Final Letter

December 13, 2016

Dear Morgan,

I have just recently finished a Cell Biology course with Dr. Christina Steel. The class was very interesting and helped me to develop a better understanding of how cells contribute to the body. In the course the topics are made interesting through videos shown in class, class representations, homework assignments, and quizzes. My favorite thing about the class was that we got to do Scientific Literacy assignments to help us understand the topics being discussed. We had two and they were both very interesting, but the Guavedoces assignment was by far my favorite. Dr. Steel introduced us to the finding in class and to read more about it was mind blowing. I never knew something of that sort could occur so it is worth looking in to. We also got to write a personal paper in which we picked our own topic to relate back to cells. In the beginning, I chose to explore how cells contribute to diseases and I wanted to somehow relate it to the brain. I changed my topic as the course went on to migraine headaches and how they contribute to cells. Over the summer when I conducted research, I focused on the cells of the brain so this topic related more closely to what I initially wanted to research further. I learned that migraine headaches can result in brain damage as the patient ages. Cell Biology was everything I expected it to be and I would highly recommend taking this course because it will expand your mind to a broader world of science.


Your future self


Personal Paper- Migraine Headaches

Morgan Roney

December 15, 2016

Migraine Headaches

The topic I chose to write on and examine more is migraine headaches. Migraine headaches affect more than 15 percent of people worldwide. They are a “…primary headache disorder characterized by recurrent headaches that are moderate to severe” (“Migraine”). Migraines can occur any time after puberty and gradually worsen as a person ages. I am interested in the topic because my mom has very bad migraines and I wanted to understand more what they resulted from. When she gets her migraine headaches she experiences dizziness, and pain in her neck. She has resulted in getting botox treatment to control her pain. The chosen article focuses on how migraines function without aura. Migraines are categorized into two different types. A person can experience migraines with aura, the early symptoms experienced during a migraine, and migraines without aura.

Twenty-one patients that did not experience aura were tested, along with twenty-eight controls who were healthy. In the study, they used two methods to examine the patients that included: a two-sample t-tests and x2. Using those methods, no differences were shown. To test the patients, a significant amount of restrictions was given. All data was captured through imaging using a MRI system. Through the process the features were first selected and underwent the multi-kernel SVM, and the subjects were then distributed and distinguished individually to get a better examination. They then used the cross-validation method to rid what was not useful in the study. Thus, they observed that the “…anterior cingulate cortex, prefrontal cortex, orbitofrontal cortex, and the insula contributed the most discriminative features” (Zhang). The charts exhibited throughout the research show many comparisons in table format; however, the methods used are spread over a large sample and the individuality report shows a more detailed approach.

Migraines relate to cells because they are known to lead to brain damage. It is believed that “…every single migraine attack may be contributing to an early onset of cell death and brain tissue loss…” (Dumas). The brain changes over time as individuals grow older, but the lesions caused by migraines are said to be more prone to damage in patients that are elderly because they can lead to strokes. Tissue volume loss also contributes to brain damage and migraines speed up the decaying of the brain. The treatment varies from patient to patient. Patients are typically on multiple medications to help with keeping the disorder from arising. Patients are also advised to keep track of when migraines occur and the patterns that occur (Dumas).

In conclusion, migraine headaches are a serious disorder that can be detrimental to one’s well-being. Without the proper diagnosis and treatment, one can suffer many different outcomes tremendously. This study helped to identify the parts of the brain that contribute most to the disorder. I will use this information to further my knowledge, and continue to research so that I am fully aware of what my mom is experiencing.




Dumas, P. (2016). Ouch! Every Migraine Attack Damages Your Brain || Migraine Again. Retrieved December 13, 2016, from

Migraine. (n.d.). Retrieved December 13, 2016, from

Zhang, Q., Wu, Q., Zhang, J., He, L., Huang, J., Zhang, J., & … Gong, Q. (2016). Discriminative Analysis of Migraine without Aura: Using Functional and Structural MRI with a Multi-Feature Classification Approach. Plos ONE11(9), 1-16. doi:10.1371/journal.pone.0163875

Guavedoces Assignment

Morgan Roney

December 9, 2016

Guavedoces Assignment

            In Salinas, a village southwest of the Dominican Republic, an epidemic called the guavedoces is seen in about one percent of males. The guavedoces is a condition where males are born without male genitalia so they are females. Around eight weeks after conception, sex hormones develop to determine the sex of a fetus. If the fetus is male, Y chromosomes instruct gonads to become testicles which produces testosterone that is sent to a tubercle. In the tubercle, the testosterone converts to a hormone called dihydro-testosterone. If the fetus is female, dihydro-testosterone will not be produced and the tubercle becomes a clitoris. The reason behind males being born without male genitalia is due to a deficiency in the 5-alpha-reductase enzyme (News, BBC). The enzyme creates the “…male sex hormone dihydro-testosterone, which prevents the development of male sex organs…” (Dockrill).

Imperato-McGinley made the discovery of the condition. They observed that “…the affected males were born with ambiguous external genitalia and therefore initially reared as girls” (Okeigwe). The males do not begin to develop male phenotypic features until they hit the stage of puberty. They develop muscle mass, enlargement of the phallus, lack of breast development, testicular descent, and deepened voices. Because they possess the deficiency, they are more likely to be subject to having little to no facial hair, a small prostate, and minimal acne. Imperato-McGinley tested their hypothesis by comparing dihydro-testosterone and testosterone levels in people who were either affected by the deficiency or unaffected. In concluding their findings, they discovered that “…a 5-alpha reductase defect resulted in decreased conversion of testosterone to DHT and furthermore that DHT functioned to facilitate differentiation of the male external genitalia and prostate” (Okeigwe).

In cell signaling, the androgen receptor is a type of nuclear receptor that is “…activated by binding either of the androgenic hormones, testosterone, or dihydrotestosterone in the cytoplasm and then translocating into the nucleus” (“Androgen”). Androgen genes are important in maintaining the male sexual phenotype. The testosterone flows to the 5-alpha reductase enzyme before it goes into dihyrotestosterone.

Dihydrotestosterone and testosterone, types of androgen, are distinct hormones for multiple reasons. Structurally, they differ only by a double bond found between the fourth and fifth carbon on the leftmost ring. Dihydrotestosterone is a hormone that stimulates growth and function of male characteristics. It is derived from testosterone and the amount of dihydrotestosterone in the body is dependent upon the amount of testosterone produced. Testosterone is produced every day in adults and is related to the prostate and testes for a male; and in the ovaries for women.

Dihydrotestosterone is related to the skin and other parts of the body due to its function. It contributes to the start of puberty because it enlarges male genitalia, growth of pubic/facial hair, and affects sexual behavior. The hormone is thought to be “…more potent than testosterone and many of the effects that testosterone has in the body can only happen after it has been converted to dihydrotestosterone” (“You”). When those affected hit the age of puberty, because they have increased levels of the enzyme, the testes produce more testosterone causing secondary male sex hormones to form. When the secondary male sex hormones are produced, the formation of a phallus and other male characteristics come in; they are then considered to be a male (Dockrill).

Works Cited

“Androgen Receptor.” Wikipedia. Wikimedia Foundation, n.d. Web. 09 Dec. 2016.

Dockrill, Peter. “In This Remote Village, Some Boys Don’t Grow a Penis Until They’re 12.” ScienceAlert. N.p., 21 Sept. 2015. Web. 08 Dec. 2016.

Mahler, Mike. “Testosterone Is Great but Is Dihydrotestosterone the King of All Male Androgens?” Testosterone Is Great but Is Dihydrotestosterone the King of All Male Androgens? – Mahler’s Aggressive Strength. N.p., n.d. Web. 08 Dec. 2016.

News, BBC. “The Extraordinary Case of the Guevedoces.” BBC News. N.p., 20 Sept. 2015. Web. 08 Dec. 2016.

Okeigwe, Ijeoma, and Wendy Kuohung. “5-Alpha Reductase Deficiency: A Forty Year Retrospective Review.” Thomson, n.d. Web. 08 Dec. 2016.

“You & Your Hormones.” You & Your Hormones | Hormones | Dihydrotestosterone. N.p., 06 Jan. 2015. Web. 08 Dec. 2016.

Scientific Writing Proposal

Morgan Roney

BIOL293- Cell Biology

TR 11:00-12:15

September 6, 2016

Scientific Writing Proposal

My name is Morgan Roney and I am a Junior here at Old Dominion University. I am majoring in Biology with a pre-veterinary focus and have thoroughly enjoyed my experiences at the university. I was drawn to major in Biology because I am very interested in the study of life and all of the various roles played by different organisms. I believe that it is interesting how each living organism has similar characteristics, but are unique at the same time. I was drawn closer to the major when I became an ambassador for the College of Sciences. As an ambassador, I get to express my interests in Biology to prospective students. The College of Sciences has also helped with ensuring that the major was the right one for my chosen career field.  Because Biology is so broad, there are many different routes available when it comes to careers and research.

In this course, I want to learn more about cells and how they contribute to the body, as well as the immune responses to various diseases. I became more interested in cells over the summer during my ten-week research internship at Virginia Tech. My research there involved Herpes Simplex Virus II Latency Associated Promoter 2 and how it contributes to neuron specificity of infection. Due to my research experience, my knowledge has expanded heavily in the study of neurons and how they work. I also have an interest in how cells contribute to different diseases and how the immune system responds to the various diseases.

My goal by the end of the course is to understand more about how cells contribute to the body as a whole, as well as the brain. I need to follow up on this because it will help in personal use and I will be more informed about how the immune system reacts to certain illnesses. Because I come from a family with various sicknesses/diseases, I have become curious about how the diseases contribute to their bodies and how exactly the sickness came about. I would like to have the ability to know more about the sicknesses in their time of need. I will relate this to course objective number two, because I am interested in seeing how cells respond to stimuli in their environments.



Final Alzheimer’s Draft

                                                                        October 30, 2016

Alzheimer’s Disease is a disease that causes brain disorder over a period and can lead to memory loss, lacking skills to think properly, and the ability to carry out simple tasks. The disease is known to be one of the leading causes of death in America, affecting more than five million people (“Alzheimer’s”). Alzheimer’s disease is formed from amyloid beta insoluble plaques that form in the brain. Amyloid beta is a short peptide that is a byproduct of amyloid precursor protein that has an unclear function. The form of the amyloid beta protein that is associated with the formation of plaques in the brain is fibrils. It is also affected by tau proteins that are expressed in neurons considering the disease to be a tauopathy (“Biochemistry”).

A monoclonal antibody is a protein made by the immune system that recognizes just one special region of just one protein. An antibody discussed was aducanumab, which was used to help reduce the amount of amyloid beta plaques found in the brain (Weintraub). Tests were run on mice to examine how the monoclonal antibody migrates to the brain. The test indicated that the antibody enters the brain and binds to amyloid beta causing the amount of plaques found to reduce (Sevigny).

The monoclonal antibody, aducanumab, is seen to selectively target the unsafe form of the plaques because it binds to the misfolded amyloid beta protein rather than the normal folded protein. Monoclonal antibodies “…target proteins that change shape and misfold, becoming toxic and triggering the hallmark beta-amyloid plaques and abnormal tau proteins…” (“Novel”). The antibody is seen to target the misfolded protein because of solubility. The antibody binds to oligomers which are soluble proteins and fibrils which are insoluble (Keller).

The data gathered in this study is used to examine how amyloid beta is affected by monoclonal antibodies in Alzheimer’s disease. The data did demonstrate, in my opinion, that the monoclonal antibody reduces amyloid beta plaques found in the brain. The antibody acts as a reducer to the plaques depending on dosage distributed. The data exhibits a change from week 26 to week 54 between the amount of amyloid plaques seen. The data concluded that the higher the dosage of aducanumab given, the lower the amount of amyloid beta plaques seen (Sevigny). This is important because this signifies the treatment is working, although it will not completely cure the disease.

The data did represent well, but not rapid enough when tested with cognitive symptoms in Child Dementia Rating (CDR) and Mini-Mental State Examination (MMSE).  The results showed that aducanumab reduced the decline in the scores of the MMSE. No improvements for the MMSE were shown between weeks 26 and 54. The results were not rapid examining that patients did not improve on the CDR when treated with placebo until week 54 of the study (Sevigny). I believe that the CDR showed better results because dose-responsiveness was seen in the tests. This means that the higher the dosage of the aducanumab, the greater the chance of positive effects to be shown.

This treatment has had a significant positive effect on the patients tested and I do believe it has promise. I believe that the FDA should cautiously approve it because I would not fully trust the treatment. The treatment should not be fully trusted because the aducanumab still produces negative effects on the patient and they could be minimized if the study is given more approach. I believe that more studies on animal models should be done before doctors start to prescribe the aducanumab once it is manufactured. This will help to avoid any errors that could come up when tested on humans. Although the drug has many negative effects, the positive effects outweigh and could be the start of something new for Alzheimer’s disease.

Works Cited

“Alzheimer’s Disease Fact Sheet | National Institute on Aging.” U.S National Library of Medicine. U.S. National Library of Medicine, n.d. Web. 15 Oct. 2016.

“Biochemistry of Alzheimer’s Disease.” Wikipedia. Wikimedia Foundation, n.d. Web. 15 Oct. 2016.

Keller, Danielle M. “Finally, a Big Win for a Monoclonal in Alzheimer’s.” Medscape. N.p., 23 Mar. 2015. Web. 16 Oct. 2016.

“Novel Monoclonal Antibodies Show Promise for Alzheimer’s Disease Treatment.” ScienceDaily. ScienceDaily, 20 July 2015. Web. 16 Oct. 2016.

Sevigny, Jeff. “The Antibody Aducanumab Reduces Aβ Plaques in Alzheimer’s Disease.” Nature. N.p., 31 Aug. 2016. Web. 15 Oct. 2016.

Weintraub, Karen. “Alzheimer’s Drug Shows Promise in Small Trial.” Scientific American. N.p., 2016. Web. 15 Oct. 2016.