!"#$%"#&'()# ONCHARACTER DEVELOPMENT
Introduction and conclusion by Larissa Roy
Introduction
Some friends refuse to watch movies with me. I don’t throw popcorn or contribute to the cinemuck latching your shoes to the ground, but I do talk. Not endless refrains of “That’s what she said,” or streams on how this actor was in this movie and is way hotter than this other actor from a di!erent movie. I rant about continuity. Continuity in the events of the movie, continuity in character, continuity of the world the movie has placed itself in, and, what is markedly the most frustrating to those friends, whether or not it is biologically sound. Noting that the EKG machine clearly says “Leads O!”— meaning that the machine is in no way hooked up to the person in question—in the dramatic blare of the "atline. Commenting that landing on the horse’s back from that height should have killed the horse. Watching Moulin Rouge and noting that she sings impossibly well for someone whose lungs are utterly deteriorating from tuberculosis and furthermore that her lover ought to be infected. The climax of the movie, however, does not seem the best moment to enter into a discussion on how soap works on the molecular level, a new trajectory, or the #ne details of digestion. Many science majors know that there are certain audiences that are simply not interested, particularly with the addition of #gures
76 from the anatomy textbook. Friends in other majors wave an invisible !ag, pleading for a subject change. Art and science do not need to be polar sides of campus. Perhaps they can "nd common ground in the goal of attempting to explain and understand this world through metaphor. Science works through metaphor, comparing lungs to balloons and the immune system to a "efdom and a new species of grass to others already known, and art functions through metaphor by becoming more than a representation, by searching for what is meant and unseen. Naturally, the metaphor needs to be brought forward in a particular way (usually by some eccentric instructor), favoring its particular method. Through the gesture of showing applicable examples that can be seen when concepts cannot, an extended metaphor, the original subject can be understood. This project is about taking concepts working at a microscopic level and making them tangible. The central dogma of biology can be simpli"ed to DNA–>RNA–>protein; all tissue and biology built from there make the larger spectrum. We can see the results of genetic change even if the causation, the chain of nucleotides itself, is murky and not instantly accessible. Herein also lies some of our fascination with deviations from the unwritten norm. We stare. We gawk. We slow down to drive by the scene of an accident, involuntarily curious. It’s in our nature, simultaneously needing to "nd an explanation and letting our imaginations wander. Mutants are cool, understanding what “goes right” by evaluating what “went wrong.” We’re further fascinated by the unfortunate souls that embody them. These individuals surely have a di#erent perspective. How does this go back to the movie thing? TV and movies are saturated with some sort of abnormal. Not every movie creature or villain is a human warped by a series of aggregating mutations, but every good villain has a back story where his or her thinking makes sense in a twisted fashion; “I’m just evil” doesn’t really cut it. Often, our “bad guy” has a physical deviation as a
77 re!ection of an inner self (though our heroes and antiheroes are not always left without some sort of mutation, notably the recent slew of superhero movies), but the discussion thereof is circular. Let’s take a look at a few extremes: the Creature from the Black Lagoon, Pyramid Head (of Silent Hill), and the Penguin (from Batman). All of these are distinctly humanoid, recognizable as basically human. If we take these "ctional characters and accept they could exist in this world, they can be further evaluated in accordance with our reality. It can take some creative thinking, fusing imagined origins with scienti"c facts, though by accepting some of the rules established in their own world and suspending disbelief, the mysterious monstrosity becomes real in a di#erent sense. In turn, they are all the more pitiable because of it, each an example of what extremes a lack of acceptance has led them; they are human after all, pitted against selective pressures. I present to you a developmental perspective— developmental in terms of from zygote to fetus to child, rather than in terms of character development—of the Creature from the Black Lagoon, Pyramid Head, and the Penguin. Their motivations are not the focus here, let alone the cinematography or the quality of acting. Instead, the thoughts represented here are how these individuals could have existed in the "rst place. The gap cinches. That space between our world and a created one is brought that much closer, all under the guise of utilizing new information and creative, critical thinking. The shocking truth: putting too much thought into things can be fun.
The Creature from the Black Lagoon a.k.a the “Gill Man” Lavinia Karl
The Creature from the Black Lagoon has been shrouded in mystery. Very little background information exists as to his origins or exact appearance, and these reports are prone to
78 exaggeration and inconsistency. Most of the information we have comes from the 1954 movie titled for the creature and reports of similar monsters which may or may not be related. Add the tendency of !lmmakers to modify for the sake of dramatic e"ect and that this !lm was not strictly a documentary, and we are left with the sad reality that the information we do have is unreliable. However, it is possible from these sources to construct a basic idea of who this individual was. What we do know about the Creature from the Black Lagoon (or “Gill Man”) was that he was undoubtedly an unfortunate human male, probably in his mid- to late- twenties at the time of discovery, who su"ered from an unusual number of dis!guring mutations. His scaly !sh skin, as well as some of his facial abnormalities, resemble some form of ichthyosis or ichthyosis-related syndrome. His webbed !ngers and toes can be attributed to a severe case of syndactyly, and his claw-like nails were possibly the result of onycogryposis. This combination of physical deformities left the poor young man with a truly monstrous appearance. Add to this his habit of living in swamps, and it is not hard to see why he was a solitary creature. There are several varieties of ichthyosis and ichthyosis- like disorders, the probable cause of much of the Gill Man’s appearance woes. Speci!c potential disorders include epidermolytic hyperkeratosis, harlequin ichthyosis, ichthyosis vulgaris, KID syndrome, lamellar ichthyosis, trichothiodystrophy, and X-linked ichthyosis. Each has its own rationale as the potential source of Gill Man’s a#ictions. All cause dry, scaly skin, varying in severity. Harlequin ichthyosis is the most severe, and infants born with this disease rarely survive. Individuals who do survive into childhood or beyond have thick scales. Their ears, mouth and nose may also be malformed due to the thick scaling, which could account for some of the Gill Man’s facial abnormalities. The shape of his mouth in particular resembles that of infants with the disease. The skin tone of those a#icted
79 with harlequin ichthyosis is resembles a burn victim, which is not in line with descriptions of the Creature from the Black Lagoon, who is usually reported with a green or brown coloring. However, it is possible that spending so much time in swamp water could tint his skin, perhaps with the help of algae and other aquatic plant matter. Epidermolytic hyperkeratosis is a mild form of ichthyosis resulting in thick scaling in the form of parallel ridges concentrated near large joints. This form of ichthyosis is also commonly associated with thickening of the nails and sparse hair growth. Given the claw-like appearance of the Creature from the Black Lagoon’s nails, the thickening accompanied by this disease sounds promising; however, in epidermolytic hyperkeratosis, the thickening of the nails is also associated with dystrophic nails. Given that claw-like nails are due to excessive nail growth rather than dystrophy, this decreases the likelihood the Creature was a!icted with this variation of ichthyosis. Ichthyosis vulgaris is characterized by "ne white polygonal scales. These are sometimes darker on the extremities, such as hands and feet, and generally do not appear on the face or large joints. Nasal allergies and eczema are commonly associated as well. Given the extreme mildness of this disease it is almost certainly not the cause of the Creature from the Black Lagoon’s abnormal skin condition. KID syndrome on the other hand is more likely. The scaling resembles that of a lizard more than that of a "sh, and is present on the face. Plugging of hair follicles is also present, resulting in sparse or absent hair, and spiny karatotic thickening of the palms is also common. Small, malformed nails are frequent as well, but not the rule. As this is one of the relatively milder ichthyosis-like syndromes, it is thus unlikely to be the a!iction from which the Gill Man su#ers. Trichothiodystrophy is another ichthyosis related syndrome. The scales are "ne and white, similar to the ones
80 present in ichthyosis vulgaris. Trichothiodystrophy is also accompanied by sparse hair, abnormally thick or thin nails, slight mental retardation, and decreased average height. Sparse hair, as previously mentioned, is a likely trait of the Creature. Abnormally thick nails agree, too, with his claws and all. Mild mental retardation is possible, and could account for his di!culty with social interactions. Shortness in stature is not usually listed among the Creature’s attributes. X-linked ichthyosis di"ers in the variety of the scaling, most prevalent on the neck and trunk, and generally not present on the face. In about 20% of cases the testes are undescended. This may or may not be an a#iction of the Gill Man, as all renditions of the individual exclude genitalia. Quite possibly this is the result of carelessness on the part of the artist, rather than an indication of the Gill Man’s appearance. Given the level of deformity with which the Creature from the Black Lagoon was a#icted, it is very unlikely that he su"ered from any of the milder forms of ichthyosis or similar disorders. The most likely scenarios are that the Creature from the Black Lagoon is a surviving individual with harlequin ichthyosis with skin color a"ected by his living environment or that he su"ered from another, as of yet unidenti$ed ichthyosis related skin disorder. It is extremely unlikely that an individual with harlequin ichthyosis could survive in a swamp due to their increased susceptibility to bacterial infections and overall sensitivity of the skin. Still, this is the only known form of ichthyosis that could account for the facial abnormalities. It is, of course, possible that they are the result of an entirely di"erent disorder. With the scant evidence we have on this individual, an exact diagnosis is impossible. In addition to his skin abnormalities, the Creature from the Black Lagoon is agreed to have unusual hands and feet. Both extremities are webbed, and he is consistently described as having claw-like nails. The webbing is attributed to syndactyly, a
81 relatively common congenital birth defect. This abnormality is caused by failure of the skin cells between the digits to die when required, i.e. lack of apoptosis. There are varieties of syndactyly, classi!ed based on severity. Complete syndactyly is when the !ngers or toes are connected along their entire length. Usually, the digits are surgically separated and allow for normal use of the hand. Incomplete syndactyly is when the digits are only partially connected. Surgery is typically unnecessary in this case since the !ngers are generally able to move independently enough of each other so as not to impede function. The two additional classi!cations are simple and complex syndactyly. Simple syndactyly is when the fusion of the digits is limited to the skin, and the bones are completely separate. Complex syndactyly is the form in which some of the bone and/or nail is fused in addition to the skin. The complex variety is much more debilitating, and as he appeared to be capable of fending for himself, the Creature from the Black Lagoon probably had simple syndactyly. Syndactyly also occurs most commonly between the middle and ring !ngers and the second and third toes. In the case of the Creature from the Black Lagoon the syndactyly would have been present on all digits and was probably severe but not complete. Complete syndactyly would have given his hands the appearance of mittens made of skin. My guess is that the !ngers were joined up to but not including the last digit. This would allow for the webbed look without creating the “mitten.” The nails are a bit more ambiguous. It is possible that he just never cut them. Living in a lagoon, as he is reported to have done, it may not have been necessary, or he could have had yet another mutation. The most likely candidate is onychogryposis. This usually occurs in the big toe as a result of trauma and causes the nail to grow thick and curved. However, it can manifest in children from genetic causes and has also been observed on multiple !ngers and toes. It is probable that the Creature from
82 the Black Lagoon was a!icted with this condition on all digits. All in all, the Creature from the Black Lagoon was a very unfortunate individual. At an early age, his appearance would have made him repulsive to members of the community in which he lived. Given that he lived in a remote area of the Amazon, it is likely that his community was tribal. The young man was probably thrown out of the community, or he eventually ran away, pressured by his inability to "t in. As for survival with his many a!ictions, it is clear that he was a remarkable human being with a strong will to live.
Works Cited
1) Cohen, Bernard, and Christoph Lehmann. “DermAtlas: Online Dermatology Image Library.” Dermatlas: Dermatology Image Atlas with 10777 Dermatology Images. 14 Nov. 2008
3) Goins, Kenneth M . “ Ichthyosis.” emedicine The Continually Updated Clinical Reference. 14 Nov. 2008
4) Hall, Jamie. “The Cryptid Zoo: Loveland Frogs.” The Cryptid Zoo: A Menagerie rie of Cryptozoology. 14 Nov. 2008
5) “ Foundation for Ichthyosis and Related Skin Types.” Foundation for Ichthyosis and Related Skin. 15 Nov. 2008
6) Kozin, Scott H., Md. “Syndactyly of the Hand.” American Academy of Orthopaedic Surgeons. 17 Nov.2008
7) Marino, Thomas A.. “Text for Pharyngeal Arch Development.” Instructional Support Center I( SC). 14 Nov. 2008
83 9) “Polydactyly and Syndactyly.” Penn State Hershey. 17 Nov. 2008
11) ”Syndactyly.” Genetics Home Reference - Your guide to understanding genetic conditions. 14 Nov. 2008
12) “My Child Has: Syndactyly.” Children’s Hospital Boston. 17 Nov. 2008
13) “onychogryposis - De!nition from Merriam-Webster’s Medical Dictionary.” Dictionary and Thesaurus - Merriam-Webster Online. 17 Nov. 2008
Pyramid Head Andrew Prendergast
Pyramid Head came to the attention of the scienti!c community in 2001 when the second “Silent Hill” incident was reported by the psychiatric patient known only as J. S. Four such incidents were reported from 1999 to 2004, all characterized by a level of grotesqueness rivaled only by their sheer paranormal inexplicability. The only survivors of these incidents exhibit severe posttraumatic stress and psychosis (for review, see the relevant case studies of H. M. 1, J. S., H. M. 2, and H. T.) and various physical scars. However, physical evidence of the town in which the related events allegedly took place remains elusive. In fact, the only common thread between the four incidents is the demonic town itself, leading some clinicians to the conclusion that the Silent Hill Incidents are merely folie a deux-like psychosomatic phenomena. The horri!c yet ephemeral nature of the Silent Hill Incidents has attracted much attention from empirical and paranormal researchers alike, and remain largely indecipherable.
84 Pyramid Head is a humanoid observed only by J. S. throughout the Silent Hill Incidents. J. S. describes him as a male !gure of normal height dragging a sword approximately the length of his own body. According to J. S., Pyramid Head’s most striking feature is his tetrahedral metal helmet, which J. S. claims was never removed in any encounters with Pyramid Head. Throughout the second Silent Hill Incident, Pyramid Head reportedly received multiple gunshot wounds, lacerations, and blunt impacts but was una"ected. J. S. also notes that Pyramid Head was incessantly violent, attacking both J. S. and the other inhabitants of Silent Hill. The Pyramid Head phenotype, if indeed an actual organism and not merely a construct of J. S.’s psyche, presents a fascinating study of cranial development. Though initial interviews with J. S. uncovered the pyramidal head as the only morphological abnormality, subsequent interviews have revealed that Pyramid Head also exhibited unusual in#amed vasculature and large #eshy growths over the torso, complicating the Pyramid Head phenotype. While some researchers have suggested that Pyramid Head has a normal-shaped head within his pyramidal helmet, we and others have dismissed this conclusion as “lame.” Normal cranial development is dependent on the delayed fusion of early cranial sutures, permitting the expansive growth of the brain (OHSU 2006). Cranial synostosis, or early fusion of any of these sutures can generate cranial abnormalities that deform one part of the skull (OHSU 2006). Trigonocephaly is characterized by an anterior cranial ridge and triangular-shaped skull (when viewed from above); it is a result of early fusion of the metopic suture (Schneider Children’s Hospital 2006). Brachycephaly is characterized by a marked dorsal elongation of the skull, a result of early bilateral fusion of the coronal sutures (Chen et al 2003). We are unaware of a case in which both phenomena occurred together in normal development. Pyramid Head’s helmet shape suggests he may be the !rst.
85 The etiology of cranial synostoses is still in dispute and may be the result of genetic or environmental factors, or perhaps some combination of the two. Candidate genes responsible for trigonocephaly have been suggested and include sox, fgfr, cer, and Mon, though these are actively disupted (Czako et al 2004, Jehee et al 2006). Mouse knockouts of fgfr2 exhibit brachycephaly, but clinical data does not yet support or reject the relevance of this gene to brachycephaly (Chen et al 2003). Other proposed environmental causes of cranial synostosis included elevated intracranial pressure and the presence of external force on the cranium or drugs such as valproic acid in utero (Shimoji and Tomiyama 2004, OHSU 2006). However the morphology arises, cranial synostosis represents a likely candidate for Pyramid Head- type development. The recent revelation that Pyramid Head also exhibits cancerous growths also suggests the possibility of additional genetic anomalies. An artist’s reconstruction of Pyramid Head following a recent interview with patient J. S. includes a protruding tumor in the torso. Although diagnosis is di!cult without histological analysis, we suggest, based on the color and size of the tumor, that the growth is a basal cell carcinoma (BCC). Susceptibility to BCC has identi"ed genetic causes. Mutations in ptchl (Patched-1) and smo (Smoothened) result in deregulation and proliferation of Sonic Hedgehog, which in turn causes BCC formation (Freier et al 2006). A common genetic pathway suggests itself in light of the two major aspects of the Pyramid Head phenotype. Ptchl is located at 9822.3, and microdeletions in chromosome 9 (albeit in di#erent locations) have previously been identi"ed as correlative genetic factors in trigonocephaly (Su et al 2005, Jehee et al 2006). In light of this speculation it seems likely that we might observe multiple aberrations at chromosome 9. For con"rmation, a direct and viable sample from the specimen is necessary for genetic analysis.
86 Recent interviews have also established that Pyramid Head exhibits an unusual raised, in!amed vasculature. We suggest that this condition is secondary to Pyramid Head’s violent and confrontational lifestyle, and perhaps represents a vascular disease brought on by infection. One possibility is systemic vasculitis, a disorder that can be secondary to infection and is characterized by in!ammation of the blood vessels (Roane and Griger 1999). However, systemic vasculitis has many subtypes, and accurate diagnosis simply cannot be made by proxy. The possibility that disease might contribute signi"cantly to the Pyramid Head phenotype is one that cannot easily be discounted. As noted above, it is essential that cell, molecular, and developmental biologists now cooperate with "eld biologists to acquire a live specimen of Pyramid Head. Though interviews with J. S. have proved constructive, they remain suspect due to the confounding factor of his multiple psychiatric disorders. This will not be an easy task; however, we remain con"dent that funded properly, "eld biologists should be able to observe, with the necessary precautions, Pyramid Head’s behavior and function. For additional information, interested investigators should see our supplementary publications: How to apply for tactical weaponry in an NIH grant, and Treatment of evisceration in the "eld.
Works Cited
1) Oregon Health and Science University. Patient information-pediatric cranial synostosis [website]. Portland: OR. 2006. [cited May 2006 Available from:
2) Schnieder Children's Hospital. Craniofacial anomalies: craniosyntosis New Hyde Park (NY). 2006 [cited May 2006]. Available from:
3) Czako, M., et al. 2004. Trigonocephaly-like syndrome in a patient with terminal deletion of 2p and partial duplication of 17q [abstract
87 American Journal of Medical Genetics. 131(3): 310-312.
4) Jehee F. S., et al. 2006. Mutational screening of FGFR1, CER1, and CDON in a large cohort of trigonocephalic patients [abstract]. The Cleft-Palate Craniofacial Journal. 43(2): 148-151.
5) Chen, L., et al. 2003. A Ser252Trp substitution in mouse !broblast growth receptor 2 (Fgfr2) results in craniosyntosis [abstract]. Bone. 33(2): 169-178.
6) Shimoji, T., and Tomiyama, N. 2004. Mild trigonocephaly and intracranial pressure: report of 56 patients [abstract]. Child’s Nervous System. 20(10): 749-756.
7) Freier, K. et al. 2006. Recurrent NMYC copy number gain and high protein expression in basal cell carcinoma. Oncology Reports. 15(5): 1141-1145.
8) Su P. H. et al. 2005. Six cases of deletion 9p24 and trisomy 19gl3.4 inherited from a familial balanced translocation [abstract]. Journal of the Formosan Medical Association. 104(7): 525-530.
9) Roane, D. W. and Griger, D. R. 1999. An approach to diagnosis and initial management of systemic vasculitis. American Family Physician. 60(5): 1421-1430.
The Penguin from Batman Returns Sarah West
In action movies and classic comics, Batman is iconic, and his villains have become the archetype for the supervillian. The strange physical appearance of these characters may be derived purely from the imaginations of their creators, yet upon closer inspection these identifying traits could be understood to have scienti!c causes—in some cases abnormalities in the embryological development—that in fact mimic developmental mutations in reality. Take for example the character of the Penguin, as portrayed by Danny DeVito in the 1992 !lm Batman Returns, directed by Tim Burton. The Penguin was originally christened Oswald Chester!eld Cobblepot by his high-society parents. Due to the gross dis!gurement of their infant son, these parents decide to
88 abandon their child by throwing him in the river rather than live with the embarrassment of having produced such a hideous creature. Downriver at the Gotham City Zoo, the child is taken in and raised by the penguin community in the sewers of Gotham. Later, after a brief career in the circus, Oswald—now known as the Penguin—attempts his vengeance against his parents by abducting the !rst-born child of every family in Gotham City. Looking at the physical characteristics of the Penguin, it is easy to imagine how the penguins at the zoo could have mistaken him for one of their own. This individual is of short stature, obese, and has little to no obvious neck. He is very pale, and his facial characteristics are predominated by a long, beak-like nose, small teeth, and dark, sunken eyes. Most striking of the Penguin’s features are his hands, where the !rst and second digits appear to be perfectly normal, yet the remaining three digits of each hand are fused together. Thus, his hands give the impression of "ippers more than hands, with thick webbing between the last three !ngers. This striking appearance naturally leads us to question what changed in early development of this individual to result in these unique characteristics. Some type of penguin- human hybrid might !rst come to mind. It is more probable that mutations in the genome of this individual, in addition to environmental factors, led to the resulting abnormalities. Growing up underground in the sewers with minimal exposure to sunlight contributes to the grotesquely pale appearance of the Penguin. While the short stature of the Penguin might be a genetic e#ect, it could also be caused by the early malnutrition of the individual while traveling downriver, resulting in slow and stunted development. However, once Oswald was taken in by the penguins, he likely was raised on the same diet—fatty !sh—as the penguins, which ultimately led to his obesity. The short legs, coupled with the obesity and learning via imitation, causes the Penguin to waddle while walking, mimicking the movements of
89 his avian counterparts. The facial features and the abnormalities of the hands are most likely caused by mutations in the genome rather than environmental factors. The lack of neck and distorted facial features suggest an error in the early development of the craniofacial region and the upper spinal cord, which both depend heavily on the migration of neural crest cells during the early stages of development (Slack, 2006). In particular, the controlled apoptosis of migrating neural crest cells is directed by the expression of Fgf-8 in surviving cells (Ahlgren, et al., 2002), which is ultimately dictated by the upstream expression of retinoic acid in this signaling pathway. Abnormal expression of Fgf-8, possibly caused by exposure of the fetus to ethanol during early development, can thus contribute to the disrupted migration of the neural crest cells, resulting in mutated craniofacial features. Furthermore, this mutation can cause the di!erentiation of the cervical vertebrae to be disrupted, leading to the lack of neck apparent in the Penguin. The phenotypic deformities of the neck and craniofacial region presented in the Penguin resemble those seen in individuals su!ering from Klippel-Feil syndrome (Hensinger, et al., 1974). Interestingly, some Klippel-Feil patients also experience syndactoly—fusion of one or more digits - accompanied by a mirroring phenomenon in which the motions of one hand are exactly mirrored by the other, and independent movement on one side is not accomplished (Hensinger, et al., 1974). Spina bi"da is seen in some individuals with Klippel-Feil, further supporting the theory that failure in the proper migration of the neural crest cells—in this case closure of the neural tube—signi"cantly contributes to the mutation of Klippel-Feil syndrome and the Penguin (David, et al., 1999). Additionally, teratogen disruption or genomic mutation of the Hox gene expression within the craniocaudal region of somite formation may lead to improper segmentation of the cervical vertebrae and resulting craniofacial
90 defects. Improper Hox gene expression can also contribute to the fusion of the digits seen in the hand. The abnormal signaling gradient of the speci!ed Hox-4 cluster of genes in the developing limb bud (Tabin, 1992) may lead to mutant downstream positioning of the AER (apical epidermal ridge), which ultimately results in improper di"erentiation of the digits. However, closer inspection of the hands of the Penguin indicates that the structural di"erentiation of the digits has occurred normally—that is, the individual bones and tissue structures are correctly developed— yet the regression of the interdigital space between digits three through !ve has failed to occur during the late formation of the limb bud. This severe webbing of the digits is a feature common to aquatic avian species, and is most likely the cause of the Penguin’s abnormalities. The normal development of the limb bud progresses with the digits connected. During the late stages of development, BMP-4 signaling induces the regression of the AER via Msx up-regulation. When this process occurs, BMP-4 directs the apoptosis of the mesenchymal cells in the interdigital spaces; thus, as the AER regresses so does the webbing between the digits (Lallemand, et al., 2005). Again, the di"erentiation of structures in the limb buds is highly dependent on signaling gradients, and the abnormal gradient expression of one or more signaling molecules can lead to phenotypic abnormalities. It is likely that in the case of the Penguin, proper BMP-4 expression is inhibited in the more posterior segments of the limb bud by either gremlin or noggin. These two inhibitors can potentially be expressed in a similar gradient, with a higher concentration of expression occurring in the most posterior segments of the developing limb bud (Guha, et al., 2002). Ultimately, incorrect expression of Hox genes, improper migration of neural crest cells, and inhibition of BMP-4 signaling pathways all contribute to the mutated phenotype presented in the Penguin. The mutations portrayed through villains in comics
91 and movies can explained scienti!cally in our world, yet, it is important to remember that the vindictive behavior of these individuals is not often the result of any developmental mutations, but rather the response to inhumane treatment by “normal” individuals in response to something that is simply di"erent. In the case of the Penguin, the motive behind his criminal activities is focused on vengeance from being abandoned because he looked di"erent; however, his villainous behavior may never have occurred if it were not for the discrimination and intolerance displayed by his parents.
Works Cited !"# Ahlgren, S.C., Thakur, V., & Bronner-Fraser, M. (2002) Sonic hedgehog rescues cranial neural crest from cell death induced by ethanol exposure. PNAS 99(16), 10476-10481. $"# David, K.M, Thorogood, P.V., Stevens, J.M. & Crockard, H.A. (1999). The dysmorphic cervical spine in Klippel-Feil syndrome: interpretations from developmental biology. Neurosurgical Focus 6(6): 4. %"# Guha, U., Gomes, W.A., Kobayashi, T., Pestell, R.G. & Kessler J.A. (2002). In Vivo Evidence That BMP Signaling Is Necessary for Apoptosis in the Mouse Limb. Developmental Biology 249: 108-120. &"# Hensinger, R.N., Lang, J.E. & Macewen, G.D. (1974). Klippel-Feil Syndrome: A Constellation of Associated Anomalies. JBone Joint Surg Am. 56: 1246-1253. '"# Lallemand, Y., Nicola, M., Ramos, C., Bach, A., Cloment, S.C. & Robert, B. (2005). Analysis of Msxl ; Msx2 double mutants reveals roles for Msx genes in limb development. Development 132: 3003-3014. ("# Slack, J.M.W. (2006). Essential Developmental Biology, 2°d ed. Massachusetts: Blackwell. Tabin, C.J. (1992). Why we have (only) !ve !ngers per hand: Hox genes and the evolution of paired limbs. Development 116: 289-296.
Conclusion
Here’s another question, then: how does one tie these up? A science paper might cut o" here to leave us with our on conclusions, the interpretations and applications o"ered without a speci!c need to restate anything more. A winding-down or
92 “what this all means” sort of note tends to be more customary for the philosophical and English paper world. This project lies somewhere in between. How to directly approach the work, too, is not easily reconciled. Each of these individual papers came from a di"erent perspective in order to gain a new perspective on the characters, more importantly innovatively applying the knowledge and functions of our world. Simultaneously, there is a depth added in the motivation and agency of the individual as a character, alongside resolutions for what genetic and environmental factors could generate such an oddity. This #nding allows for more sympathy in either case. In truth, I could easily make this a public service announcement, stating that mutants cannot necessarily help themselves or that aberrations are (or were, or could have been) just like us and deserve to be treated as such, but while the method of understanding these characters, in both senses of the word, is unique, the real story here is the exploration. The analyses presented by their respective author—though each centers on an unfortunate human male— are all undertaken with a scienti#c tone but to a very di"erent analysis. A grand conclusion does not immediately present itself. The merit lies in dissecting the world from all angles, falling back again to that intersection of art and science. To achieve the most out of our imagined creations, the intersection needs to become an integration. An integrative process between art and science may not function precisely how this project has represented it; neither art nor science are so con#ned. The art in science writing may be hidden in ciphering the patterns and trying to explain in a di"erent kind of metaphor just as the science in a story may veer from this example in dissection of genetic code to considering a logical process of actions and reactions. A di"erent vantage point changes interpretation, driven by a curiosity that makes us human.
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