syphilis is a severe and life threatning multisystem infection caused by the vertical transmission of the spirochete Treponema palladium to the foetus. The transplacental transmission rate is 60-80% Vertical transmission of congenital syphilis can occur at anytime during pregnancy although the infection is more likely to be transmitted by women in the primary and secondary stages of the disease as opposed to the latent stage.Just like in adult syphilis, this infection is categorised into early disease which is seen in children two years or younger and late disease which is seen in children over the age of two(http://www.merck.com). During child birth organisms such as N. gonorrhoea, B. streptococci and C. trachomonas bacteria that are naturally found in the female reproductive system can also colonise the newborn. A list of these bacteria are shown in fig 1 of the appendix attached. Vertical transmission of Immunity during pregnancy is complex and one that intrigues many a soul. Till this date its mechanisms are not fully known. What is known is that a number of complex systems are involved in the process and without the foetus will either be rejected or infected by pathogens.

The Beasts and Monsters in Dantes Inferno Essay example -- Divine Com

The Inferno is the first section of Dante's three-part poem, The Divine Comedy. Throughout Dante's epic journey into the depths of Inferno he encounters thirty monsters and five hybrid creatures.   The most significant of these monsters are of central importance to his journey and to the narrative, as they not only challenge Dante's presence in Inferno, but are custodians of Hell, keeping in order or guarding the "perduta gente".   In this essay I am concentrating on these prominent beasts, namely Minos, Cerberus, Plutus and Geryon, establishing why they feature in Dante's eschatological vision and discussing the sources which influenced his inclusion of these particular creatures. These four monsters all fulfil important functions as well as representing important themes in Inferno, establishing them as symbols which reinforce Dante's allegory. Minos, as the infernal judge and agent of God's justice, represents our own conscience and morality.   When the sinners come before him "tutta si confessa", which causes the reader to reflect on their own sins.His terrifying treatment of the souls is significant as after Charon, he is one of the first figures who they encounter on their passage into Hell, and his unique method of demonstrating which area of Hell that the souls should be sent to increases the horror and adds to the alarming atmosphere. His warning to Dante, is similar to several of the infernal custodians, who continually remind him that he should not be in the Otherworld, tu che vieni al doloroso ospizio, guarda com'entri e di cui tu ti fide non t'inganni l'ampiezza de l'intrare (1) However, Cerberus's reaction to Dante is one of obvious malice and vice, and rather than comment on his presence he... ...s Minos's warning to Dante and his unusual illustration of how the sinners are judged.   The monsters also form strategic narrative devices, as their confrontations with Dante and Virgil continue the pattern of incident and movement in the text, adding variety and tension. The beasts form an inherent and essential part of the narrative because of the excitement and terror that they add to Dante and Virgil's journey, as well as reinforcing Dante's classification of sin.   They also illustrate the traditional motifs of Otherworld visions, whilst simultaneously expanding and developing previous representations of the afterlife in order to form original and exciting creations.   This shows the importance Dante placed on the inclusion of these beasts as they not only express the influence of other works on Inferno, but also his own spectacular creativity and fantasy.

Kemosabe

He loved the solitude of the mountains, and as he dismounted his horse he smiled as the usual thoughts and emotions washed over him His ex-wife sarcastically called it the Zen of the Mountain Man, which he thought was a perfect fit. To him, well, to family going back a half-dozen generations these mountains were home, and in a lot of ways he knew his way around here better than his apartment complex.He led his horse to a tiny glade and tied the reins to a low branch where he could nibble on the mountain grass. For a brief moment he gazed at the steed and his hand-tooled saddle and was proud that everything he needed to live in the woods and mountains was right there in front of him. It gave him the comfort self-reliant people have, knowing how to use the best tools and equipment and keeping it all in good shape and neatly organized.He took his binoculars from a saddle bag and strapped it around his neck. From the scabbard came a well-used Ruger Number 1 rifle, a single-shot chambered in 7mm Remington Magnum topped with an equally worn Unertl scope. He was equally proud of his marksmanship; even after he lost the eye he rarely if ever needed a second shot. Besides, if you missed the first shot chances are your prey spooked and ran.He climbed a hundred yards or so to a rocky ridgeline that gave him a perfect view of the valley below and the mountainside opposite his position. Any shot at an elk here could be up to 500 yards, well within the lethal range of his gun and optics. He reloaded his own ammo, learning the hard way never leave anything to chance or someone else’s control. Soon he spied several younger bucks and a stag too big for the youngsters to challenge—for now.He loved the natural order of nature, how it provided for those who took care of it, and in his mind he was already butchering the bounty that would feed him well for months. He said a silent prayer the stag would keep grazing and present him a solid broadside shot. Suddenly he no ticed the elk froze, ears perked and eyes alert and just as suddenly they bolted out of sight. A brief moment later the sound that spooked his quarry rolled up the hill.â€Å"Fuck! Ignorant mother-fucking assholes!† he swore, already up and moving down to his horse as the distant growl of a big ‘dozer washed the hills. He unloaded his rifle and leaned the rifle against a tree. He found the ammo pouch he was looking for, each shell tipped with an especially hardened solid metal-piercing bullet.It took him a while to get a good view of the bright yellow machine as it tore into trees. â€Å"Just great, asshole,† he whispered to himself. Whack down another couple dozen trees and show yourself.† He waited until the moment the machine throttled up, certain the engine’s noise would mask his gunfire. He knew that from experience. He also knew that the metallic ‘bang’ of the bullet slamming through the engine cover and impacting on the engine, al ong with the sudden appearance of a shiny hole would get the operator’s attention.The heavy recoil of his shot rocked against his shoulder. He was halfway to his mount when he heard the motor die into silence. He shook his head in disgust and patted his horse. â€Å"Well, Jumper, just another day in fucking paradise.†On the way home he remembered the days when his oath and badge would have compelled him to search out and arrest the sneaky SOB vandal. It was both just a few years as well as a lifetime past. If anyone had the right to a hard-on for the logging interests, he did. He had tried to restore order in a bar full of loggers and lost his eye in the vicious brawl that ensued. At least a half-dozen loggers set upon him, kicking and laughing as the other patrons watched, either uncaring or too frightened to come to his aid. Miraculously he was able to draw his back-up revolver and shoot three of them, killing one, before they surrendered. Luck was with him—it was a five shot revolver.Insult was added to injury when he was taken off the road and given a job as a dispatcher. His brother-in-law lawyer was able to secure a decent monetary settlement for his injuries and partial loss of sight. Then a new sheriff was elected, nothing but a pawn of the logging coalition, and he was, in the vernacular, â€Å"adios’d†. Pissed as he was. he knew he couldn’t kill anyone, at least not without the heat of battle. But it wouldn’t stop him from ruining their day. Or months and years, he was happy to admit.As much as he liked the solitude, he wasn’t anti-social, and had more than a few good friends he regularly met up with at old bar. He thought his pal Barney summed it up: the kind of place Hemmingway would be comfortable barfing in. He loved Barney and his bullshit, and found him holding court with a bunch of coeds and beatniks. Barney held his lecture and beamed at him. â€Å"Yo! The Great White Hunter returns! Ar e we gonna have an elk bar-be-que tonight?†He glanced at the cleavage of the young girl putting his beer on the table. â€Å"No such luck. Busted. Goddam noise from the logging scares ‘em into fucking Canada.†Ã¢â‚¬Å"Well,† Barney said, â€Å"maybe you need to chase other game.†Ã¢â‚¬Å"Like hell I will.†Ã¢â‚¬Å"Take bulldozers for instance. The news says someone nailed a trophy Cat in Gates Valley this morning.†He raised his glass. â€Å"No shit? Here’s to ‘em!†Ã¢â‚¬Å"Yep.† Barney had a drunken grin. â€Å"Damn shame they’re too heavy to quarter and take home. It’d make a hellofa mount!†

Are There Blind Spots in Our Eyes?

Are There Blind Spots in Our Eyes? ABSTRACT Our eyes are vital organs because they help us visualize our surroundings. But are our eyes perfect in seeing what’s right in front of us? Sadly I learned in our evolution, nature messed up at one point and gave us blind spots in our eyes. This project shows why we have these blind spots, how to discover them, and how big they are. I researched on how our eyes see things; why when one eye is closed, the other eye sometimes can’t see what’s in front of it. I also found during my research a formula that is used to estimate the size of a human eye’s blind spot.I performed an experiment using Blind Spot Test card I made to verify the existence of blind spots in my eyes. I also collected data while testing to find the size of my blind spot. I learned the size of eyes’ blind spots varies in relation to the size of the human eyes. QUESTION Are there any blind spots in our eyes? If there are, how do we find them, and how big are they? VARIABLES Dependent Variable: Size of the blind spot in our eye Independent Variable: Diameter of the eye Experimental Group Controlled Variables For Each Group Child Test Subject MeAdult Test Subject My Mom HYPOTHESIS If I close one of my eyes, using a test card marked with different symbols then I can find my other eye’s blind spot. Add a ruler/yard stick to take measurements; I can estimate the size of that blind spot too. I think the bigger the human eye, the bigger the blind spot is. BACKGROUND RESEARCH The following diagram shows the anatomy of a human eye (New Translation of Laruelle’s ‘Biography of the Eye’). Our eyes see things when light reflects off the objects goes through the pupil and sends the information to our brains.The eye and brain work together as a group that after the information gets delivered to the brain as electro-chemical signal, it is interpreted, or â€Å"seen†, as images (WebMD). The first layer o f our eye is the cornea. It is made of a clear tissue and protects the eye like a see through glass cover. More importantly, it helps the eye focus on an object while light passes through it. The iris, a colorful part of the eye around the pupil behind the cornea contracts or dilates to control the amount of light that goes into the pupil. The pupil at the center of the iris is an opening that lets the light into the eye (Your Eyes).After light enters the pupil, it passes through the lens behind. The lens functions just like a camera lens so that it focuses the light and beams it onto the retina, the light receptor at the back of the eye. The retina’s surface is flat and smooth, and it acts like a movie screen or the film of a 35mm camera. However, unlike a screen or a film, the retina also has some other features, one of which is the light sensors that detect light. After the retina detects light, it converts the light into electro-chemical signals. These signals then exit t he back of the eye via optical nerves and get sent to the brain for processing (WebMD).There is a little area on the retina where the optical nerves are attached to the eyeball at one end and connects to the brain on the other end. This spot of the retina contains no light sensors. Without light sensors the retina cannot sense light, therefore if light hits that spot, it cannot convert the light into electro-chemical signal and pass the information to the brain to â€Å"see†. This forms a blind spot on the eye. The blind spot however, doesn’t affect our vision because our brain â€Å"ignores† it. Also having a pair of eyes, one eye can back up the other eye’s blind spot so that we have a clear vision most of the time.This is why people usually don’t notice the effects of blind spots (Kingfisher 114). There are ways to test human eye’s blind spot. Scientists also discovered formula to estimate the size of our blind spots. Depending on the siz e of our eyes, we each have unique blind spots. MATERIAL LIST A cardboard card approximately 3 x 5 in (or 8 x 10 cm) in dimension Black Marker to draw symbols on the cardboard card Ruler/Yard Stick A pencil to record the data EXPERIMENTAL PROCEDURE Often people use the following experiment (Exploratorium), or its variation to test for blind spots existing in our eyes:Make a test card using the cardboard material. Use a black marker pen to draw a black dot and a cross on the two edges of the card. Make sure the dot and the cross are on the same level. Hold the test card away at an arm’s length and at eye level, while the other hand holds a yardstick just below the left eye. Put the test card on top of the meter stick. Make sure the cross on the test card is on the right hand side. Close your right eye and stare at the cross with your left eye. At this point, you should also be able to see the black dot. Focus on the cross and move the test card towards you by sliding it along the yardstick slowly.At a certain point, the black dot will disappear from your vision. Record the measurement on the meter stick when that happens. Continue to move the test card forward; you’ll notice the black dot will reappear again. You can also test for the other eye by closing your left eye instead. This time you should look directly at the black dot with your right eye, and as you move the test card closer to you, you should notice the cross disappear and reappear again. DATA AND DISCUSSION The following is the formula for finding the size of the blind spot of a human eye: S/m = d/DIn this equation, S is the size of the blind spot on the eye, m is the distance of pupil to retina, estimated by the diameter of the eye, d is the size of the black dot on the test card, and D is the distance from eye to the test card (Exploratorium). Thus, to solve for S, we have: S = d/D * m To perform the experiment, I have two test subjects: my mom and myself. We measured the diameter o f each of our eyes as following: my eye is roughly 2 cm, and my mom’s eye is about 2. 5 cm. Then we stepped through the above-mentioned experimental procedure, and wrote down the data.Experimental Data Black Dot SizeDistance between eye to test card when black dot disappeared Andy Eye diameter = 2 cm0. 25 in ~= 0. 635 cm11. 75 in ~= 29. 845 cm Andy’s Mom Eye diameter = 2. 5 cm 0. 25 in ~= 0. 635 cm13 in ~= 33. 02 cm Based on the data collected, I calculated my blind spot is approximately 0. 0426 cm, or 4. 26 mm in diameter; and my mom’s blind spot is roughly 0. 048 cm, or 4. 8 mm in diameter. Since her eye is slightly larger than mine, her blind spot is a tiny bit bigger than mine as well. I wish I were able to find more test subjects for my experiment.However, I couldn’t find other people to try the experiment. CONCLUSION In conclusion there are blind spots in the eyes and my hypothesis was correct. The experiment shows there is a blind spot in the corne r of our eye because of the optic nerve, and that the size of the blind spot differs from person to person. Our blind spots are an evolutionary defect. Nature was able to correct it by making us have two eyes so we could see clearer and we have a bigger vision field. With that being said we are at the end of my research paper. I hope you enjoyed our little adventure. ACKNOWLEDGMENTI would like to thank my mom, Jane, for being my test subject for my experiment. WORK CITED 1. â€Å"Blind Spot: To see, or not to see†, Exploratorium, http://www. exploratorium. edu/snacks/blind_spot/index. html 2. â€Å"New Translation of Laruelle’s Biography of the Eye†, Fractal Ontology, Nov 21, 2009 http://fractalontology. wordpress. com/2009/11/21/new-translation-of-laruelles-biography-of-the-eye 3. â€Å"The Kingfisher Science Encyclopedia†, Kingfisher Publications, 2006 4. â€Å"Your Eyes†, Kids Health, http://kidshealth. org/kid/htbw/eyes. html 5. â€Å"Your Gui de to How the Eye Sees†, WebMD, http://www. webmd. com/eye-health/amazing-human-eye