Before arriving at Old Dominion University in 2022, my life was nearly perfect. I was vice president of my senior class at Hopewell High School, vice president of our Student Council Association (SCA), and I graduated with an associate of science at only 18, before graduating high school, might I add. On top of all of this, I was valedictorian of my class at Hopewell High School. While in high school, I took an Intro to Nurse Aid I course that really set the way of how I wanted to spend the rest of my life. This did not push me to be a nurse necessarily, but it did tell me that I could picture the rest of my future in medicine. A white coat is in my future.<\/p>\n\n\n\n
Growing up without health insurance and proper stability, it really makes me question how the rest of my future will go. Am I willing to be in debt for years on end for a career that is so competitive? Am I willing to sacrifice all my time to something that might not go my way in the end? How quickly will I give up on my dreams if I fail too many times? The truth is though, I will never know if I don\u2019t try. If I am so worried about failing and the financial aspects of the rest of my future, I will never obtain what my dreams are. Learinng to come to terms with the fear of failure is something I work towards every day and will continue to do so in medical school.<\/p>\n\n\n\n
With my goals in mind, I knew that after I graduated high school, going to college would be my next step. I applied to many colleges, and I got into all of them except one. One of those being a full ride to William and Mary. An influential factor for me when picking a university to spend the next four years of my life at is the atmosphere. Based on my experience at William and Mary, the atmosphere was not something I could picture for my life. So, here I am now at Old Dominion University.<\/p>\n\n\n\n
With this being my sophomore year at Old Dominion University, my chosen major is Public Health, with the hopes to advance into physician assistant (PA) school after I finish my undergraduate degree. As of right now, I have passed all my prerequisites for PA school with a B+ or higher. As I have taken these classes, while they may be very difficult, they have really shown me that this career is what I’m destined to do. The versatility, the competitive atmosphere, the white coat, the compatibility with your team; I want it all, and I intend to achieve it.<\/p>\n\n\n\n
Right now, I am only 19 years old. I don\u2019t have any experience in the field, but I am lined up to shadow a PA in the hospital in my hometown over the summer. As for my future, I hope to work as an EMT during my Junior year for lots more hand-on experience, as well as the possibility of working in a nursing home. From my experience being on the Y Street Leadership Team (YSLT) in high school, I know that I have the ability to become a great doctor one day, and an even better person. My leadership potential has really blossomed since being a part of the leadership team, as well as working with teams, my communication skills, and my ability to adapt. I know, despite having no experience, that I can and will succeed in this profession.<\/p>\n\n\n\n
With this being said, I belive that I have what it takes to become a successful and great physician assistant. I have the skills required for the career and will achieve more experience as I become exposed more to the field in the future. As my mom says, \u201cwith time, comes greatness.\u201d As my future to PA school quickly approaches, I will focus on the reason why I am doing it all; to become a great person and doctor. I see a white coat with Dr. Harper embroidered on it and will every day until I achieve greatness.<\/p>\n\n\n\n
A primary article is the first publication of a scientific report of new research findings, and they are typically peer reviewed. The individual who writes a primary article has a direct connection with what they are writing about, so they are typically the researchers themselves. The usual sections found in a primary article include the introduction, methods, results, discussions, and references.<\/p>\n\n\n\n
A review article is written to bring together a combination of existing research on a certain topic. These types of articles summarize the results\/conclusions of multiple research studies and articles. These articles are particularly useful when you are not yet familiar with a body of research and want to get a better understanding of it. These articles are not meant to retrieve all of the research on a certain topic. Unlike usual research papers, review articles do not contain new results.<\/p>\n\n\n\n
During the scientific peer review process, a researcher will write a draft article describing his findings and submit that article for publication. Once the article is submitted, the journal’s editor will read over the article to decide if it\u2019s a good fit for said journal. Then, they will send the article over to a group of experts to go over the article’s quality. These experts are called \u201cpeers\u201d since their area of research is the same area. Each of the \u201cpeers\u201d will ask questions to judge the accuracy\/significance of that research. These experts then decide if the article is suitable for the journal, so it\u2019s either approved or rejected. This is a very lengthy process and can take quite a bit of time before the article is finally published in the journal. Remember, peer reviewed articles and review articles are not the same.<\/p>\n\n\n\n
Based on the article provided, the Oxford Human Molecular Genetics <\/em>journal is the primary article, while the Cold Spring Harbor Perspectives in Medicine <\/em>journal is the review article. The Oxford Human Molecular Genetics <\/em>journal is the primary article because the authors did the research they are writing about, and there are specific sections like an introduction, results, method, and an abstract section. The other article in the Cold Spring Harbor Perspectives in Medicine <\/em>journal is simply bringing together existing research on a topic, and in this case, Huntington’s Disease. The findings shown in this article have already been done, and they are simply summarizing the results of multiple studies done previously.<\/p>\n\n\n\n Hovestadt, V. et al. Resolving medulloblastoma cellular architecture by single-cell genomics. Nature <\/em>572<\/strong>, 74-79 (2019).<\/p>\n\n\n\n https:\/\/www.nature.com\/articles\/s41586-019-1434-6<\/a><\/p>\n\n\n\n In this article, the authors are discussing a study about the molecular and cellular heterogeneity Hovestadt, V. et al. Resolving medulloblastoma cellular architecture by single-cell genomics. In this article written by Hannah Seo, published on October 10, 2023, the topic of Seo, H. Why some people don\u2019t feel the buzz of caffeine. The Washington Post<\/em>; 1. WHAT CHROMOSOME DID YOU CHOOSE? I chose Chromosome 4<\/strong> <\/p>\n\n\n\n 2 & 3. STATE THE NUMBER OF GENES AND<\/strong> BASE PAIRS ON THE CHROMOSOME YOU CHOSE. Chromosome 4 contains approximately 1600 genes and approximately 190 million base pairs.<\/strong> <\/strong> <\/p>\n\n\n\n 4. LIST ONE GENE THAT IS LOCATED ON THIS CHROMOSOME. One gene located is FGFR3.<\/strong> <\/p>\n\n\n\n 5. STATE THE FUNCTION OF THE GENE YOU LISTED IN #4.\u00a0The function of the FGFR3 gene is\u00a0to slow down the formation of bone by inhibiting the proliferation of chondrocytes, the cells that produce cartilage. This is a common cause of dwarfism. <\/strong>\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/p>\n\n\n\n 6. WHAT IS THE SECOND<\/strong> SEQUENCE DESCRIPTION MATCH FOR YOUR QUERY SEQUENCE? Homo sapiens CFTR (CFTR) gene, partial cds<\/strong> <\/p>\n\n\n\n 7. WHAT DOES THE ENCODED PROTEIN DO IN THE BODY? This gene encodes a member of the ATP-binding cassette transporter superfamily. The encoded protein functions as a chloride channel and controls ion and water secretion and absorption in epithelial tissues. <\/strong> <\/p>\n\n\n\n 8. FOR WHAT DISEASE IS A MUTATED FORM OF THIS GENE RESPONSIBLE? Cystic Fibrosis<\/strong> <\/p>\n\n\n\n 9. ON WHAT CHROMOSOME IS THE GENE LOCATED? This gene is located on chromosome 7.<\/strong> <\/strong> <\/p>\n\n\n\n 10.CHOOSE A SPECIES (STATE THE SCIENTIFIC NAME) OTHER THAN HOMO SAPIENS<\/em> THAT ALSO HAS A 100% IDENTITY (Per. Ident) FOR THIS SEQUENCE? Pongo abelii.<\/strong> <\/p>\n\n\n\n 11. WHAT IS THE COMMON NAME FOR THIS SPECIES? Sumatran orangutan<\/strong> <\/p>\n\n\n\n 12. DOES IT SURPRISE YOU THAT THIS SPECIES ALSO HAS A 100% SIMILARITY IN IDENTITY? WHY OR WHY NOT? No it doesn\u2019t surprise me because human and chimp DNA is so similar, which explains how closely related we are.<\/strong> <\/strong> <\/p>\n\n\n\n 13a. WHAT IS THE GENUS AND SPECIES WITH THIS NUCLEOTIDE SEQUENCE? Nomascus leucogenys <\/strong> <\/p>\n\n\n\n b. WHAT IS THE COMMON NAME? northern white-cheeked gibbon<\/strong> <\/p>\n\n\n\n c. HOW MANY GAPS OCCUR BETWEEN THE TWO SEQUENCES (THE ONE YOU ORIGINALLY SUBMITTED AND ONE THAT HAS LESS THAN 100% QUERY COVER)? Both of the sequences have 0\/120 gaps, so zero (0).<\/strong> <\/strong> <\/p>\n\n\n\n 14. WHAT IS A GAP IN SEQUENCE ALIGNMENTS? Gaps in a sequence alignment are<\/strong> the pieces that get left behind when you try to align DNA or protein sequences and have to use padding or null characters to match homologous residues.<\/strong> <\/p>\n\n\n\n FOR EACH, STATE WHAT THE GENE IS (#15-18). (Again, give the description of the gene or gene product, not the nucleotide sequence.) <\/p>\n\n\n\n 15. NM_145556- Mus musculus TAR DNA binding protein (Tardbp), transcript variant 1, mRNA<\/strong> <\/p>\n\n\n\n 16. NM_013444- Homo sapiens ubiquilin 2 (UBQLN2), mRNA<\/strong> <\/p>\n\n\n\n 17. NM_001010850- Homo sapiens fusion (involved in t(12;16) in malignant liposarcoma) (FUS), transcript variant 2, mRNA<\/strong> <\/p>\n\n\n\n 18. KJ174530- Homo sapiens superoxide dismutase-1 (SOD-1) gene, exon 1 and partial cds<\/strong> <\/p>\n\n\n\n 19. WHAT DISEASE IS ASSOCIATED WITH MUTATIONS OF THE GENES REFERENCED IN #15-#18? WHAT IS A \u201cCOMMON NAME\u201d OF THE DISEASE? ALS<\/strong> <\/p>\n\n\n\n 20.\u00a0WHAT IS GENBANK?\u00a0 GenBank is a comprehensive database that contains publicly available nucleotide sequences for more than 300 000 organisms named at the genus level or lower, obtained primarily through submissions from individual laboratories and batch submissions from large-scale sequencing projects.<\/strong>\u00a0<\/p>\n\n\n\n 21. First, answer this question: WHAT IS cDNA? <\/p>\n\n\n\n Complementary DNA or copy DNA (cDNA) is synthetic DNA <\/strong>that has been transcribed from a specific messenger RNA (mRNA). <\/strong> <\/p>\n\n\n\n 22. WHAT IS THE SEQUENCE MATCH? beta-globin [Homo sapiens]<\/strong> <\/p>\n\n\n\n Assignment:<\/strong> While still on BLAST, choose \u201cProtein BLAST\u201d. Check the box which says, \u201cAlign two or more sequences\u201d. <\/p>\n\n\n\n 23. DO YOU SEE ANY DIFFERENCES BETWEEN THE TWO AMINO ACID SEQUENCES? Yes, there is a gap and a dash in query 779.<\/strong> <\/p>\n\n\n\n 24. IF YOU SAW DIFFERENCES, WHAT WERE THEY? There was a gap and a dash.<\/strong> <\/strong> <\/p>\n\n\n\n 25. ARE THERE ANY GAPS IN THE SEQUENCE ALIGNMENT? Yes<\/strong> <\/p>\n\n\n\n 26. WHAT GENE ENCODES FOR THE POLYPEPTIDE YOU WERE ANALYZING? This gene encodes a member of the fibroblast growth factor receptor (FGFR) family.<\/strong> <\/p>\n\n\n\n 27. WHAT IS THE FUNCTION OF THIS PROTEIN? It plays a role in bone development and maintenance and it binds acidic and basic fibroblast growth hormone. <\/strong> <\/p>\n\n\n\n 28. WHAT HUMAN DISEASE IS CAUSED BY A MUTATION IN THIS GENE? Skeletal dysplasia<\/strong> <\/p>\n\n\n\n 29. WHAT IS THE CONNECTION AMONG THE FOLLOWING: NIH, NLM, NCBI, and HHS? The connection among the National Institutes of Health (NIH), the National Library of Medicine (NLM), the National Center for Biotechnology Information (NCBI), and the Department of Health and Human Services (HHS) is that they are all connected within the U.S. government with the primary goal of medical research. <\/strong> <\/p>\n\n\n\n 30. REFLECT ON ONE THING THAT YOU LEARNED FROM DOING THIS ASSIGNMENT. One thing I learned from doing this assignment is the function of the FGFR3 gene. This gene slows down bone formation, which is something that I didn\u2019t know before starting this assignment. <\/strong>\u00a0<\/p>\n\n\n\n https:\/\/doi.org\/10.1093\/nar\/gkp1024<\/a><\/p>\n\n\n\n
\n\n\n\nWriting Assignment #3: Citation of a Primary Article <\/h1>\n\n\n\n
\n\n\n\nWriting Assignment #4: Genetics Related Article Summary<\/h1>\n\n\n\n
of medulloblastoma, the most common type of cancerous brain tumor in children. In this study,
they are focusing on single-cell genomics to examine in further detail the cellular architecture of
this cancerous brain tumor. This type of tumor starts in the lower back portion of the brain called
the cerebellum. This part of the brain, the cerebellum, is involved in the muscle coordination,
balance, and movement of the body. For this type of cancer, there are many advances being
made in the field of medicine, but many of these patients suffer from consequences of this cancer
if they survice, or they ultimately succumb to the cancer.<\/p>\n\n\n\n
In this study, there are four main molecular subgroups being examined: WNT, SHH, Group 3,
and Group 4. Each of these four groups are characterized by genotypes, transcriptional profiles,
and the age of the patient at their diagnosis. From these groups and characteristics, we can see
how these groups have different cellular origins and how they show up in gene expression
patterns. Due to these differences and patterns, we can grasp a better understanding of
medulloblastoma cellular composition and structure.<\/p>\n\n\n\n
Single cell genomics plays a very critical role in advancing our understanding of what exactly
medulloblastoma is. In this RNA sequencing, we can discover the cellular diversity, cells of
origin, and heterogeneity. In shorter terms, this single cell RNA sequencing provides us with a
detailed understanding of the cellular architecture in medulloblastoma tumors.<\/p>\n\n\n\n
In this study, single-cell RNA sequencing is being used, as it is a method to characterize cellular
states in healthy and diseased tissues. This method has never been used in medulloblastoma
subgroups before. Because of this never been done before on medulloblastoma single-cell RNA
sequencing, the data did in fact provide some insight into architecture of medulloblastoma. Due
to the positive data, there is some potential to improve patient outcomes in the future.<\/p>\n\n\n\n
The researchers obtained twenty-five fresh surgical tumor resections from different subgroups of
patients with medulloblastoma. By doing this, the researchers could see and examine the gene
expression profiles of individual cells within the tumors and identify different cell types and
states. This is the main method being used, but they also used DNA methylation analysis to
further characterize the tumors and validate their findings and research.<\/p>\n\n\n\n
The WNT, SSH, and Group 3 subgroup tumors comprised of differentiated and undifferentiated
neuron-like malignant populations, while group 4 focused on differentiated neuron-like
neoplastic cells. The SSH group tumors resembled granule neurons of varying differential states
that correlated with the patient’s age. Despite multiple methods of extensive characterization and
subgroup therapies, a deeper understanding of the cellular basis of medulloblastoma is needed to
fully decipher the research findings, particularly for Group 3 and 4.<\/p>\n\n\n\n
This research was aimed to create a better understanding of the complex nature of
medulloblastoma, and hopefully find better diagnosis and treatment. While the study does offer
valuable insights into what exactly single-cell genomics is and what medulloblastoma is, more
research is needed to fully understand the cause and molecular underpinnings of MB.<\/p>\n\n\n\nCitation<\/h2>\n\n\n\n
Nature <\/em>572<\/strong>, 74-79 (2019).
10.1038\/s41586-019-1434-6
(link to article)<\/p>\n\n\n\n
\n\n\n\n Writing Assignment #5: Genetics Related Article W\/ Supporting Evidence<\/h1>\n\n\n\n
discussion is why some people are affected by caffeine, and why some others are not. There are
many reasons why an individual does not feel the effects or the \u201ckick\u201d of caffeine: genetic
variability, tolerance, sensitivity, timing and dosage, age, etc. The author mentions how she has
never felt the effects of caffeine, and she can drink it at any time during the day and still fall
asleep with no problems. I chose this article in particular because I also tend to not feel caffeine
effects. As it turns out, according to this article, the way our body reacts to having caffeine is
highly impacted by our genes. There is one gene in particular, the CYP1A2 gene, that appears to
severely affect our body’s sensitivity to caffeine. This gene, CYP1A2, controls the enzyme,
CYP1A2. The gene controls the enzyme that is responsible for breaking down caffeine and
removing it from the body. There are different variants of this gene, and depending on what
variant you have, this controls how fast you metabolize caffeine. About 50% of individuals have
two copies of the \u201ccaffeine\u201d gene, making caffeine metabolize much quicker. This means these
individuals are less likely to have effects, like staying awake, from consuming caffeine. About
40% of individuals only have one copy of the gene, making them metabolize caffeine slowly.
The other 10% have no copies of the gene making them particularly slow at metabolizing
caffeine. Caffeine has a wide half-life of either two hours or eight hours, so depending on which
variation of the gene you have is how long your body might take for the caffeine to be removed
from your body.<\/p>\n\n\n\n
This article relates to genetics in the way that there is a particular gene that can affect the way
your body reacts to the effects of caffeine, meaning you either feel the effects of caffeine or you
don\u2019t. This is a gene that depends on which variant you have of the gene, and that variant
determines how long the caffeine will be removed from your body. In simpler terms, the main
topic of discussion in this article is the gene associated with the effects of caffeine, which is what
genetics is all about.<\/p>\n\n\n\n
In a review article by Amy Yang and other various authors, they are also discussing the topic of
caffeine consumption and the genetics behind it. This article proves that the popular press
information is in fact correct. This article goes into a deeper explanation of what the popular
press information says about caffeine and genetics. The review article says that the gene that
most significantly affects the way your body reacts to caffeine is the CYP1A2 gene. Variations
in the CYP1A2 gene determine how efficiently your body metabolizes caffeine. There are two
common genotypes associated with this gene: slow metabolizers and fast metabolizers. There are
other genes mentioned in this article that play a role in influencing the effects of caffeine that are
not mentioned in the popular press, but the main one is the CYP1A2 gene.<\/p>\n\n\n\n
As we have gathered from both articles, the review and the popular press, there is in fact a
genetics role in the effects of caffeine consumption. Based on both studies, genetics does in fact
play a role in individual caffeine consumption and the effects.<\/p>\n\n\n\nReferences:<\/h2>\n\n\n\n
https:\/\/www.washingtonpost.com\/wellness\/2023\/10\/10\/caffeine-sensitivity-coffee-heart-genes\/
(2023).<\/p>\n\n\n\n
Yang, A., Palmer, A. A., de Wit, H. Genetics of caffeine consumption and responses to caffeine.
Psychopharmacology<\/em> 211<\/strong>, 245-257 (2010).<\/p>\n\n\n\n
\n\n\n\nGenome Assignment<\/h1>\n\n\n\n
Chromosome Maps<\/h3>\n\n\n\n
Introduction to Nucleotide BLAS<\/strong>T\u00a0<\/h3>\n\n\n\n
Introduction to Protein BLAST<\/strong>\u00a0<\/h3>\n\n\n\n
Citations\u00a0<\/h3>\n\n\n\n
\n
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