Spectrum Volume 5(1)(1) Fall 2014

SPECTRUM Journal of Student Research at Saint Francis University

Volume 5 (1) Fall 2014

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SPECTRUM: Journal of Student Research at Saint Francis University Faculty Editors: Balazs Hargittai Professor of Chemistry bhargittai@francis.edu

Grant Julin Assistant Professor of Philosophy gjulin@francis.edu

Student Editorial Board: Shannon Adams Hayden Elliott Daniel Hines ’13 Paul Johns ’07 Cecelia MacDonald Gabrielle McDermott Jonathan Miller ’08 Morgan Onink Aaron Rovan ‘09 Margaret Thompson

Cover: Photo by Balazs Hargittai

Allison Bivens ’12 Cathleen Fry Eric Horell ’13 Jennifer Kirchner Lauren McConnell ’12 Sarah McDonald Steven Mosey ‘14 Rebecca Peer ‘14 William Shee Jennifer Yealy ‘13

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SPECTRUM Table of Contents From Purity to Pollution: The Transformation of Baseball in the Steroid Era Dennis J. Ryan; Arthur Remillard

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Synthesis and Characterization of Azo Dyes Michelle Lipski; Lauren E. McConnell; Lauren E. Grabowski; Kristen N. Ritchey; Michele R.S. Hargittai; Balazs Hargittai

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A Study of the Risk Factors of Degenerative Joint Disease of the Knee leading to Total Joint Arthroplasty and their Influence on Therapeutic Outcomes Stephen D. Kowalski; Stephen M. LoRusso

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Call for papers

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(Student authors’ names underlined.)

Erratum: The following paper appeared with the incorrect list of authors in Volume 4, Issue 4 of Spectrum. The Editors of Spectrum apologize for the mistake.

Organized Body, Organized Mind: The Association between Yoga and Cognitive Abilities Irene M. Boyle; Margaret H. Calvert

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From Purity to Pollution: The Transformation of Baseball in the Steroid Era Dennis J. Ryan Literature & Languages Department School of Arts & Letters djr100@francis.edu

Arthur Remillard Religious Studies Department School of Arts & Letters aremillard@francis.edu

A Major League Baseball dispute in 1994 almost struck out the sport forever, until the unlikeliest hero stepped up to bat, steroids. The postponement of the 1994 season lasted 234 days and led to the first cancellation of the World Series since World War One. Although the game resumed, its lasting effects continued to be felt the next season when attendance dropped 28 percent.

Baseball would not peak again until Mark McGwire’s historic 1998 season when he broke Roger Maris’ homerun record that had stood for 37 years. Meanwhile, baseball’s other prime player, Barry Bonds, watched his status as an elite player fade away and resolved to use illicit drugs. Bonds’ use of performance enhancing drugs elevated steroids to a topic of national debate as fans wrestled with the violation of baseball’s purity. To resolve this conflict fans need to return to the origins of the game, and come to terms with the history of pollution hidden by the illusion of purity.

baseball as an American game. When the commission published their findings, Abner Doubleday, a Civil War hero, became the founder of baseball. To convey the significance of baseball as the American the game, Tim Arango writes “Myth of Baseball’s Creation Endures, With a Prominent Fan” for The New York Times. In the article Arango quotes a baseball historian, John Thorn who states, “We have a peculiar country in which we do not have a national creed, we do not have a king, we have no national set of beliefs,” and as a result Thorn asserts, “Baseball became a secular religion” (quoted in Arango).

Joseph L. Price establishes the characteristics baseball shares with religion in his book Rounding the Bases. He begins by discussing professional baseball’s commencement in 1876 with the National League who instructed Brooklyn police to arrest anyone playing baseball on Sunday. The opposition would not last long however, as The Sporting News predicted 10 years later, “Sunday is getting to be the great day for sports in America, which if present trends continued would make the Sabbath remembered only as a tradition of the past” (qtd. in Price 13). The Sporting News statement held true as religious leaders lost control on their reign of sports as a new generation abandoned pews and instead occupied sold out stadium seats across America.

Henry Ward Beecher was a minister during the Civil War era who supported a movement identified today as muscular Christianity. Beecher noted how Christian connotations share a core identity with religion by engaging young men in physical activities that promotes health instead of a life of leisure. Beecher’s message of muscular

Origins of Belief Ninian Smart, a major theorist in religious studies, defines religion in seven dimensions. In his mythic dimension, Smart explains the need of religion to possess a history because people desire a story to make sense of the intangible. Furthermore, Smart notes how an understanding of the past gives us an identity in our life long search of meaning.

The vitality of origins extends beyond religion, evident when a British sportswriter published an article in 1903 reasoning the founding of baseball to have British roots. Consequently, the American identity became shattered and in response baseball’s chief executive in the early 1900s formed a commission to decisively reestablish

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Christianity resonated with twentieth century baseball players who gave religious testimonies.

Specifically, Norman Vincent Peale a pastor of the Marble Collegiate Church in New York City and the pioneer of positive thinking theory oversaw the publication of Faith Made them Champions, a book of inspirational baseball stories. Famous testimonies were contributed by Mickey Mantle, Jackie Robinson, and Babe Ruth who promoted “the effectiveness of disciplined work, the significance of loyal friendship, and the creative possibilities of courageous action” (Price 23).

The early interplay of sports and religion becomes apparent in fans that develop a deep faith in their teams, a devotion which transcends the game to become a national identifier. One way fans experience their faith in sports is through Mircea Eliade’s definition of a hierophany, a manifestation of a higher being. When this occurs Eliade reasons, “Experience of the sacred space makes possible the ‘founding of the world’ where the sacred manifests itself in space, the real unveils itself, the world comes into existence” (59). In his book, Something Like the Gods, Stephen Amidon discusses his founding of the world with the New York Yankees. In brief, Amidon worships the sacred area in the old Yankee Stadium where Mickey Mantle’s well known hit landed on May 22, 1963 during the 11th inning against the Kansas City A’s. This ball, if it did not land in the area the fans dubbed “the facade,” may have traveled 600 feet. Ironically, the physical area of worship, “the facade,” conceals Mantle’s personal vices which include alcoholism, adultery, and his contempt for fans. When fans become aware of Mantle’s or any other athlete’s facade, the sacred becomes profane and the world continues in ordinary existence.

The PED scandal also revealed the existence of a facade which became so large America’s chief executive had to address the issue. On January 20, 2004 in his State of the Union address, George Bush stated, “To help children make right choices, they need good examples: Athletics play such an important role in our society, but unfortunately, some in professional sports are not setting much of an example” (FDCH E-Media). Bush continued,

5 singling out PED’s and advised the sports community “to take the lead, to send the right signal, to get tough, and to get rid of steroids now” (FDCH E-Media). This passage, which came to be known as “the crazy two sentences” on Capitol Hill, concisely exposes how baseball became a game of personal achievement, even at the expense of the game’s sacred origins.

Constructing the Chief Facade The disturbance of baseball’s mythological origin began when two players competed for the sole glory of eclipsing Roger Maris’ homerun record. Sammy Sousa and Mark McGwire’s legendary race satiated a fan base still bitter over the 1994 lockout season. McGwire in particular came to represent everything that was right in baseball as Mark Fainaru-Wada highlights in Game of Shadows. On America’s fascination with McGwire during this season Fainaru-Wada indicates, “And from acting baseball commissioner Bud Selig down to its ordinary fans---all agreed that McGwire’s pursuit of the home run record was hugely important. It had made watching the sport of baseball enjoyable again, for the first time in quite a while” (xi). Unbeknownst to the fans at the time, McGwire’s homerun record was assisted by performance enhancing drugs and would establish steroids as the new norm instead of sacrifice and fair play.

The epitome of baseball’s new design came when McGwire crushed the 37 year long home run record baseball out of the park on September 8, 1998 in St. Louis, finishing the season with 70 homeruns in total. His rival, Barry Bonds had once been the premier star, as he signed with the San Francisco Giants in 1993 for the richest deal in history at 43.75 million dollars for six years. Yet, at 33 during the 1998 season Bonds watched the attention shift away from all around skilled athletes to pure power sluggers. Fully aware McGwire’s achievement was aided by steroids, Bonds became increasingly jealous and resolved to begin using what he called “the shit” (Fainaru-Wada xvi). The effects of Bonds’ steroid use would not only alter his game, but more notably transform the sport of

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baseball forever, by creating the largest facade sports has yet to witness.

Bonds began his makeover during the 1998 offseason by firing his well respected trainer, Raymond Farris for a man who dubbed himself the “Weight Guru.” Although Farris had previously worked with Jerry Rice, whom many consider the greatest wide receiver in NFL history, he did not include performance drugs into his training. The “Weight Guru,” formally known as Greg Anderson did however and Bond’s sought him out to increase his power. Anderson began by designing intense workout sessions to isolate specific muscle groups, and pushed Deca-Durabolin and Winstrol to his clients under the table. To explain the benefits of steroid use Fainaru-Wada details, “The drugs could quicken recovery after workouts, build stamina, add muscle. They could eliminate that slump in August, when the minor injuries and fatigue of the long season would otherwise wear a ballplayer down” (39). Combining his natural talent with unnatural substances soon gave Bonds foreshadowing into his prolific future.

When he reported to spring training for the 1999 season Bonds bulked up from 210 to 225 pounds. His teammates questioned his shocking transformation calling him “the incredible hulk,” but sports writers feared to broach the topic (Fainaru-Wada 72). Major League Baseball failed to care too as they rode baseball’s recent resurgence and disregarded testing their athletes for preforming enhancing drugs.

Consequently, Bond’s new edge was on full display throughout his first twelve games as he batted with a .366 average, four homeruns, six doubles, and 12 runs batted in. The new power abruptly came to a halt when as a result of steroid use, Bonds tore a triceps tendon, an injury which required surgery and kept him out of the game for seven weeks. He finished the 1999 season playing only 102 games and watched McGwire bat in 65 homeruns with growing frustration. Recognizing a need to adjust his drug use, Anderson switched Bonds off of Winstrol and started him on human growth hormone (HGH). Even though it is not a steroid, Fainaru-Wada points out its appeal, “Like a steroid,

6 Growth had a strong anabolic effect, and it could help the user increase muscle mass. But it was also thought to strengthen joints and connective tissues and thus was often cocktailed with Deca or other steroids” (75). At age 35 Bonds was supposed to feel his body in decline but instead he felted primed to establish himself as a prolific hitter and a catalyst to the MLB purity debate.

After the disappointing 1999 season Bonds returned in 2000 with a .306 batting average and totaled 49 homeruns. HGH aided Bonds in an undeniable improvement but he required an additional edge if he wanted to surpass McGwire.

Anderson found the edge for Bonds through Victor Conte’s company, The Bay Area Laboratory CoOperative, an organization which analyzed athletes blood and urine for mineral deficiencies. With BALCO Conte would prescribe his original supplement, ZMA to his clients to camouflage his real business of supplying cutting edge steroids.

Conte was ecstatic to work with Bonds, providing him with new drugs like Mexican beans, trenbolone, (a steroid to improve the muscle quality of beef cattle) and even insulin. Additionally, Bonds’ partnering with BALCO gave fans an excuse for his change in appearance as the world believed the natural ZMA supplement explained his growth. Yet, to his credit Bonds would work hard around steroids, dedicating five days of intense weight training, and eating six 350 calorie meals a day. Adding up hard work, hard drugs, and serious determination would result in a product Bonds’ himself couldn’t predict.

On October 6, 2001 Bonds hit homerun number 71, inaugurating himself as the all-time single season leading homerun hitter in Major League Baseball History. When he reached this milestone Bonds only became more addicted to steroids even against the urging of his dying father who became concerned with PED’s negative long term effects on Bond’s health. Disregarding advice from all except himself, Bonds continued to use and post unnatural results for a player at his advanced age. To highlight this fact, FainaruWada points out,

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Over the 13 seasons of his career, from 1986-1998, Bonds hit .290 and averaged 32 homeruns and 93 RBI. He hit one homerun at every 16 at-bats. But in the six seasons after he began using performanceenchanting-drugs – that is, from 1999 to 2004, between the ages of 34 and 40 – Bonds’ batting line averaged .328, 49, and 105. That represented 17 additional home runs and 12 additional RBI per year. He would hit a home run at every 8.4 at-bats.

(145) Prior to the 2003 fans of baseball rarely questioned Bond’s unnatural performance spike, yet when they learned of steroid use they treated Bonds as an enemy of purity.

The Sacred Becomes Profane The steroid scandal in Major League Baseball broke due to the determination of Special Agent Jeff Novitzky of the Internal Revenue Service’s Criminal Investigations Unit.

Digging through BALCO’s trash, Novitzky discovered disposed needles, pill bottles, and records which incriminated a wide variety of athletes. In September of 2003, a federal grand jury convened to investigate BALCO. Many athletes would be called to testify to their alleged steroid use, including Bonds who would later be convicted of perjury. The mastermind of BALCO Victor Conte, served four months in prison and another four on house arrest. When details of the grand jury emerged in 2005 Bonds would face criticism on the road. Instead of cheering when he hit his 706th homerun, fans booed, chanting “steroids” and “BALCO.” Capturing the collective pulse of baseball fans Christine Brennan, a USA Today sports columnist wrote, “How we wish he would do what was best for his game and leave the records of Babe Ruth and Hank Aaron intact” (qtd in FainaruWada 261). In this critique, Brennan identified the ultimate paradox, to save the game its greatest player would have to be exiled.

Before specifically examining Bonds’ role in pollution, the purity which he defiled needs to be established. In baseball, purity is best illustrated

7 through the ritual activity various elements of the game undergo to be made sacred. First, before players take the field for practice, the grounds crew preforms the rituals of consecration. This includes removing the tarpaulin, chalking the batter’s box, raking the pitcher’s mound, and sprinkling water on dirt to settle the dust. Without these consecration rituals Price contends that any team has the right to call foul and contest the validity of the game. In the game itself, Price identities the baseball to hold the most ritualistic significance. The ball enters the game through the umpire who inspects and rubs it with Delaware River mud to remove sheen and introduce it to the earth. Physically, Price points out that the ball is white with red stitching, representing purity and blood. During the game however, the ball transcends purity to become what Price establishes as, “The ball itself manifests the clear dualism of the game, consummately expressed in the conflict between the forces of creation (the pitcher delivering the pitch) and the forces of destruction (the batter swatting the ball)” (87). Evidently, the painstaking ritual processes enacted during the game not only affirms purity but also protects it from the profane forces of pollution.

Musing on steroids stain on baseball, Alex Tzelnic puts forward Mirca Eliade’s hypothesis, “However impure it may have become, the world is continually purified by the sanctity of sanctuaries” (“Baseball Mundi”). Tzelnic interprets Eliade’s statement and infers, “Perhaps this is what has been so upsetting about the steroid era in baseball-the tarnishing of our sanctuaries” (“Baseball Mundi”).

Due to the corruption of steroids, the ritual process of baseball has been disrupted and as a result one of places of worship is made ordinary. The vitality of maintaining ritual is made evident by Mary Douglas who writes, “Ritual recognizes the potency of disorder. In the disorder of the mind, in dreams, faints and frenzies, ritual expects to find powers and truths which cannot be reached by conscious effort” (117). In the disorder of steroids, baseball players discovered truths and power not attainable through their natural ability. If then the players who saved Major League Baseball by

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reaching outside their own talent are impure, the definition of impurity requires a reevaluation.

In Purity and Danger Douglas sets forth her definition of pollution as “...powers which inhere in the structure of ideas itself and which punish a symbolic breaking of that which should be joined or a joining of that which should be separate. It follows from this that pollution is a type of danger which is not likely to occur except where the lines of structure, cosmic or social, are clearly defined” (140). Should baseball be joined with steroids or should the two be separate? At the beginning of the steroid era, Major League Baseball did not test for PEDs and issued no opinion on them. Only in 2003 when the Major League Baseball clearly banned steroid use was pollution able to permeate the ritual space. Yet, even when they began enforcing in 2003 their tests were mocked because of their weak standards and minimal consequences. For this reason we can deduce that pollution always existed in the game until 2003, and the outlawing of PED’s made what was once pure a contamination.

Meanwhile, the fans where just as unknowing to the lack of cosmic structure in baseball and took their outrage on the only reasonable people, the athletes using steroids. Although most of the world condemns steroid abusers, in this light they are the scapegoat in a larger organization’s failure to provide a structure on which to evaluate and purge pollution.

From the initial founding in the 19th century, baseball has promoted fair play, religious rituals, and teamwork as its core values. Nevertheless, baseball has ignored the distinct facade concealing cheating in the game for nearly a century. The

8 transformation of the game during the steroid era was too obvious to ignore and became the spark for a powder keg of controversy. Left to reestablish their identity, Major League Baseball has created their definition of purity though steroid testing, thus allowing pollution to become apparent. The realization of purity and pollution as members of the same team came too late, as fans now have to isolate the two as bitter rivals locked in a future of discontent.

Works Cited Amidon, Stephen. Something Like the Gods. New York: Rodale, 2012. Print.

Arango, Tim. “Myth of Baseball’s Creation Endures, with a Prominent Fan.” The New York Times 12 November 2010: D1. Nytimes. Web. Douglas, Mary. Purity and Danger. New York: Routledge, 1966. Print.

Eliade, Mircea. The Sacred and Profane. New York: Harcourt, Brace and Company, 1959. Print.

FDCH E-Media. “Text of President Bush’s 2004 State of the Union Address.” The Washington Post 20 January 2004.

Washingtonpost. Web. Fainaru-Wada, Mark and Lance Williams. Game of Shadows.

New York: Penguin Group, 2006. Print.

Price, Joseph. Rounding the Bases. Macon: Mercer University Press, 2006. Print.

Tzelnic, Alex. “Baseball Mundi.” Killing the Buda.Web. 3 December 2013.

Dennis Ryan ('14, B.A., English) was the vice president of the Psi Upsilon Fraternity, as well as a member of the English Honors Society, Sigma Tau Delta. After graduation, Dennis has returned to Saint Francis University to study for a Masters Degree in Human Resource Management.

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Synthesis and Characterization of Azo Dyes Michelle Lipski Chemistry Department School of Sciences mxl105@francis.edu

Lauren M. McConnell Chemistry Department School of Sciences lemst6@francis.edu

Lauren E. Grabowski Chemistry Department School of Sciences legst5@francis.edu

Kristen N. Ritchey Biology Department School of Sciences knrst20@francis.edu

Michele R. Hargittai, Ph.D. Chemistry Department School of Sciences mhargittai@francis.edu

Balazs Hargittai, Ph.D. Chemistry Department School of Sciences bhargittai@francis.edu

Dyes are colored compounds that bind to fabric. For nearly five thousand years, human have been using dyes to create and improve aesthetically pleasing clothing and fabrics.1 The specific type of dyes in our experiments are azo dyes, discovered by a brewer, Peter Griess. In our research we synthesized a vast array of azo dyes, using diazonium salts, identified the color of each dye, focusing on the identities of the two organic components of the dyes, and looked at the indicator properties of the dyes – how well can they be used to differentiate between acidic and basic solutions by detecting a change in the color of the dye.

Introduction The earliest of dyes were often plant extracts and have since evolved to become synthetic compounds exhibiting a variety of colors. The versatile dyes are used in clothing, food, and pigments in paints, ink, and printing facilities.1 Our method for the synthesis of the various azo dyes mimics the creation of a large array of pharmaceutical compounds during the search for new drugs. With ongoing advancements being made daily in the scientific and medical fields, new pharmaceuticals are needed to keep up with everchanging technology. In order to design a drug with specific biological activities, chemists use a research technique known as combinatorial chemistry.2 It is the creation of a vast numbers of molecular substances that are tested for desired properties.2 As this popular technique has immense money- and time-saving properties, combinatorial

chemistry has expanded past pharmacology to catalysis and materials chemical research.3 Two methods commonly used in the combinatorial synthesis of a new molecular substance are the split synthesis method and the parallel synthesis method.2 In a split synthesis, a library of compounds is synthesized and tested in combinations of the compounds. In a parallel synthesis, each compound is prepared and tested individually. Both are effective in allowing for the researcher to draw conclusions regarding the structure and function of the molecules.3 In this experiment we used the parallel synthesis method to synthesize azo dyes – compounds comprised of two aromatic derivatives joined by a nitrogen-nitrogen double bond.

Depending of the diazonium salt that is coupled with an aromatic derivative, each dye exhibits a specific color and has unique chemical properties.

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10

The general structure of an azo dye is depicted in Figure 1 where Q and R are representative of any functional group and Y is representative of an electron-withdrawing group.

Y N N R Q

Figure 1. General structure of azo dyes.

The first of the two steps needed to synthesize nearly all azo dyes is called diazotization, which involves adding nitrous acid to an aromatic amine in order to obtain its respective diazonium salt (Figure 2).1 NH2

N HNO2 H2SO4

Q

N HSO4

Q

Figure 2. Formation of diazonium salts.

The salt is then coupled with a highly electronrich aromatic derivative to yield an azo dye (Figure 3).1 In a number of our studies the electron withdrawing group was a hydroxyl group, thus these reactions were run with phenol derivatives (Y = OH).

N

N HSO4

Y

Q N

+

N

Q Y

R

Figure 3. Diazonium coupling.

R

Materials and Methods All chemicals and materials were purchased from Sigma-Aldrich (Milwaukee, Wisconsin) Miniscale diazotization of the aromatic amine1 10 mmol of the desired aniline derivative was dissolved in 8 mL of 3 M hydrochloric acid (HCl) in a 125-mL Erlenmeyer flask. The solution was heating gently over a hot plate, and if needed, up to 10 mL of deionized (DI) water was added to the solution to ensure the solid was fully dissolved.

After dissolving the solid, the solution was simultaneously stirred with stir bar and cooled over an ice bath to roughly 5 째C. In a few cases, some solid precipitated out of solution; however, no experimental complications were met.

While stirring, 10 mL of newly-prepared 1 M sodium nitrite (HNO2) solution was slowly added via Pasteur pipet. The addition rate of the sodium nitrite was adjusted to ensure the reaction temperature did not exceed 10 째C. The solution was tested with starch-iodide paper to verify that enough 1 M sodium nitrite solution had been added.

If needed, a few more drops of sodium nitrite solution was added to ensure that the oxidizing agent was in excess. As diazonium salts are highly explosive, the solution was not allowed to dry and was kept on an ice bath as the coupling agent was prepared.

Miniscale coupling of a phenol derivative1 10 mmol of the desired phenol derivative was dissolved or suspended in 20 mL of 1 M sodium hydroxide (NaOH) solution in a 250 mL Erlenmeyer flask. While stirring and cooling the solution of the phenol derivative in an ice bath, the diazonium salt was slowly added. The solution was allowed to stand in the ice bath for at least 15 minutes until all the product has crystallized out of solution. If necessary, to induce crystallization, the pH of the solution was adjusted by added drops of dilute HCl or NaOH. The dye was collected via vacuum filtration as the crystals were washed with cold distilled water (DI H2O). About a week was given for the dyes to completely air dry before characterization.

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Characterization The various azo dyes were characterized by Ultraviolet-Visible Spectroscopy (UV-Vis) and their pH indicator range was determined using 0.1 M HCl and 0.1 M NaOH solutions. In preparation for the UV-Vis spectroscopy, roughly 5 mg of dye was dissolved in 10 mL of 95% ethanol/water. The UV-Vis spectrum was recorded from 800-350 nm and the λmax(s) was/were found for each. To determine the pH indicator range of the dye, ~5 drops of ethanol-dye solution were added to three test tubes and dissolved in 10 mL of H2O. The first, neutral, test tube was recorded for appearance of color and clarity and the pH of the solution was determined. To the second test tube 0.1 M HCl solution was added drop-wise until a color change occurred. Color, clarity, and pH of the solution were recorded. To the final test tube 0.1 M solution NaOH was added drop-wise until a color change occurred. Color, clarity, and pH of the solution were recorded.1 Results and Discussion The color of the ethanol solutions, the UV-Vis characterization results and the pH and color for the neutral, acidic and basic solutions are found in Tables 1 – 11 (“no ” means no change in the color of the solution upon addition of 0.1 M HCl or 0.1 M NaOH solution, respectively). Combinations of aniline derivatives (A – K) and coupling agents (1 – 20) where the amount of dyes formed was not sufficient for further characterizations are not included in the tables.

Each azo dye was unique to the aniline derivative (Figure 4) that formed the diazonium salts in the first step and to the coupling agents with the electron withdrawing groups (Figure 5). Some dyes proved to be excellent indicators of pH; drastic color changes were seen as drops of dilute HCl and NaOH solutions were added to each – this was especially true for basic solutions. For example, dyes with p-nitroaniline and p-anisidine as their aniline derivative were very good indicators of basic pH, while their ability to indicate an acidic environment was minimal.

11 The polarity of the dyes was also dependent on their aniline derivative. Dyes synthesized from aniline, m-nitroaniline, 1-naphthlyamine, or naphthlyamine behaved quite differently in water when compared to other dyes. As most of the dyes were clear in solution with ethanol and water, these dyes were extremely cloudy and sometimes even chunky in texture.

While most dyes were usually orange, red, or yellow in color – even when tested with acid and base – some produced beautiful, deep colors. For example, the dye synthesized from sulfanilamide (D) and N,N-dimethylaniline (20) was bright orange-yellow in a neutral solution, but extremely vibrant pink when 0.1 M HCl solution was added.

Works Cited 1. Schoffstall, A.M.; Gaddis, B.A.; Druelinger, M.L. Microscale and Miniscale Organic Chemistry Laboratory Experiments, McGraw Hill, 2nd Ed., 2004, New York, NY, pp. 450-456.

2. Furka, A.; Sebestyen, F.; Asgedom, M.; Dibo, G. “General method for rapid synthesis of multicomponent peptide mixtures.” Int. J. Peptide Protein Res. 1991, 37, 487-493.

3. Smith, J.G. Organic Chemistry, McGraw Hill, 4th Ed., 2014, New York, NY, pp. 2010-2031.

Michelle Lipski (‘16) is a Chemistry major. She plans to earn a Doctor of Pharmacy degree following graduation. She is a member of the Atlantic 10 Saint Francis University Women’s Field Hockey Team.

Lauren McConnell ('12, B.S., Chemistry) was the founding president of the Rho Nu chapter of Gamma Sigma Epsilon: National Chemistry Honor Society.

She plans to become a Physician Assistant.

Lauren Grabowski (’12, B.S., Chemistry) is a doctoral student in the Chemistry program at the University of South Carolina.

Kristen Ritchey (’11, B.S., Biology) is a student of Veterinary Medicine at the Ohio State University.

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A

12

B

C

NH2

D

E

NH2

NH2

F

NH2

NH2

NH2

O O2N

H3CO

p-Anisidine

p-Nitroaniline

H

G

S

H2N

m-Toluidine

Aniline

Sulfanilamide

NH2

K

NH2

NH2

Sulfanilic acid

J

NH2

I

HO3S O

NH2

NO2

H2 N

NO2

o-Nitroaniline

m-Nitroaniline

-Naphthylamine

-Naphthylamine

Benzidine

Figure 4. Aniline derivatives used in study.

1

2

3

OH

4

OH

5

OH

OH

O

NO2 OH

O2N

OH

OH

NO2

Resorcinol

4-Nitrophenol

Phenol

6

7

2,4-Dinitro-1-naphthol

8

9

O

OH

N H

HO

p-Hydroxybenzoic acid

4-Methoxyphenol 11

12 O

OH

NH

HO

4-Acetamidophenol 13

HO3S

Adrenaline 14

O

5-Sulfosalicylic acid

O OH

OH

NO2

3,5-Dinitrosalicylic acid 17

3-Nitrosalicylic acid 18

OH

OH

4-Nitrosalicylic acid

Phenyl salicylate 20

O

OH

Figure 5. Coupling agents used in study

OH

19 O NH2

2-Naphthol

O2N

NO2

Salicylaldehyde

OH

1-Naphthol

O

H OH

16

15

O

O

OH

OH OH

OH

O2N

O

HO

OH H3CO

10 OH

OH

O

Salicylic acid

Salicylamide

O Na

N

OH

Sodium salicylate

N,N-Dimethylaniline

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13 Ethanol solution color

λmax (nm)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol

red-orange

440

phenol p-nitrophenol 2,4-dinitro-1-naphthol

faint blood red navel orange lemon yellow

488 486 431

light yellow

2: no Δ

12: bright purple

light orange orange lemon yellow

1-2: light yellow 3-4: light yellow 3: faint yellow

13: light red 13-14: deep red 11: navel orange

salicylic acid p-methoxyphenol

light yellow, slightly cloudy peach-orange

< 400 448

bright yellow light peach

1-2: pale yellow, cloudy 2: no Δ

14: blood red, clear 13-14: bright purple

p-hydroxybenzoic acid

faint yellow

4-acetamidophenol

peach-orange

< 400

light yellow

2: no Δ

14: fuchsia

447

peach-orange

3: no Δ

14: faint red-purple

adrenaline sulfosalicylic acid 3,5-dinitrosalicylic acid

yellow-orange neon yellow-green light yellow

< 400 402 < 400

light yellow-orange bright yellow-green bright yellow

2: no Δ 3: no Δ 3: no Δ

14: orange, purple hue 12: fuchsia 13: orange

salicylaldehyde 3-nitrosalicylic acid

light orange light yellow

465 401

yellow-orange neon yellow

2: faint yellow 3-4: no Δ

14: red-orange 13-14: blood red

5-nitrosalicylaldehyde phenylsalicylate

orange-yellow deep yellow-orange

411 410

light orange-yellow yellow-orange

2: no Δ 2: light yellow, cloudy

14: red-orange 14: red-pink

1-naphthol

faint orange-red

458

light red

1: no Δ

10: very deep purple

2-naphthol

light brown-red

475

light brown-red

1: light red

14: light green, brown hue

salicylamide sodium salicylate N,N-dimethylaniline

red-orange light yellow yellow-orange

417, 484 410 475

navel orange neon yellow deep yellow-orange

2-3: lemon yellow 1: pale yellow, cloudy 2: faint rose pink

9-10: red-orange 13: blood red 14: no Δ

Coupling agent

Initial Water Solution color (pH = 7)

Table 1. p-Nitroaniline (A) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol phenol p-nitrophenol 2,4-dinitro-1-naphthol salicylic acid p-methoxyphenol

yellow-orange yellow-orange neon yellow, green hue neon yellow light yellow-orange bright lemon yellow

382, 412 389 425 394, 434 391 438

bright yellow-orange bright yellow-orange neon yellow lemon yellow bright yellow-orange bright yellow-orange

3-4: no Δ 2: no Δ 2-3: off white, clear 1: faint yellow, cloudy 3: yellow, cloudy 1: bright orange-yellow

13: navel orange 11-12: true orange 9-10: neon yellow 13: no Δ 10-11: no Δ 12: blood red

4-acetamidophenol 3,5-dinitrosalicylic acid 5-nitrosalicylaldehyde

light yellow, brown hue light yellow-orange light yellow-orange

397 388 407

deep orange faint yellow-orange bright yellow-orange

1-2: darker orange 1-2: light orange 1: light peach

12: brick red 11-12: bright orange 13-14: no Δ

1-naphthol

light orange-red

407

deep brick red

2: brown-purple

13: blood red

2-naphthol

light orange-red

459, 521

fruit punch red

2-3: no Δ

14: no Δ

salicylamide sodium salicylate N,N-dimethylaniline

light orange faint yellow faint yellow

378 388 408

bright yellow-orange lime yellow lemon yellow

2: light peach 1: faint yellow, cloudy 2: fuchsia, purple hue

9-10: no Δ 14: bright yellow-orange 14: no Δ

Table 2. p-Anisidine (B) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol phenol 2,4-dinitro-1-naphthol

pale yellow bright yellow bright yellow-orange

413 432 393, 439

light yellow-orange bright yellow, green hue bright orange-yellow

2: no Δ 2-3: light peach 1: light peach, yellow hue

14: dark orange-yellow 13-14: dark orange-yellow 14: no Δ

salicylic acid 4-acetamidophenol salicylaldehyde 3-nitrosalicylic acid 5-nitrosalicylaldehyde 1-naphthol 2-naphthol salicylamide

pale lemon yellow bright yellow-orange light yellow light lemon yellow orange-yellow red-orange orange-yellow, red hue yellow-orange

381 430 373 390 414 410, 484 489 423

faint lemon yellow dark orange, brown hue pale lemon yellow bright yellow-orange bright yellow-orange dark cherry red red-orange bright yellow-orange

2-3: no Δ 2: same color, cloudy 2-3: faint yellow 1: no Δ 2: orange-peach 2: red, cloudy 1: navel orange,cloudy 2: no Δ

13: dark yellow-orange 12: cherry red 12-13: bright yellow 13-14: dark orange-red 14: dark orange-yellow 13: blood red 14: no Δ 13: red-orange, clear

N,N-dimethylaniline

yellow-orange, cloudy

418

yellow-orange, cloudy

1: bright red-pink,cloudy

14: yellow, cloudy

Table 3. m-Toluidine (C) dyes synthesized.

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14 Ethanol solution color

λmax (nm)

resorcinol

light yellow

421

phenol 2,4-dinitro-1-naphthol salicylic acid

neon orange neon yellow light yellow

478 441 384

p-methoxyphenol p-hydroxybenzoic acid

bright orange bright orange-yellow

472 382, 456

bright orange bright yellow-orange

4-acetamidophenol

bright orange-yellow

434

yellow-orange

2: no Δ

14: cherry red

sulfosalicylic acid

very light yellow

381

very light yellow

2: light yellow, cloudy

13: bright orange-yellow

3,5-dinitrosalicylic acid salicylaldehyde 3-nitrosalicylic acid

light orange-yellow neon yellow light lemon yellow

409 447 394

light orange-yellow neon yellow light lemon yellow

2-3: no Δ 2-3: light yellow 2-3: no Δ

14: deep dark yellow 11-12: no Δ 14: deep dark yellow

5-nitrosalicylaldehyde phenylsalicylate

bright yellow-orange bright yellow-orange

421 411

bright yellow-orange light yellow, cloudy

1-2: light peach 2: no Δ

14: dark orange 14: bright orange, clear

1-naphthol 2-naphthol

orange-red bright navel orange

471 482

deep cherry red bright navel orange

1: deep orange 2: no Δ

13: dark red-purple 14: dark red-orange 14: dark yellow-orange

Coupling agent

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

light yellow

3-4: no Δ

14: light rose pink

neon orange neon yellow light yellow

1: neon yellow 1: light yellow, cloudy 1-2: no Δ

14: no Δ 14: no Δ 13: deep orange

2: dark orange 1-2: no Δ

13-14: deep cherry red 13-14: purple, red hue

salicylamide

neon yellow, orange hue

424

bright yellow-orange

1-2: light yellow

sodium salicylate

bright yellow-orange

427

bright yellow-orange

1: light yellow

13: bright red-orange

N,N-dimethylaniline

bright yellow-orange

467

true orange

2: bright red-pink

11-12: dark orange-yellow

Table 4. Sulfanilamide (D) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol phenol

bright yellow-orange bright yellow-orange

429 417

orange-yellow orange-yellow

1: no Δ 2: no Δ

14: red-orange 14: red-orange

p-nitrophenol 2,4-dinitro-1-naphthol salicylic acid p-hydroxybenzoic acid 4-acetamidophenol sulfosalicylic acid

bright yellow-orange neon yellow neon yellow light orange, brown hue neon yellow nearly clear, yellow hue

431 467 383, 483 400, 724 424 381, 563, 723

bright yellow-orange neon yellow neon yellow light orange, brown hue bright yellow-orange off-white, clear

1-2: light orange peach 1: light yellow, cloudy 2-3: no Δ 2: light peach 2-3: no Δ 3-4: no Δ

11-12: dark yellow-orange 14: no Δ 10-11: red-orange 14: dark orange 12-13: blood red 14: light yellow

3,5-dinitrosalicylic acid salicylaldehyde phenylsalicylate

very light yellow bright yellow-orange dark orange-yellow

409, 565, 724 398, 446, 558, 730

420, 556, 726

very light yellow bright yellow yellow-orange, cloudy

2: no Δ 1: no Δ 2: no Δ

14: neon yellow 13-14: bright yellow 14: dark orange

1-naphthol

cherry red, orange hue

520, 725

deep red-orange

2: no Δ

12: deep black-purple

2-naphthol

dark red-orange

506, 725

deep red-orange

2-3: no Δ

10-11: deep black-red

salicylamide N,N-dimethylaniline

light yellow peach, orange hue

396, 445, 570, 726

yellow-orange light peach

2: neon yellow 3: bright baby pink

13: dark yellow 14: no Δ

413, 558, 732

Table 5. Sulfanilic acid (E) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol phenol p-nitrophenol 2,4-dinitro-1-naphthol

orange red true orange neon yellow neon yellow

469, 723 481, 724 454, 564, 733 460, 559, 723

red-orange yellow-orange neon yellow bright yellow-orange

3-4: bright orange, cloudy 1-2: yellow-orange, cloudy 1-2: very light peach 1-2: light yellow, cloudy

10-11: dark orange 9-10: red-orange 11-12: light orange-yellow 11-12: light orange-yellow

salicylic acid 4-acetamidophenol 3,5-dinitrosalicylic acid salicylaldehyde 1-naphthol

lemon yellow orange, red hue dark orange bright orange dark brown red

400, 561, 725 420, 557, 723 413, 565, 723 470, 728 506, 726

lemon yellow dark orange, cloudy orange, brown hue yellow-orange, cloudy dark brown-red

2: yellow-orange, cloudy 2: dark orange, cloudy 1: no Δ 1: light yellow, cloudy 2: brown-red, cloudy

13: bright navel orange 13: dark red-orange 14: very dark red-brown 11: bright orange 13: deep cherry red

Table 6. Aniline (F) dyes synthesized.

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15

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol

orange-yellow

484

bright orange-yellow

1-2: orange, cloudy

10-11: blood red

phenol p-nitrophenol

red-orange bright orange

490 447

neon orange, opaque bright orange-yellow

1: neon yellow, cloudy 1-2: light yellow, cloudy

9-10: deep red-orange 11-12: burnt orange

2,4-dinitro-1-naphthol salicylic acid p-methoxyphenol

bright yellow-orange orange, peach hue orange, peach hue

471, 563, 724 470, 719 471, 724

neon yellow, orange hue orange-peach orange-peach

1: light yellow, cloudy 1-2: orange-peach, cloudy 1: no Δ

12+: burnt orange 12+: deep purple-red 12+: deep purple

p-hydroxybenzoic acid 4-acetamidophenol

yellow-peach burnt orange

405, 556, 723 483, 720

bright yellow burnt orange

1: yellow-peach, cloudy 1: bright orange, cloudy

12+: dark burnt orange 12: deep black-red

3,5-dinitrosalicylic acid

light yellow

410, 558, 725

light yellow

3-4: no Δ

12: bright yellow-orange

salicylaldehyde phenylsalicylate

bright orange deep red-orange

456, 558, 724 489, 722

neon yellow light yellow-orange

1-2: light yellow, opaque 1: no Δ

11-12: dark yellow-orange 11: deep red

1-naphthol 2-naphthol

brown-red bright orange

458, 565, 617, 727

480, 557, 722

bright red bright orange-pink

1-2: brown-orange, cloudy 1: orange-pink, opaque

12+: purple-red 12+: red-orange

salicylamide

bright red-orange

491, 731

bright orange-yellow

2: bright yellow

12: red-orange

sodium salicylate

bright orange

427, 568, 744

bright orange-yellow

2-3: neon yellow, opaque

9-10: red-orange

Table 7. m-Nitroaniline (G) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol p-nitrophenol

bright yellow-orange bright orange

459, 563, 726 438, 728

bright orange-yellow bright orange

1-2: no Δ 2: bright orange, cloudy

11: burnt orange 13: blood red

p-methoxyphenol 4-acetamidophenol 3,5-dinitrosalicylic acid salicylaldehyde 1-naphthol

red-orange dark burnt-orange bright yellow neon yellow burnt orange-red

458, 738 390, 480, 739 421, 558, 725 439, 563, 747 447, 725

brown-red, cloudy brown, cloudy bright yellow neon yellow burnt orange, red hue

2-3: no Δ 1: no Δ 2-3: no Δ 1-2: neon yellow, cloudy 2-3: light burnt orange

12-13: deep red-purple 13-14: deep blood-red 12: bright yellow-orange 14: orange-yellow 14: brick red

2-naphthol

bright orange

407, 492, 741

orange-pink

1: no Δ

14: orange-brown

Table 8. o-Nitroaniline (H) dyes synthesized.

Coupling agent

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

resorcinol p-nitrophenol salicylic acid

bright orange-red red-brown burnt orange

519, 737 439, 498, 723 446, 473, 729

red-orange red-brown, cloudy brown, cloudy

2-3: dark red, cloudy 2-3: red with purple hue 3-4: pale orange, cloudy

13-14: cherry red, cloudy 10-11: no Δ 14: red-orange

p-methoxyphenol p-hydroxybenzoic acid

brown-orange red-brown

505, 727 488, 721

brown-orange, cloudy brown-red,cloudy

2: no Δ 1-2: no Δ

13: deep red-purple 14: no Δ

4-acetamidophenol sulfosalicylic acid 3,5-dinitrosalicylic acid salicylaldehyde phenylsalicylate 1-naphthol 2-naphthol salicylamide

brown-orange dark purple brown burnt orange dark orange red-orange magenta red orange-brown

493, 723 428, 531, 728

440, 556, 722 414, 474, 779

brown-orange, cloudy blue-periwinkle, cloudy dark brown-purple burnt orange, cloudy burnt orange, cloudy dark purple-brown, cloudy magenta-red burnt orange

3-4: pale orange, cloudy 1: no Δ 1: no Δ 1-2: no Δ 2: no Δ 3-4: no Δ 1: magenta-purple 2-3: orange-brown

13: cherry red 14: dark brown 12: dark brown-orange 12-13: brown-orange 13: red-orange, cloudy 14: very deep purple-red 13-14: magenta-brown 10-11: dark orange-red

sodium salicylate

brick red

438, 491, 738

brick red

2-3: purple-brown, cloudy

12-13: no Δ

407, 441, 476, 730

469, 721 429, 469, 723 412, 464, 558, 740

Table 9. -Naphthylamine (I) dyes synthesized.

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16

Ethanol solution color

λmax (nm)

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

resorcinol

tangerine orange

472, 751

tangerine orange, cloudy

3-4: no Δ

11-12: red-orange, clear

phenol p-nitrophenol

bright orange-red brown-orange

490, 747 413, 479, 723

strawberry red, cloudy brown-red, cloudy

1-2: no Δ 1-2: no Δ

9-10: blood orange, cloudy 11-12: dark brown-orange

p-methoxyphenol p-hydroxybenzoic acid 4-acetamidophenol

extremely light peach orange-brown bright orange

420, 565, 620, 739

410, 482, 732 412, 487, 734

very light peach brown-brick red, cloudy red-orange, cloudy

1: no Δ 3-4: no Δ 1-2: no Δ

12-13: no Δ 12: no Δ 13: blood red

sulfosalicylic acid 3,5-dinitrosalicylic acid

bright red burnt orange

393, 508, 745 419, 437, 486

bright red, cloudy brown-purple, cloudy

1: no Δ 2-3: no Δ

14: bright orange, cloudy 13-14: coffee brown

Coupling agent

0.1 M NaOH pH: color

salicylaldehyde

light brown-orange

398, 556, 746

light brown, cloudy

2-3: no Δ

10-11: burnt orange

phenylsalicylate 1-naphthol

burnt orange red-orange

414, 478, 725 391, 493, 723

light orange, cloudy red-brown

2: dark orange,cloudy 1: red-brown, cloudy

13-14: burnt orange 12: cherry red

2-naphthol salicylamide

bright red, orange hue brown-orange

437, 509, 539, 719

398, 472, 741

brick red,cloudy burnt orange, cloudy

1-2: no Δ 2: no Δ

13-14: no Δ 13: dark burnt orange

sodium salicylate

dark orange, brown hue

399, 445, 477, 744

brown-orange, cloudy

1: brown-purple, cloudy

10-11: orange-brown

Initial Water Solution color (pH = 7)

0.1 M HCl pH: color

0.1 M NaOH pH: color

3-4: light peach 1-2: light brown-orange 2-3: very light peach

13: blood red 13-14: bright orange-red 9-10: no Δ

1-2: light yellow

12-13: bright orange

Table 10. -Naphthylamine (J) dyes synthesized.

Coupling agent

Ethanol solution color

resorcinol phenol p-nitrophenol

bright orange-yellow bright orange-yellow bright yellow

398, 446, 729 432, 566, 725

dark orange dark orange, brown hue bright yellow

salicylic acid

bright yellow

422, 566, 722

bright orange-yellow

Table 11. Benzidine (K) dyes synthesized.

λmax (nm) 457, 556, 730

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17

A Study of the Risk Factors of Degenerative Joint Disease of the Knee leading to Total Joint Arthroplasty and their Influence on Therapeutic Outcomes Stephen D. Kowalski Physical Therapy Department School of Health Sciences

Stephen M. LoRusso, Ph.D. Physical Therapy Department School of Health Sciences slorusso@francis.edu

The purpose of this study is to determine the influence of risk factors on total knee replacement (TKR) treatment outcomes, duration and recovery. Our method involved the random selection review of 15 anonymous female patients aged 57-85 who had TKR in the last 5 years. To meet HIPAA provisions the data was collected by a third party employee at an outpatient Physical Therapy Clinic. The data was analyzed using two-sample t-tests, paired t-tests, and correlation statistical analysis. Paired t-tests revealed statistically significant findings in comparing pre- to post-treatment active ROM in extension (p=0.001) and flexion (p=0); pre- to post-treatment passive ROM in extension (p=0.001) and flexion (p=0). Additionally significant (all p<0.05) positive correlations were identified between BMI and treatment duration (r=0.818), pre-treatment active and passive ROM in extension (r=0.952) and flexion (r=0.954), post-treatment active and passive ROM in extension (r=0.960) and flexion (r=0.926), and preand post-treatment active ROM in extension (r=0.553). Significant negative (all p<0.05) correlations were found between the incidence of past-knee trauma and treatment duration (r=-0.508); Session number and active and passive post flexion (-0.668; -0.618) and extension ROM (-0.556; -0.556;). No relationships were found to exist between age and number of sessions, and no correlations were found between smoking and any outcome measure. Our conclusion was that following TKR surgery current methods of physical therapy treatment are effective in restoring range of motion. Additionally, as hypothesized, BMI’ extends treatment duration while smoking history, and age do not appear to directly impact extent and/or duration of recovery. The negative correlations with session number and ROM suggests a point of diminishing returns with therapy sessions once a treatment goal is achieved. The influence of past-knee trauma is not understood without knowledge of those injuries and outcomes.

Introduction and Purpose Osteoarthritis, also referred to as Degenerative Joint Disease, is widely accepted as the most common condition affecting weight bearing joints of the lower extremity. Approximately one-third of all individuals over the age of 65 show some radiological indication of it, characterized by a visible narrowing of the affected joint margins on a standard radiograph. As this joint space narrowing may compromise the integrity of the joint’s functioning components, this type of condition can be seriously debilitating for affected patients due to resulting muscle and joint pain/weakness, loss of

mobility, and deformity eventually leading to overall functional disability. Because of the importance of lower extremity function and strength during conventional activities of daily living (ADLs), especially for the elderly, Osteoarthritis is a condition that must be adequately addressed to preserve or restore a patient’s functional capacity.[6,9] Osteoarthritis is believed to originate in the cartilage of the affected joint, impacting the mechanics of the underlying bones, soft tissue, and synovial fluid associated with the area. It can be classified as being either primary, having an

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unknown cause and insidious onset, or secondary, being associated with trauma, infection, hemarthrosis, osteonecrosis, and/or another condition.[2] As previous research has put an emphasis on the articular cartilage of the joint alone being the focus of responsibility for recalcitrance in Osteoarthritis, recent evidence indicates that the issue is caused by a combination of factors influencing multiple joint components. As osteoarthritis progresses specifically in the knee, patients will experience pain and lose joint function as a result of cartilage degeneration, diminished bone density caused by an aberrant bone repair process, a weakened joint capsule construct, synovial inflammation, and potentially the additional structural involvement of the menisci, surrounding ligaments, and/or tendons. These structural degenerations in knee joint components are facilitated by the over-production and release of specific proteins and cytokines, and the rate of release of these is dependent on the presence of etiologic and risk factors for Osteoarthritis.[9] As with most conditions, there are certain etiologic and risk factors that are associated with an increased risk in developing Osteoarthritis. These factors deal with multiple areas of a personâ&#x20AC;&#x2122;s bodily composition, including biomechanics, dealing with the forces through a joint and the strength of the surrounding soft tissue to accommodate these forces, and biochemistry, referring to genetics as numerous studies have defined the roles of Interleukin-1 beta receptor variations, singlenucleotide polymorphisms, Interleukin-6 abnormalities, and SMAD3 anomalies among other genetic irregularities in determining prevalence and severity of knee Osteoarthritis[1,2,3,5]. Weight control and obesity have been identified as significant in the prevalence and severity of knee Osteoarthritis[4]. It is accepted that traumatic injury to a joint combined with a genetic predisposition to the condition account for roughly half of the existing cases of Osteoarthritis, with many of these injuries arising from strenuous athletic (football, hockey, etc.) or occupational (repetitive stooping, squatting, twisting, kneeling) activities.[7,22] After the initial injury is sustained, these risk factors may

18 accelerate the degenerative process by either loading the joint with excess weight, promoting an abnormal functional interaction of joint parts, or decreasing the supportive capacity in bone density or muscle strength of the joint. Although there are additional syndromes and conditions that further accelerate this degenerative joint process, they function in one or more of the three previously mentioned processes.[11,19-21] As the effects of these etiologic and risk factors on the development and progression of Osteoarthritis over time have been studied expansively and have become well understood, the impact of the presence of these risk factors during therapy following a joint replacement surgery have not been. It is the goal of this study to determine a relationship, if any, between particular risk factors for Osteoarthritis in the knee and both the extent of recovery compared to normal and the duration of treatment required for it following a total joint replacement operation.

Methods In this study, the risk factors identified for review were the effects of weight and height, i.e., Body Mass Index (BMI), past knee trauma, smoking, and age. A random chart review of 15 patient total knee replacement cases from an outpatient physical therapy clinic was performed to obtain information regarding the presence of these risk factors as well as the length of time and number of Physical Therapy visits as our outcome measure. The success of the rehabilitative process of each patient was measured by the improvement in functional range of motion in the affected knee; although normal knee motion is considered 135 degrees flexion and 0 degrees extension for healthy individuals, the target values for knee flexion and extension range of motion in the physical therapy clinic for total knee replacement cases are 120 and 0 degrees, respectively, and so the success of each patient was measured by the time it took them to reach these values, if in fact they were reached.[15] From the physical therapy clinic, 15 random patient cases in which the patient had undergone a total knee replacement surgery were selected from

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the last five years using an online documenter archive. From these cases, the patient’s age, height, weight, smoking history, incidence of past knee trauma, and pre-rehabilitation range of motion values were taken from the record of the initial evaluation, while the patient’s post-rehabilitation range of motion values, total number of physical therapy visits, and episode of care duration (initial evaluation and discharge dates) were taken from the discharge summary. A third party employee at the physical therapy clinic performed the random chart review selection process to ensure that all patient privacy rights were upheld as per the Health Insurance Portability and Accountability Act (HIPAA). The results of this chart review were then statistically evaluated to determine possible correlations between the risk factors and posttreatment range of motion values and number of physical therapy visits required for each patient.

Statistical analysis included ‘two-sample t-tests’, ‘paired t-tests’, and ‘correlation tests’.

Results and Discussion General Data Limitations in range of motion are different from patient to patient and can be caused by any number of factors, ranging from disuse and physical inactivity to traumatic injury.

Functionally, a range of motion value below the average for a particular movement leaves the patient at a disadvantage for performing activities that incorporate that action. In post-surgical treatment for a total knee replacement, therapists are greatly concerned with the patient’s ability to both actively (patient performed) and passively (therapist performed) flex (bend) and extend (straighten) the knee because these motions are vital to the ability to walk normally. Even with limited range of motion, patients can still adapt to walk either with an apparent limp, excessive rotation of the hip to thrust the leg forward, or other compensations, but these adaptations often lead to additional injury, underlining the importance for a complete recovery of motion without compensations from other muscle groups.

19 Statistically, positive correlations were found between pre-treatment active and passive extension (r=0.952, p=0.0) and flexion (r=0.954, p=0.0) and post-treatment active and passive extension (r=0.960, p=0.0) and flexion (r=0.926, p=0.0). This relationship indicates that limitations in active range of motion in both flexion and extension are limitations in passive range of motion as well, meaning that the greater the restriction in active range the greater the restriction will be in passive range. Furthermore, a negative correlation was discovered between number of physical therapy sessions and post-treatment active extension (r=-0.556, p=0.031) and flexion (r=-0.668, p=0.006) and post-treatment passive extension (r=-0.556, p=0.031) and flexion (r=-0.618, p=0.014), suggesting that physical therapy treatment yields diminishing returns in recovered range of motion as treatment duration increases.

Finally, paired t-testing revealed statistically significant findings in comparing pre- and posttreatment active extension (t=-4.38, p=0.001) and flexion (t=-6.84, p=0) and pre- and post-treatment passive extension (t=-4.22, p=0.001) and flexion (t=-9.46, p=0), indicating that on average, all patients showed improvements in both active and passive extension and flexion during physical therapy treatment.

Body Mass Index (BMI) The body mass index measurement is used to assess a person’s overall body composition and is calculated by dividing the patient’s weight in kilograms by their height in meters squared.

Although this measurement does not take into account the actual body composition of a person, that is whether the bulk of their weight is predominantly comprised of fat or muscle, it does provide an accurate assessment of how much weight is placed on the knee joint. The classification categories for body mass index range from underweight (body mass index less than 18.5 kgm2) to obesity class III (body mass index great than 40 kgm2), with the normal (18.5 – 24.5), overweight (25-29.5), and obesity class I (30-35) and II (35-40) designations in between.

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Conventionally, the body mass index measure is used as a cursory screening tool to determine an individual’s level of risk for developing cardiovascular related health problems, but for the purposes of this study, it can also yield an accurate, baseline assessment of the weight/height relationship of each patient allowing direct comparison of each individual patient case to another.[12,13] Therefore, it can be determined that a patient in the study with a higher body mass index value than another patient has a greater force of weight put through the knee joint during weight bearing activities.

Statistically, a positive correlation (r=0.818, p=0.0) was found between a patient’s body mass index measurement and the number of sessions required to achieve the range of motion goals for total knee replacement therapy, indicating that as the body mass index increases, so does the number of session required for complete rehabilitation. Figure 1 below depicts this correlation well as the fluctuations in the blue line (body mass index) are closely mimicked by the changes in the red line (number of physical therapy sessions). Similarly, Figure 2 reveals the linear

Figure 1. BMI index of study participants and the number of Physical Therapy sessions they attended.

Figure 2. Number of Physical Therapy sessions as function of BMI.

20 relationship between these variables. This correlation likely suggests that the ‘wear and tear’ damage associated with knee osteoarthritis leading to a total knee replacement operation is magnified by the amount of weight that the joint must constantly support during weight bearing activities.[16] Understandably, a knee that must support an increased weight may be more damaged than a knee with significantly reduced weight bearing responsibilities, and therefore may take a greater time in repairing the functionality and synergy of its components following surgery.

Additionally, trends in the collected data suggest that a relationship may exist on some level between body mass index and the amount of active extension and flexion range of motion that is recovered. As these are only trends and as the data did not clearly show statistical significance in this area, it cannot be stated with assurance that a definite relationship exists here.

Prior Knee-Trauma Statistically, a negative correlation (r=-0.508, p=0.053) was discovered between a prior incidence of knee trauma or injury and number of physical therapy visits. In other words, the rehabilitation process took less time in number of physical therapy visits on average for patients that indicated that they had suffered previous knee injury. Since the specific injury or number of injuries that were sustained by each patient was not available, the only relationship that can be determined form this information is that past knee injury leads to a reduced rehabilitation timeframe. This relationship may be based on any number of factors, including that past treatment could have helped to strengthen parts of the joint that undergo healing following a total knee replacement, or that prior exposure to physical therapy intervention may have a positive influence on future physical therapy interventions.

Nevertheless, it is unclear how behaviors related to past-knee trauma impact treatment duration because it was not possible to evaluate these from the patient histories that were provided.

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Smoking The adverse effects of smoking over a long period of time have been well researched and documented within the last 15 years.

In the case of a total knee replacement, an increased demand is placed on the bodyâ&#x20AC;&#x2122;s immune system as the joint capsule that is replaced must undergo a healing process. Physical therapy rehabilitation aims to maximize the recovery potential of the affected knee by augmenting the healing process with the proper amount of exercise and pain control treatment.[14] In smokers, it is plausible to suggest that this healing process, and therefore treatment duration, may require an additional amount of time due to the fact that healing must occur in multiple locations simultaneously.[17] Statistically, no relationship was observed within the 15 patient sampling that would indicate smoking having a direct impact on the duration and/or effectiveness of treatment following a total knee replacement and all tests performed yielded non-significant results. However, it should be noted that only 4 of 15 subjects were active smokers, perhaps a percentage too small to see any meaningful trends in the data.

Age As the human body ages, its responses to abnormal health statuses become prolonged and less effective. This phenomenon has been observed in cases dealing with infection and the immune system, musculoskeletal healing and cancer treatment.

As both the immune and musculoskeletal systems come into play when discussing the healing process following a total knee replacement, it is understandable that these systems may be less effective in achieving the level of post-surgical healing that younger individuals may experience. Bisschop, Brouwer, and Van Rayy showed in their study that patients younger than 60 years of age that underwent total knee replacement operations experienced better treatment outcomes.[23] In this study, no correlation was found between patientâ&#x20AC;&#x2122;s ages and their respective treatment durations. As indicated in Figures 3 and 4 no trend in the data is suggested.

21

Figure 3. Age of study participants and the number of Physical Therapy sessions they attended.

Figure 4. Number of Physical Therapy sessions as function of age

Summary Many studies have been performed examining the effects of risk factors leading to total knee replacement surgery but none could be found regarding the influence of these risk factors on both the success and duration of post-surgical therapy and treatment. As such, a great deal of information seems to be unknown about how these risk factors come into play when discussing treatment outcomes in the physical therapy setting. From the results of the data and its statistical analysis, we have confirmed information that has already been known, discovered possible answers to some questions asked in the study, and have laid a potential path for future studies in that some of our questions remain unanswered.

From the data, we see clear relationships between active and passive range of motion measurements, confirming the fundamentals of joint motion as we have known them. As active range of motion is limited, so is passive motion, but to a lesser extent. Additionally, the data confirmed that current physical therapy treatments are effective in restoring knee range of motion in both directions following a total knee replacement

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operation, as 14 out of the 15 patients showed marked and normal recovery responses. As many unknown variables concerning the specific surgical interventions used and health histories still remain regarding the patient pool, it is difficult to speculate as to why the one patient did not respond well to post-surgical treatment.

The data also revealed a distinct association between body mass index and the number of physical therapy sessions required for recovery, as well as a possible connection between body mass index and the amount of active range of motion recovered in both flexion and extension. On average, patients that maintained a higher body mass index value required a greater duration of treatment to reach the goals of post-knee joint replacement range of motion. Also, the data showed trends of a lower body mass index value corresponding with greater active range of motion values following treatment, although statistical testing did not show clear significance in this association. No significant correlations were found between smoking history and treatment success and/or duration, and age did not seem to play a role in post-treatment outcome either.

Surprisingly, a negative correlation was observed between an incidence of prior-knee trauma and the duration of treatment required to achieve post-surgical goals. As the original hypothesis was that prior-knee trauma would lead to more significant damage to the joint preceding surgical intervention and therefore would take a greater time to rehabilitate following surgery, this was most interesting. As there are a number of elements regarding patient histories n terms of the specific injury or injuries sustained, time since the injury, treatments received for the injury, and others, it is impossible to define the meaning of this relationship, however, this is an area that can be marked for further study.

Limitations Some limitations of the study include the small sample size of patients used for evaluation during the study, the use of a single clinical site for obtaining the data, the potential for selection bias

22 and the limited age range of patients that were selected for the study are not to be discounted.

Although some definite correlations and statistically significant results were discovered, it must be stressed that these trends come from a very small sample size of 15 patients, and that it is understandable that the sampling of a larger population may yield different results.

Furthermore, the inclusion of patients from multiple clinical sites may yield different results as well, as therapies, patient demographic factors, and therapists vary from location to location. Finally, the age range of patients that were randomly selected for participation in the study was from 5785 years, however, the bulk of the patient sample ranged from 60-78 years. A more evenly distributed age sampling may potentially yield different results as well.

Conclusion The study confirmed relationships between active and passive extension and flexion knee range of motion, and identified influences of body mass index and past-knee trauma on physical therapy success and duration in a knee following a total knee replacement operation. Because of these relationships and the associated impact of them on physical therapy treatment, it is important for therapists in the field to understand them, identify potential patient cases where these they may come into play, and plan/amend treatment strategies accordingly.

Works Cited 1. Abramson, S. B., N. K. Arden, M. Attur, S. D. Bos, C. Cooper, E. M. Dennison, M. Doherty, S. A. Doherty, E. Evangelou, D. J. Hart, A. Hofman, K. Javaid, I. Kernad, K. Kisand, M. Kloppenburg, S. Krasnokutsky, R. A. Maciewicz, I. Meulenbelt, K. R. Muir, F. Rivandeneira, J. Samuels, M. Sezgin, E. Slagbloom, A. J. Smith, T. D. Spector, A. Tamm, A. G. Uitterlinden, A. M. Valdes, J. B. Van Meurs, M. Wheeler, G. Zhai, and W. Zhang. "LargeScale Meta-Analysis of Interleukin-1 Beta and Interleukin1 Receptor Antagonist Polymorphisms on Risk of Radiographic Hip and Knee Osteoarthritis and Severity of Knee Osteoarthritis." Osteoarthritis Cartilage3rd ser. 19 (2011): 265-71.

2. Arden, N. K., C. Cooper, E. M. Dennison, M. Doherty, S. A. Doherty, D. J. Hart, I. Kerna, K. Kisand, R. J. Lories, M.

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Mangino, T. D. Spector, A. Tamm, A. M. Valdes, and M. Wheeler. "Genetic Variation in the SMAD3 Gene Is Associated with Hip and Knee Osteoarthritis." Arthritis and Rheumatology 8th ser. 62 (2010): 2347-352.

3. Arden, N. K., C. Cooper, M. Doherty, S. Doherty, D. Hart, I. Kerna, R. A. Maciewicz, K. R. Muir, F. O’Neil, E. Pola, T. D. Spector, A. Tamm, A. M. Valdes, and W. Zhang. “A Meta-Analysis of Interleukin-6 Promoter Polymorphisms on Risk of Hip and Knee Osteoarthritis.” Osteoarthritis Catrilage 5th ser. 18 (2010): 699-704.

4. Bao, C., F. Hu, L. Jiang, X. Li, J. Rong, Y. Wang, and Y. Zhao. "The Relationship Between Body Mass Index and Hip Osteoarthritis: a Systematic Review and MetaAnalysis."Joint Bone Spine 2nd ser. 78 (2011): 150-55.

5. Chen, D., K. Dai, J. Fan, Q. Jiang, J. Laio, Z. Lin, T. Nakamura, P. Norman, A. Qin, D. Shi, J. Xu, Z. Xu, M. Zheng, and Q. Zheng. "Association of Single-Nucleotide Polymorphisms in HLA Class II/III Region with Knee Osteoarthritis." Osteoarthritis Cartilage 11th ser. 18 (2010): 1454-457.

6. Colby, Lynn Allen, and Carolyn Kisner. Therapeutic Exercise Foundations and Techniques. 5th ed.

Philadelphia: F. A. Davis, 2007.

7. Doherty, M., B. F. Leeb, D. F. McWilliams, S. G. Muthuri, and W. Zhang. "Occupational Risk Factors for Osteoarthritis of the Knee: a Meta-Analysis." Osteoarthritis Cartilage (2011).

8. Fransen, M., G. Hernandez-Molina, S. McConnell, and S. Reichenbach. “Does land-based exercise reduce pain and disability associated with hip osteoarthritis? A metaanalysis of randomized controlled trials.” Osteoarthritis Cartilage 5th ser. 18 (2010): 613-20.

9. Fuller, Kendra S., and Catherine Cavallaro Goodman. Pathology Implications for the Physical Therapist. 3rd ed. St. Louis: Saunders, Elsevier, 2009.

10. Gunther, K. P., U. Hubel, S. Kirschner, F. Krummenauer, and J. Lutzner. "Long-term Results in Total Knee Arthroplasty : A Meta-Analysis of Revision Rates and Functional Outcome." Chirurg 7th ser. 82 (2011): 618-24.

11. Jiranek, W. A., X. Kong, and D. L. Riddle. "Factors Associated with Rapid Progression to Knee Arthroplasty: Complete Analysis of Three-Year Data from the Osteoarthritis Initiative." Joint Bone Spine (2011).

12. Gordon, Neil F., Linda S. Pescatello, Walter R. Thompson. “ASCM’s Guidelines for Exercise Testing and Prescription.” 8th ed. Philadelphia: Wolters Kluwer, Lippincott Williams & Wilkins, 2010.

13. Dean, Elizabeth, Donna Frownfelter. “Cardiovascular and Pulmonary Physical Therapy.” 4th ed. St. Louis: Mosby Incorporated, 2006.

23 14. O’Sullivan, Susan B., Thomas J. Schmitz. “Physical Rehabilitation.” 5th ed. Philadelphia: F.A. Davis Company, 2007.

15. Norkin, Cynthia C., D. Joyce White. “Measurement of Joint Motion, A Guide to Goniometery.” 4th ed.

Philadelphia: F.A. Davis Company, 2009.

16. Engstrom G, Gerhardsson de Verdier M, Lohmander LS, Nilsson PM, Rollof J. “Incidence of Severe Knee and Hip Osteoarthritis in Relation to Different Measures of Body Mass: A Population-Based Prospective Cohort Study.”

Ann. Rheumatology Dis. 4th ser. 68 (2008): 490-6.

17. Bishop M, Campagna EJ, Hawn M, Henderson WG, Houston TK, Maddox G, Ponce BA, Richman J, Singh JA. “Smoking is a Risk Factor for Short-Term Outcomes Following Primary Total Hip and Total Knee Replacement in Veterens.” Arthritis Care Res. (2011).

18. Benevides L, Basati MZ, Coletta RD, da Silva JS, Goncalves RB, Nociti FH Jr., Silverio KG. “Impact of Smoking on Inflammation: Overview of Molecular Mechanisms.” Inflammation Res.5th ser. 60 (2011): 40924.

19. Kokoszka P, Lapaj L, Markuszewski J, WieruszKozlowska M. “Total Knee Replacement in Joints With Severe Varus and Bone Deficiency.” Chir Narzadow Ruchu Ortop Pol. 6th ser. 75 (2010): 375-9.

20. Abram F, Choguette D, Dorais M, Haraoui B, MartelPelletier J, Pelletier JP, Raynauld JP, Wildj LM. “Risk Factors Predictive of Joint Replacement in a 2-Year Multicentre Clinical Trial in Knee Osteoarthritis Using MRI: Results From Over 6 Years of Observation.” Ann. Rheumatology Dis. 8th ser. 70 (2011): 1382-1388.

21. Abram F, Beary JF, Berthiaume MJ, Choguette D, Cline GA, Haraoui B, Martel-Pelletier J, Meyer JM, Pelletier JP, Raynauld JP. “Risk Factors Associated With the Loss of Cartilage Volume on Weight-Bearing Areas in Knee Osteoarthritis Patients Assessed by Quantitative Magnetic Resonance Image: a Longitudinal Study.” Arthritis Res. Ther. 4th ser. 9 (2007): R74.

22. Ishii T, Motojima S, Ryu J, Saito S, Suzuki G, Tokuhashi Y. “Previous Fracture Surgery is a Major Risk Factor of Infection After Total Knee Arthroplasty.” Knee: Surgery, Sports, Traumatology, Arthroscopy (2011).

23. Bisschop R, Brouwer RW, Van Rayy JJ. “Total Knee Arthroplasty in Younger Patients: a 13-Year Follow-Up Study.” Orthopedics 12th ser. 33 (2010): 876.

Steve Kowalski (’11, B.S., Health Science,’13 DPT) is working at HealthSouth Altoona in inpatient rehabilitation.

Call for papers Sub m ission G uid elines The purpose of SPECTRUM is not merely to disseminate new results, but also to inform and enlighten.

Our readership is a general and multidisciplinary audience who may not be an expert in your field of study. Consequently, please explain all pertinent concepts essential to understanding your article as well as any concepts that might not be common knowledge. Please submit your file in Microsoft Word format as an attachment to the following email address: spectrum@francis.edu. The text should be single spaced, using 12-point Times New Roman font. Please use italics, rather than underlining, for emphasis.

O r ganiz at ion of M anuscr ip t s SPECTRUM is an interdisciplinary journal accepting submissions from the natural sciences, the humanities as well as the professional schools (health sciences and business), therefore, the structure and style of each manuscript will differ from discipline to discipline. Regardless, all submissions must provide a cover sheet, a thorough introduction of the problem your research addresses, the conclusion(s), result(s) or findings of your research, as well as some form of bibliographic citation. Below are the general guidelines for these requirements, some of which may not apply to your area of research.

C ov er Sheet Title Names and departments of undergraduate researcher(s) and faculty advisor(s) Abstract (200 â&#x20AC;&#x201C; 300 words) Six key words Int r od uct ion Include general background of the relevant field and the larger problem your research addresses as well as its relevance within the field. In addition, explain what prompted your investigation, a summary of previous findings related to your research problem and what contributions your project brings (or was expected to bring) to the issue.

M et hod s and M at er ials (If ap p licab le) Summarize important methods and materials used in your research.

R esult s/C onclusions Give detailed report of the results and or conclusions reached through your research.

Discussion Results should be evaluated in the context of general research problem, the implications of which should be explained with conclusions, predictions or suggestions (if applicable) for further study.

T ab les (if ap p licab le) Create tables in Microsoft Word format and insert into general text accompanied by a table legend. Each table needs a number based on its appearance in the paper, where it is referenced.

Figur es (if ap p licab le) Please submit figures at the end of the article, one image per page; we will fit these in as we organize the manuscript. Each figure needs a number (the figures shall be numbered consecutively in the order of their appearance in the paper) and a title. SPECTRUM will be printed black and white, but there will be an online version where figures submitted in color will appear in color.

R efer ences You may use any referencing style you choose so long as it is a standard format or your discipline (IEE, APA, ACS, PubMed) and that you use it consistently and to the appropriate bibliographical standards.