This essay strives to answer the question, " How and Why Does Peer Influence Affect Adolescents?" Peer influence "...involves changing one’s behavior to meet the perceived expectations of others”. This phenomenon primarily affects adolescents—“the age between puberty…and the age at which you [they] attain a stable, independent role in society”—because of structural metamorphoses in the brain. Understanding why peer influence occurs and analyzing its effect on adolescents can help juvenile facilities create environments where adolescents can learn from their mistakes and grow.  Recently, the University of Chicago Press conducted a study where adolescents were randomly assigned into peer groups to study together for an exam. The organization initially measured a student’s work ethic by four categories: how determined they were in the face of challenges, how confident they were of their academic skills, how anxious they were about their future success, and how prone they were to “engage in risky behavior”. Results of the experiment showed how studying with more persistent peers raised one’s overall GPA, whereas studying with risk-prone students had the opposite effect.  The extent of peer influence lies far beyond how adolescents perform at school, however. Dr. Laurence Steinberg from Temple University created the “Spotlight Game”—an online game where an adolescent within a Magnetic Resonance Imaging (MRI) scanner must decide to stop or go at a yellow-light intersection. The first time, the participant plays, assuming no one is watching them. The second time, however, the adolescent hears their friends’ voices through a speaker and is notified that their friends are observing them. Adolescents had more car accidents in the virtual game when informed of their peers' presence. To explain this phenomenon, Sarah-Jayne Blakemore, a psychology and cognitive neuroscience professor at the University of Cambridge, studied how the social brain—“the network of brain regions that are involved in understanding other people”—undergoes a rapid transformation during adolescence. First, the limbic system—the brain region that triggers human reward systems—is sensitive in adolescents because there is an increase in chemicals that heighten pleasure from risk-taking. In other words, adolescent brains directly view social acceptance from their peers as a reward for their risky behavior. Furthermore, the prefrontal cortex—the brain region that affects "judgment, impulse control, and planning”—develops much later than the limbic system, explaining why adolescents rely more on emotions than reasoning.  Consequently, this raises the dilemma of how adolescents should be punished for crimes. In the United States, two-thirds of juvenile facilities are correctional-style, meaning that adolescent criminals are confined from society when they commit a crime. Yet, since adolescent behavior changes with different peer influences, Michael Corriero—the founder of the New York Center for Juvenile Justice—advises that the primary goal when addressing juvenile crimes “…should be that of rehabilitation and not a punitive one”.  As explored in this essay, peers have an increasing presence in one’s habits and decision-making skills during adolescence because of their developing limbic system and prefrontal cortex. While there is still debate on how to address juvenile crimes, examining the effect of peer influence on adolescents can eventually design a world that leads adolescents one step closer to adulthood. Bibliography Brains on Trial with Alan Alda: Peer Influence and Adolescent Behavior [online video], Brains on Trial, 26 September 2013, https://youtu.be/rt9MyNo65eI?si=th1Wu_0vsn8aEG9h , (Last Accessed: 30 December 2023) Burns A. and Darling N., “Peer Pressure Is NOT Peer Influence”, The Education Digest, 82:1 (2002): 4-6 https://ucolibinstruction.files.wordpress.com/2010/10/ed-article-4.pdf Department of Psychology, “Professor Sarah-Jayne Blakemore”, University of Cambridge,  [ https://www.psychol.cam.ac.uk/staff/professor-sarah-jayne-blakemore/  Last Accessed: 30 December 2023] Golsteyn B. H. H., Non A., and Zölitz U., “The Impact of Peer Personality on Academic Achievement”, Journal of Political Economy , 129:4 (2021): 1052–1099 https://doi.org/10.1086/712638 How friendship affects your brain – Shannon Odell  [online video], TED-Ed, 16 September 2022, https://youtu.be/YmVpwXH4jhA?si=cQOV4NX6bLOmkISy , (Last Accessed: 30 December 2023) Jones T., “Brain Development During Adolescence”, Lumen Learning , [ https://courses.lumenlearning.com/wm-lifespandevelopment/chapter/brain-development-during-adolescence/#footnote-2982-1 / Last Accessed: 30 December 2023] “Michael Corriero”, Virtue Foundation , [ https://virtuefoundation.org/committee/michael-corriero/#:~:text=Judge%20Corriero%20is%20the%20Executive,York%20Center%20for%20Juvenile%20Justice./  Last Accessed: 30 December 2023] Sarah-Jayne Blakemore: The mysterious workings of the adolescent brain  [online video], 18 September 2012, https://youtu.be/6zVS8HIPUng?si=7XIffBg_9I_xdnxk , (Last Accessed: 30 December 2023)  The juvenile system is broken. Here’s what actually works. [online video], PBS NewsHour, 29 October 2021, https://youtu.be/q1fsysGy_hM?si=i7tw5YsN-AV3zb0D , (Last Accessed: 30 December 2023).  The Neuroscience of the Teenage Brain—with Sarah-Jayne Blakemore  [online video], The Royal Institution, 22 August 2018, https://youtu.be/yQXhFa8dRCI?si=d5tWUOtyjMZGeAXl , (Last Accessed: 30 December 2023). © 2023 Kaylyn K. | All rights reserved  Originally published at themedtales.com

Cramming for your finals last minute, watching your favorite k-drama, or listening to music staring at the ceiling—these are all “valid” reasons for pulling an all-nighter…right? Rory Gilmore is studying hard for her finals! What about you? *Image credit: Screenshot from Gilmore Girls, via Screen Rant* Well, what exactly happens to our bodies when we do not sleep for 24 hours? Do not fret! I’m Kaylyn Kim, your favorite teen blogger, and I’ve got scientific evidence to explain what’s going on when you pull an all-nighter. Let us dive in! 🌙 The Science of Sleep A circadian rhythm  refers to the 24-hour cycle all organisms undergo. This rhythm is influenced by light. As the sun goes down in the evening, your eyes detect this signal and send it to the brain—specifically to the suprachiasmatic nucleus  (SCN). Then, the SCN signals to the pineal gland  to release a hormone called melatonin  that communicates that you need to fall asleep. Melatonin typically spikes about 2 hours before your bedtime. At the same time, neurons in the hypothalamus and brainstem  releases GABA , a compound that allows you to relax. Around your “typical” bedtime (I know you sneaky ones sleeping at 3 am every day!), your body temperature drops, and attention decreases . ☕ Fake Energy? Adenosine  is a waste product that builds up in the brain during the day. At night, it latches onto nerve cell receptors to make you sleepy—but caffeine blocks adenosine , giving you a false boost of energy . That moment when you realize you've been reading the same sentence for 10 minutes. *Image credit: Screenshot from Gilmore Girls, via Screen Rant* 🧠 Studying Without Sleep? Your hippocampus  stores all of the information that you are trying to memorize during your late-night cramming sessions. But to convert short-term memories into long-term memories , your brain needs sleep—specifically, the neocortex . So, if you’re studying for a test far in advance , sleep is important! ⚠️ What One All-Nighter Does FUN FACT:  Did you know that being awake for 19 hours can make you behave like individuals who have been drinking alcohol ? Some people experience a brief sense of euphoria , but don’t let that tempt you into making this a habit! In the morning, your pineal gland stops releasing melatonin , so you might feel falsely alert —but your problem-solving skills and focus  will still be impaired. Later in the day, your amygdala  (which controls emotions) becomes unstable, making you irritable . (Don’t snap at your mom, kids!) Rory's facial expression = me after pulling an all-nighter and running into Paris + a math test *Image credit: Screenshot from Gilmore Girls, via Screen Rant* 💤 Why It Matters One sleepless night won’t kill you. But know that your sleep schedule impacts everything—from your risk of depression and chronic illness  to your grades . Studies show that students with a consistent sleep routine tend to have higher GPAs , so choose wisely! Balancing school, sleep deprivation, and student gov like a pro. 🌟 All-Nighter Survival Tips If life throws you into a situation where you have  to stay up, here’s what to do: Drink caffeine , but keep it under 400 mg/day (~4 cups) . Turn on the lights  and get morning sunlight  to feel alert. Avoid driving —sleep-deprived driving is dangerous. Eat balanced meals . Sleep loss can cause cravings for sugary junk that messes with your metabolism. Take a nap  once your test or task is done. You deserve it. 📌 Final Thoughts Sleep is your secret weapon —for health, mood, memory, and success. So next time you're about to stay up all night... maybe just watch one K-drama episode and go to bed. References: TED-Ed: https://youtu.be/idrbwnWLJ7w?si=FnVDDzndsVCYE0uO National Sleep Foundation: https://www.sleepfoundation.org/sleep-hygiene/why-are-all-nighters-harmful Gilmore Girls screenshots via Screen Rant All Gilmore Girls images are copyrighted by Warner Bros. Television and used here for educational and commentary purposes.

A leading cause of death worldwide, Chronic Obstructive Pulmonary Disease (COPD) is characterized by restricted airflow and breathing difficulties over time. With early intervention, COPD can be managed to slow disease progression. However, in low- and middle-income countries (LMICs), the underdiagnosis and misdiagnosis of COPD is a significant problem due to the inaccessibility of respiratory specialists and existing diagnostic methods like spirometry. This often leads to years of inadequate, costly treatment before a proper diagnosis is made.  To  address this issue, this study introduces SMART Screening, an innovative biomedical engineering solution for early COPD detection. The system leverages deep learning techniques, which is a branch of artificial intelligence that involves using filters to extract specific features or patterns from a dataset. In this case, we are analyzing cough sounds, which are unique biomarkers to identify the presence of COPD. SMART Screening employs convolutional neural networks (CNNs), which consist of various layers that each serve a specific function in the extraction process, to detect specific acoustic features from cough recordings and provide a reliable preliminary diagnosis. To enhance the model’s performance, the study implements data collected from West China Fourth Hospital and Chengdu International School, along with public databases like the Kaggle and Zenodo datasets. We trained and tested our model on around 1,800 audio recordings, and preliminary results indicate an accuracy of around 99% when tested on an unseen set of data with 188 recordings. This model is then integrated into a user-friendly mobile application to improve accessibility in low-resource settings.  Designed to complement existing diagnostic tools, this technology has the potential to significantly improve early COPD detection in underserved populations. The next step will be to focus on how well this technology works on various demographics in the world, along with how it could be implemented for other respiratory diseases. Bibliography Alqudaihi, K., Aslam, N., Khan, I., Almuhaideb, A., Alsunaidi, S., Ibrahim, N., Alhaidari, F., Shaikh, F., Alsenbel, Y., Alalharith, D., Alharthi, H., Alghamdi, W., & Alshahrani, M. (2021). Cough sound detection and diagnosis using artificial intelligence techniques: Challenges and opportunities. IEEE Access, 9, 102327–102344. https://doi.org/10.1109/ACCESS.2021.3097559 Boers, E., Barrett, M., Su, J. G., Benjafield, A. V., Sinha, S., Kaye, L., Zar, H. J., Vuong, V., Tellez, D., Gondalia, R., Rice, M. B., Nunez, C. M., Wedzicha, J. A., & Malhotra, A. (2023). Global Burden of Chronic Obstructive Pulmonary Disease through 2050. JAMA Network Open, 6(12), e2346598. https://doi.org/10.1001/jamanetworkopen.2023.46598 Cleveland Clinic. (2022, May 17). What Is COPD? Symptoms, Treatment & More | Cleveland Clinic: Health Library. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/8709-chronic-obstructive-pulmonary-disease-copd Elgendi, M., Menon, C., & Ghrabli, S. (2024). Identifying unique spectral fingerprints in cough sounds for diagnosing respiratory ailments. Scientific Reports, 14(1). https://doi.org/10.1038/s41598-023-50371-2 Kuluozturk, M., Kobat, M. A., Barua, P. D., Dogan, S., Tuncer, T., Tan, R.-S., Ciaccio, E. J., & Acharya, U. R. (2022). DKPNet41: Directed knight pattern network-based cough sound classification model for automatic disease diagnosis. Medical Engineering & Physics, 110, 103870. https://doi.org/10.1016/j.medengphy.2022.103870 Liu, Y., Carlson, S., Watson, K., Xu, F., & Greenlund, K. (2023). Morbidity and Mortality Weekly Report. In Centers for Disease Control and Prevention. https://www.cdc.gov/mmwr/volumes/72/wr/pdfs/mm7246-H.pdf National Health Service. (2021, August 18). Spirometry. NHS. https://www.nhs.uk/conditions/spirometry/ Panagiotis Kapetanidis, Fotios Kalioras, Tsakonas, C., Pantelis Tzamalis, Kontogiannis, G., Karamanidou, T., Stavropoulos, T. G., & Sotiris Nikoletseas. (2024). Respiratory diseases diagnosis using audio analysis and artificial intelligence: A systematic review. Sensors, 24(4), 1173–1173. https://doi.org/10.3390/s24041173 Patel, K., Smith, D. J., Huntley, C. C., Channa, S. D., Pye, A., Dickens, A. P., Gale, N., & Turner, A. M. (2024). Exploring the Causes of COPD Misdiagnosis in Primary care: a Mixed Methods Study. PLOS ONE, 19(3), e0298432–e0298432. https://doi.org/10.1371/journal.pone.0298432 Plum, C., Stolbrink, M., Zurba, L., Bissell, K., Ozoh, B. O., & Mortimer, K. (2021). Availability of diagnostic services and essential medicines for non‐communicable respiratory diseases in African countries. The International Journal of Tuberculosis and Lung Disease, 25(2), 120–125. https://doi.org/10.5588/ijtld.20.0762 Smith, J., Ashurst, H., Jack, S., Woodcock, A., & Earis, J. (2006). The description of cough sounds by healthcare professionals. Cough, 2(1), 1. https://doi.org/10.1186/1745-9974-2-1 Spencer, P., & Krieger, B. (2013). The Differentiation of Chronic Obstructive Pulmonary Disease from Asthma: a Review of Current Diagnostic and Treatment Recommendations. The Open Nursing Journal, 7, 29–34. https://doi.org/10.2174/1874434601307010029 World Health Organization. (2024, November 6). Chronic Obstructive Pulmonary Disease (COPD). World Health Organisation. https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd) Yao, L.-P., & Tao, R. (2021). Does Chronic Obstructive Pulmonary Disease Affect Workers’ Health? Frontiers in Public Health, 9. https://doi.org/10.3389/fpubh.2021.711629 Cover page via CreakyJoints © 2025 Kaylyn K. | All rights reserved  Originally published at themedtales.com

On January 31st at around 9 PM, American Eagle Flight 5432 collided with a UH-60 Black Hawk Helicopter while arriving at Ronald Reagan National Airport. The plane contained 60 passengers and 4 crews, while the helicopter contained 3 military members, all of whom, unfortunately, passed away. With 55 of the victims currently identified, I want to recognize all of the heroes from this tragedy, each of whom had personal backstories and lives that they could not continue. I hope my readers will understand how this event exemplifies the unexpected nature of life, provide our deepest condolences to all of the members involved in this incident, and embrace gratitude as we go on with our lives. Here is a tribute to Asra Hussain Raza, a 26-year-old wife, daughter, and daughter-in-law. Asra was born in a household of Indian immigrant parents. She graduated from Indiana University in 2020 with a master's degree in hospital management and married her husband, Hamaad Raza, in August 2023. Since then, she has always made an effort to care for others and was actually returning from a work trip to a hospital. In fact, Asra was helping others until the very end. This did not make the news of the tragedy any easier on her husband and family members, though. Asra's final message to her husband, "We're landing in 20", was soon disproved as her husband, waiting in the airport, saw that there were lines of emergency medical service (EMS) vehicles and his texts were not sending. Hamaad expresses how he often heard of events like this in the news but never expected his own loved ones to be in danger of such tragedies. Just after being married for two years, Hamaad now has to face the hurt of organizing a funeral for his wife. However, he also has a message for the world: " Life is short. Hug your loved ones. Tell them you love them when they’re getting on a flight". As consumers and readers of the news, I think it is important for us to acknowledge that these victims could easily have been our loved ones, significant others, or relatives. Taking that into account, I encourage you to be there for anyone who is suffering from the loss of their loved ones due to tragic accidents and continue to live with gratitude today. Sources: https://www.bbc.com/news/articles/cwyjpwxx22ko https://www.financialexpress.com/world-news/who-was-asra-hussain-raza-daughter-of-indian-immigrants-killed-in-us-plane-crash/3732039/   https://www.nbcwashington.com/news/local/hug-your-loved-ones-dc-man-mourns-wife-killed-in-potomac-crash/3831661/   https://www.usatoday.com/story/news/nation/2025/01/31/victims-dc-plane-crash-asra-hussain-raza/78087903007/   Cover page via Financial Express © 2025 Kaylyn K. | All rights reserved  Originally published at themedtales.com

On January 31st at around 9 PM, American Eagle Flight 5432 collided with a UH-60 Black Hawk Helicopter while arriving at Ronald Reagan National Airport. The plane contained 60 passengers and 4 crews, while the helicopter contained 3 military members, all of whom, unfortunately, passed away. With 55 of the victims currently identified, I want to recognize all of the heroes from this tragedy, each of whom had personal backstories and lives that they could not continue. I hope my readers will understand how this event exemplifies the unexpected nature of life, provide our deepest condolences to all of the members involved in this incident, and embrace gratitude as we go on with our lives. Here is a tribute to Kiah Duggins, a daughter, student, and professor missed by many in her community. Kiah Duggins was on her way home to Washington D.C. after being in Wichita, Kansas, her hometown, to support her mother undergoing surgery. Yet, her future, including being a Howard University law professor in the coming fall semester, drastically changed overnight. After graduating from Wichita East High School, Kiah entered Wichita State University, where she taught students in Taiwan English after receiving a grant from a government-funded organization called Fullbright . She participated in Full Bright's 2017 Advocacy Petition Campaign, an exchange program for sharing education worldwide, and having both beauty and brains, Kiah was also crowned Miss Butler Country in 2014 and 2015 . Fast-forward a few years, she graduated from Harvard Law School in 2021 with a Clinical and Pro Bono Outstanding Student Award. Kiah, whether it be through being the president of the Harvard Legal Aid Bureau to receiving the 2021 Cravath International Fellow Award, always strived to make a positive impact on the community around her. Following graduation, she worked at the firm Neufeld,  Scheck & Brustin and worked as an attorney at the Civil Rights Corps, constantly fighting against police misconduct and calling for reforms in the prison system across Texas and Washington D.C. Yet, even as Kiah transitioned to different phases of her career, she never forgot the path that led her there, leading workshops for Harvard Law School and encouraging the Environmental Protection Agency (EPA) to address Wichita's groundwater contamination problem. Considering the significant role that Kiah played in her community, many expressed sorrow and grief at her passing. Kiah's minister at her church in Wichita emphasized how she brightened everyone's day and loved God with all her heart. Kiah's father, Maurice Duggins, expressed , " We are coming to terms with the grief associated with the loss of our beautiful and accomplished firstborn.” Even her classmates from Harvard Law School stated, "She was the best of us". Kiah Duggins was a hero, and she will truly be missed by the world. As consumers and readers of the news, I think it is important for us to acknowledge that these victims could easily have been our loved ones, significant others, or relatives. Taking that into account, I encourage you to be there for anyone who is suffering from the loss of their loved ones due to tragic accidents and continue to live with gratitude today. Cover page via Harvard Law Today © 2025 Kaylyn K. | All rights reserved  Originally published at themedtales.com

On January 31st at around 9 PM, American Eagle Flight 5432 collided with a UH-60 Black Hawk Helicopter while arriving at Ronald Reagan National Airport. The plane contained 60 passengers and 4 crews, while the helicopter contained 3 military members, all of whom, unfortunately, passed away. With 55 of the victims currently identified, I want to recognize all of the heroes from this tragedy, each of whom had personal backstories and lives that they could not continue. I hope my readers will understand how this event exemplifies the unexpected nature of life, provide our deepest condolences to all of the members involved in this incident, and embrace gratitude as we go on with our lives. Here is a tribute to Elizabeth Anne Keys, an attorney, daughter, and partner who will be greatly missed. Elizabeth was born on January 29th, 1992 . Yet, just 33 years later on the same day, she passed away from this tragic incident. Keys' partner, David Seidman, articulated that the couple was going to celebrate her birthday once she arrived. While Elizabeth could not celebrate, she greatly contributed to the community around her during her time on Earth. Born in Cincinnati, Ohio , she graduated from Maderia High School in 2010 as her school's valedictorian. Elizabeth then studied economics and community health at Tufts University , while also being an active member of the varsity sailing team, marathon team, and Tufts Concert. Since graduating, Keys worked as an attorney at Wilkinson Skeloff Law Firm based in Washington DC. At her workplace, she was renowned for her pro bono cases, even being on the D.C. Court of Appeals Capital Pro Bono Honor Roll . In fact, she was arriving from a work trip when this accident occurred, also leading to the death of her co-worker Sarah Lee Best. While we, as readers, might not have known Elizabeth Keys on a personal level, her mother expresses that "Liz was a dear friend to so many, offering her best self to them all", and her friends and close connections all attest to her "fearlessness, humor, and sharp wit". As we step into the next chapter in our own lives, let us take a moment to recognize that all the victims of the Washington DC plane crash were as "human" as we are now with the same passions, dreams, and goals for the future. Hence, this common ground between humans further underscores the need to recognize the victims of these unfortunate accidents, just as we would want to be recognized after our deaths. Cover page via Spectrum News © 2025 Kaylyn K. | All rights reserved  Originally published at themedtales.com

Abstract  This literature review explores the role of PTEN expression in the progression of endometriosis, focusing on its impact on the cell cycle, the severity of endometriosis, and the rate of apoptosis and autophagy. Drawing on recent studies from 2009 to 2024, this review explores the underlying cellular mechanisms behind endometriosis progression concerning PTEN expression. Findings indicate that loss of PTEN gene expression leads to increased cell division, more severe forms of endometriosis, and reduced control over apoptosis and autophagy. Further research, however, is necessary to explore the complex interplay between gene expression that leads to endometriosis.  The Role of PTEN Gene Expression in the Progression of Endometriosis Endometriosis is a gynecological disorder involving abnormal endometrial growth outside of the uterus. The endometrium, also called the “innermost lining of the uterus”, typically develops during puberty but regenerates every menstrual cycle in response to steroid hormones estrogen and progesterone (Mirzaei, et al., 2021, p.45). Although endometriosis affects 10 to 15% of the female population worldwide, its exact cause remains unknown (Chycezewski et al., 2009). Endometriosis can be characterized by abnormal growth of tissues, invasion of other organs, and bleeding outside the uterus, affecting the quality of life of many women worldwide. However, currently available treatments have side effects like liver damage, weight gain, gastrointestinal discomfort, and menopause-like symptoms. Hence, research dedicated to determining the cause of endometriosis is critical in improving the diagnosis and treatment of this benign yet debilitating condition. One of the key limitations in current endometriosis research is the fact that endometriosis can only be diagnosed via invasive methods, such as a laparoscopy or laparotomy, leading to fewer diagnoses in areas without access to proper medical technologies and assistance.  Phosphatase and Tensin Homolog, often referred to as PTEN, is a type of tumor suppressor gene that regulates the cell cycle comprised of nine exons and 403 amino acids on chromosome 10q23.3 (Jia et al., 2016). Loss-of-function mutations in PTEN have been reported in around 14 to 18% of endometriosis cases, with the most common mutations being nonsense mutations (where there is a premature stop codon in the nucleotide sequence), frameshift (the insertion or deletion of nucleotides that lead to a change in the reading frame of the mRNA), missense (a nucleotide sequence change that results in coding for a different amino acid than the normal amino acid), and deletion mutation (a deletion of a single nucleotide), along with epigenetic changes (Allaire, et al., 2025).  PTEN has two significant roles during the cell cycle, including regulating the transition from G1 to S and G2 to M phases. First, during the G1 phase, cells typically grow, obtain resources from the environment, and prepare for DNA replication in the S phase. Cells can pass through this phase by activating G1 cyclin-dependent kinase and cyclin complexes, including CDK 4/6 with the D-type cyclin and CDK2 with the E-type cyclin. The activated D-CDK4/6 complex then phosphorylates the retinoblastoma protein (RB), which causes the histone deacetylase 1 (HDAC1) and transcription factor E2F-1 to detach from RB, thereby activating the genes downstream, which include cyclin E, that then attaches to CDK2 to form another complex. PTEN, located in the nucleus and cytoplasm, works by catalyzing the reaction that converts phosphatidylinositol-3, 4, 5-triphosphate (PIP3) into phosphatidylinositol-4, 5-bisphosphate (PIP2), which results in decreased cell growth and survival. PTEN inhibits the PI3K/AKT pathway, preventing the activation of cyclin-CDK complexes necessary for cells to enter the S phase, effectively halting the development of uncontrolled cell division. In the meantime, PTEN also controls the cell cycle in the G2-M transition, where cells prepare to divide in mitosis by being involved in many checkpoints requiring DNA replication to be completed successfully before division. In mitosis, PTEN facilitates the structure and binding of the mitotic spindle to the chromosomes, ensuring that an equal number of chromosomes are distributed to each daughter cell.  This literature review examines the relationship between the PTEN tumor suppressor gene and endometriosis, contending that the presence or absence of loss-of-function mutations in the PTEN gene will impact the severity of endometriosis. While many different types of genes are involved in endometriosis-like symptoms, this review focuses on the presence of the PTEN gene in cell cycle progression, the severity of endometriosis, and the rate of apoptosis and autophagy.  Review It is known that the PTEN gene controls the PI3K/AKT signaling pathway, thereby negatively regulating angiogenesis and vascular endothelial growth factor (VEGF), both of which are key processes necessary for the growth and division of cells. Many previous studies have also observed a high frequency of loss of heterozygosity (LOH) in the PTEN gene in patients with ectopic endometriosis as a result of a structural frameshift and insertion mutation at the N-terminal phosphatase region of PTEN. A study by Jia et al. (2016) aimed to isolate the role of PTEN in endometriosis in primary human endometrial cells and human-mouse chimeric endometriosis animal models, and more specifically, examine how the expression of PTEN affects the cell cycle of the primary endometrial cells after PTEN transfection and how re-initiating the PTEN expression may impact cell apoptosis, angiogenesis, and VEGF expression of endometriosis in the animal model.  To first identify the role of the PTEN gene on human primary endometrial cells, the study first synthesized and cloned the PTEN gene into pLV-IRES-PURO Plasmid. Short-hairpin RNA (shRNA)---or RNA used to prevent gene expression through a process known as RNA interference—was synthesized and inserted into pLV-2shPTEN and pLV2-shNC vectors, which carry these foreign genes into 293T cell-packed lentivirus. Ultimately, the lentivirus was used to infect the endometrial cells in vitro. The study used five groups and performed gene knockout to identify the effect of different environmental conditions on PTEN gene expression. The five groups include a blank group (used as a control), a vector group (transfected with pLV-PTEN, acting as the negative control to the over-PTEN group), an over-PTEN group (transfected with pLV-PTEN), a siNC group (a negative control to the siPTEN group), and the siPTEN group. Then, after each group was washed and centrifuged, the study used a Western blot analysis to identify patterns in the cell cycle.  The study's results supported their initial hypothesis that PTEN expression influences cell division in primary human endometrial cells. The study found that PTEN overexpression significantly increased the levels of apoptosis of endometrial cells. In contrast, low levels of PTEN expression were associated with higher levels of angiogenesis, or the growth of new capillaries, which may support tumor growth.  The journal also discovered how the overexpression of PTEN resulted in a greater proportion of cells in the G0/G1 phase, where cells are non-dividing or not yet in mitosis, while fewer cells were present in the G2/M phase, indicating that the cell cycle was arrested at the G0/G1 phase when PTEN was overexpressed. This result suggests that a loss-of-function mutation of the PTEN gene may induce increased cell division, forming an endometrial lesion or any abnormal change to an organ.  In the meantime, to isolate the role of the PTEN gene in endometriosis in animal cells, the study utilized cells from 18 female severe combined immunodeficiency (SCID) mice that were provided with food, water, and shelter and randomly selected to be studied. Their endometrial samples were then pre-cooled, washed, and centrifuged. The study quantified PTEN expression in animal models through the presence or absence of brown granules in the cytoplasm and the nucleus. The researchers then used a score ranging from 0 to 3 to categorize the level of PTEN expression; a score of 0 signified no PTEN expression, a score of 1 signified 1-25% of cells with PTEN expression, a score of 2 signified 26–49% of cells with PTEN expression, and a score of 3 signified >50% cells with PTEN expression. The study also considered the intensity of the brown color to truly identify whether the difference between the control and experimental groups was significant.  Eventually, Jia et al. found that the percentage of PTEN-positive cells, or those that displayed brown granules, was significantly greater in the over-PTEN group than in the control and si-PTEN groups. The VEGF-positive cells, however, were greater in the si-PTEN group than in the control and over-PTEN groups, confirming the general theory that PTEN is responsible for negatively regulating the expression of VEGF.  While the results of this study display how angiogenesis and the expression of VEGF are critical to providing the energy and resources necessary for mutated/abnormal tissues to survive and continue proliferating, they do not yet guarantee that re-introduction of the expression of the PTEN gene in patients will lead to positive clinical outcomes. Hence, this may suggest that PTEN has a multifaceted role in preventing ectopic tissue growth by regulating angiogenesis, apoptosis, and cell cycle checkpoints.  Building on these findings,  Allaire et al. (2025) observed patterns of PTEN somatic loss in individuals at different stages of endometriosis, categorizing individuals as having SUP (superficial peritoneal endometriosis), DE (deep endometriosis), and OMA (ovarian endometrioma). DE and OMA were considered the "severe" anatomic subtypes of endometriosis. In contrast, SUP was classified as the "mild" anatomic subtype to test the hypothesis that somatic PTEN loss is more common in patients with severe types of endometriosis (DE and OMA) than in those with mild forms (SUP).  This longitudinal study was conducted from 2013 to 2017 at the BC Women's Center for Pelvic Pain and Endometriosis. It used immunohistochemistry staining to identify the presence of the loss of PTEN gene expression in the cytoplasm of endometrial cells. The IHC scoring had four primary categories to identify whether there was a loss of PTEN expression in patients with the categories ranging from 0% loss in epithelial cells, 1-10% loss, 11-49% loss, and 50-100% loss. This study only considered loss in the expression of the PTEN gene of a patient with endometriosis if there were at least 10 nearby endometriosis epithelial cells with the PTEN loss.  Allaire et al. used endometriosis patients' anatomic subtypes, the rARSM scale (I-IV)—a scale used to determine the severity of endometriosis—, and patient outcome (quantified via pain score and surgical difficulty) to identify whether there is an actual correlation between the PTEN gene expression and endometriosis severity and outcome.  While the study did not specifically identify what mutation in the PTEN gene led to the loss of expression of the PTEN, the study ascertained that PTEN somatic loss is present more frequently in severe anatomic subtypes and higher stages of endometriosis with around 72.7% of participants with DE or OMA (either but not both conditions) having PTEN loss. In contrast, only 46.4% of the SUP patients had PTEn somatic loss. Moreover, 81% of individuals with Stage IV endometriosis had a somatic loss of PTEN expression, whereas only 47.8% of individuals with Stage I endometriosis did not express PTEN. Indeed, it is difficult to determine whether this correlation can also be considered a cause-and-effect relationship; however, these findings display how a loss-of-function mutation of the PTEN tumor suppressor gene may be responsible for severe conditions associated with endometriosis. Also, other genes may be involved in the presence or absence of endometriosis, including ARID1A, suggesting further research in this area. As a result of this association between PTEN loss and severity of endometriosis, this could lead to greater disease burden and difficulties during surgery. This study found that PTEN loss was correlated with longer surgical times in non-white ethnicity/race demographics. However, non-white ethnicity/race groups also had greater pain levels and scored higher on the rARSM scale, indicating that factors other than PTEN loss may have contributed to this result. In general, however, the study did not find any association between PTEN loss and post-operation pain level or the frequency of reoperation.  Although the previous two studies primarily focused on the role of PTEN expression on the cell cycle and endometriosis severity, Choi et al. (2017) studied how PTEN affects the PI3K/AKT/mTOR pathway to change levels of apoptosis and autophagy. Apoptosis is a type of programmed cell death (PCD), and reduced apoptosis in endometrial cells has been associated with increased survival of endometrial cells in abnormal locations of the body, potentially causing the symptoms of endometriosis. Autophagy is another type of PCD, where autophagosomes—areas of cytoplasm enclosed in double membranes—mature and combine with lysosomes to be degraded. Previous hypotheses believed that autophagy was an evolutionary mechanism that resulted from a response to a lack of nutrients or resources in an environment for the survival of organisms. However, autophagy has also been shown to play a significant role in the development of endometriosis, since mTOR, a negative regulator of autophagy, is de-repressed in endometriosis, leading to decreased autophagy and apoptosis. As a result, PTEN has been speculated to be involved in the negative regulation of the mTOR pathway. However, based on the limited research on the effect of the PTEN gene expression on the regulation of autophagy, Choi et al. exposed endometrial cells to progesterone, a hormone produced in the ovaries, to identify how a lack of PTEN gene expression affects apoptosis and autophagy. This study initially hypothesized that the percentage of cells in apoptosis and autophagy in normal endometrial cells would increase in the presence of progesterone.  To start, the study collected normal endometrial stromal cells (NESCs) and endometriotic cyst stromal cells (ECScs), rinsed them with PBS to eliminate unwanted debris, and cultured them with 1 mL of culture medium. (Stromal cells are tissue cells that connect other tissues and organs.)  All NESC and ECSC groups were treated with sex steroids, oestradiol, or progesterone, for 72 hours and pre-cultured in a serum-free Earle's Balanced Salt Solution (EBSS) medium. Then, some groups of cells were exposed to PTEN and progesterone inhibitor treatments so that the researchers could observe the effect of blocking progesterone on apoptosis and autophagy. Ultimately, by using a Western blot technique, the researchers determined AKT activity by identifying the number of phosphorylated (activated) AKT, mTOR pathway activity by finding the number of phosphorylated ribosomal protein S6 kinase (S6K), which is a substrate in this pathway, and endometrial cell apoptosis rate by evaluating the number of cleaved poly ADP-ribose polymerase (PARP) and cleaved caspase-3. This study used immunofluorescence to identify each of the factors involved in these pathways, along with transmission electron microscopy to assess whether the level of AKT activity, mTOR pathway, and apoptosis rate in the NESCs significantly differed from that of the ECSCs.    The study found, as expected, that the estrogen-treated NESCs in the presence of progesterone had increased levels of PTEN and decreased AKT and S6K levels. Yet, after using the progesterone and PTEN inhibitors, PTEN expression decreased, and AKT and S6K phosphorylation decreased.  This study, however, did not solely want to confirm the theory that PTEN expression leads to increased apoptosis. Hence, researchers went a step further by evaluating whether PTEN-mediated autophagy stimulated apoptosis in NESCs. Results showed that the progesterone-treated NESCs had increased levels of cleaved PARP and cleaved caspase-3 compared to those of the estrogen-treated NESCs, displaying how apoptosis increased by around 2.23-fold when progesterone was present. Finally, when the amount of phosphorylated AKT and S6K was measured in estrogen-treated and progesterone-treated NESCs, the study found that the removal of both steroids led to significantly higher levels of PTEN expression and decreased levels of phosphorylated AKT and S6K expression, providing insight into how PTEN regulates these proteins in the presence of steroid hormones.  This study determined that steroid hormones increase PTEN expression, which regulates the AKT/mTOR signaling pathway in normal endometrial stromal cells, leading to autophagy, which, in turn, leads to increased apoptosis. On the other hand, endometriosis stromal cells do not adequately respond to progesterone, which decreases PTEN expression, preventing the inhibition of the AKT/mTOR pathway, and leading to decreased apoptosis.  At the end of the day, endometriosis continues to be an obscure medical condition. Previous studies have found that endometriosis may have a genetic basis, with Simpson et al. discovering in 1980 that individuals with endometriosis had 5.9% of mothers and 8.1% of sisters with endometriosis as well; on the other hand, individuals without endometriosis had a significantly lower percentage of mothers and sisters with endometriosis. Additionally, patients with endometriosis in families with endometriosis also tend to display more severe symptoms of endometriosis, posing the question of whether endometriosis can be inherited across generations as well.  Cardon et al. (2004) hypothesized that endometriosis may display familial clustering—or the chance that a disease or trait might appear more frequently in members of the same family than by random chance alone—and used a large rhesus monkey population to identify whether this pattern was valid. The study found that monkeys have a higher risk of being affected by endometriosis if they are closely related to other female monkeys currently affected by endometriosis, indicating that endometriosis may have a hereditary basis.  Conclusions In overview, tumor suppressor genes like PTEN often play significant roles in various biological pathways, including pathways that control apoptosis, cell division, and the progression of endometriosis. From the studies reviewed, PTEN expression is critical in limiting excess cell division or creation by regulating the PI3K/AKT/mTOR pathway. Loss-of-function mutations in the PTEN gene, however, may lead to the formation of ectopic cysts and more severe stages of endometriosis, leading to greater surgery difficulty or increased pain levels. As a result, a deeper understanding of the cellular mechanism that drives endometriosis and identifying the genes involved in this condition can lead to the establishment of more effective diagnostic tools and treatments in the future. References Brandmaier, A., Hou, S.-Q., & Shen, W. H. (2017). Cell cycle control by PTEN. Journal of Molecular Biology , 429 (15), 2265–2277. https://doi.org/10.1016/j.jmb.2017.06.004 Choi, J., Jo, M., Lee, E., Hwang, S., & Choi, D. (2017). Aberrant PTEN expression in response to progesterone reduces endometriotic stromal cell apoptosis. Reproduction , 153 (1), 11–21. https://doi.org/10.1530/rep-16-0322 HANSEN, K. A., & EYSTER, K. M. (2010). Genetics and genomics of endometriosis. Clinical Obstetrics and Gynecology , 53 (2), 403–412. https://doi.org/10.1097/grf.0b013e3181db7ca1 Lv, J., Zhu, Q., Jia, X., Yu, N., & Li, Q. (2016). In vitro and in vivo effects of tumor suppressor gene PTEN on endometriosis: An experimental study. Medical Science Monitor , 22 , 3727–3736. https://doi.org/10.12659/msm.901091 P Laudanski, J Szamatowicz, Kowalczuk, O., M Kuźmicki, M Grabowicz, & L Chyczewski. (2009). Expression of selected tumor suppressor and oncogenes in endometrium of women with endometriosis. Human Reproduction , 24 (8), 1880–1890. https://doi.org/10.1093/humrep/dep175 Simpson, J. L., Elias, S., Malinak, L. Russell., & Buttram, V. C. (1980). Heritable aspects of endometriosis. American Journal of Obstetrics and Gynecology , 137 (3), 327–331. https://doi.org/10.1016/0002-9378(80)90917-5 Tucker, D. R., Lee, A. F., Orr, N. L., Alotaibi, F. T., Noga, H. L., Williams, C., Allaire, C., Bedaiwy, M. A., Huntsman, D. G., Köbel, M., Anglesio, M. S., & Yong, P. J. (2024). Somatic PTEN and ARID1A loss and endometriosis disease burden: A longitudinal study. Human Reproduction , 40 (2), 296–309. https://doi.org/10.1093/humrep/deae269 Zahmatkesh, E., Khoshdel-Rad, N., Mirzaei, H., Shpichka, A., Timashev, P., Mahmoudi, T., & Vosough, M. (2021). Evolution of organoid technology: Lessons learnt in co-culture systems from developmental biology. Developmental Biology , 475 , 37–53. ScienceDirect. https://doi.org/10.1016/j.ydbio.2021.03.001 Zondervan, K. T. (2004). Familial aggregation of endometriosis in a large pedigree of rhesus macaques. Human Reproduction , 19 (2), 448–455. https://doi.org/10.1093/humrep/deh052 Cover photo via PTEN Research © 2025 Kaylyn K. | All rights reserved Originally published at themedtales.com

There are two primary types of strokes, including ischemic and hemorrhagic strokes. Ischemic strokes occur when there is a paucity of blood supply to the brain, which depletes oxygen and key nutrients necessary for the brain to function. This leads to the degradation of brain cells, which can have significant long-term consequences on an individual. In the meantime, hemorrhagic strokes occur when there is a brain hemorrhage, or in other terms, blood vessels in the brain break, causing an accumulation of blood in the brain that increases pressure and leads to brain cell damage as well. To identify whether you or someone around you has a stroke, look for the following symptoms: Inability to comprehend speech Sudden numbness in body parts (including the inability to raise both of one's arms or mouth to stay firm) Reduced, double, or blurred vision Headache, vomiting, or dizziness Reduced coordination (difficulty in walking properly) When you notice these initial symptoms, you must remember the acronym FAST. F stands for face. Check if the person's face is drooping or paralyzed. A stands for arms. Check if the person can still move both arms. S stands for speech. Is the person able to repeat a phrase word-by-word without slurring? T stands for time. If you notice any of the symptoms above, you must prioritize acting quickly by calling for emergency medical guidance. There are various underlying causes of stroke and risk factors that can increase the possibility of its occurrence. For ischemic strokes---the most frequent type of stroke---, fatty deposits, blood clots, or debris blood vessels accumulate in the brain's blood vessels, leading to the constriction of blood flow through these vessels (a condition referred to as ischemia, and hence, the name ischemic stroke). Since risk factors like obesity, having a sedentary lifestyle, excess drinking, or consumption of illegal drugs can all lead to the narrowing or blocking of blood vessels, individuals must be wary of what they consume and are exposed to. Hemorrhagic strokes are typically caused by high blood pressure, head trauma, protein deposits in blood vessels, or ischemic strokes. Hence, individuals must manage hypertension with medicine, a diet without excess cholesterol or saturated fat, and nearly 30 minutes of physical activity every day. Current medications for strokes include anti-platelet drugs and anticoagulants. To start, platelets are types of cells that are responsible for blood clot formation. Hence, anti-platelet drugs like Plavix (for individuals who have experienced minor strokes) or Ticagrelor are effective in decreasing the chance of blood clot formation in blood vessels. Likewise, anticoagulants, also called blood-thinning medications, prevent blood clotting. The most common anticoagulants are Heparin, which is often used as a quickly effective response in hospitals, and warfarin with a slower yet powerful effect. I hope this article taught you more about the mechanism behind strokes, along with symptoms, causes, potential preventative measures, and medications for stroke. By understanding the initial signs of strokes and how to act accordingly, you may one day be able to help a fellow human in need, which I believe is the ultimate goal of medicine. Source: https://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/syc-20350113 Cover photo via Hamilton Health Sciences © 2025 Kaylyn K. | All rights reserved  Originally published at themedtales.com

This excerpt attempts to inform readers on how stem cells are being used to advance genetic engineering, along with addressing some of the current controversies regarding this research. Stem cells are uncategorized cells that can infinitely divide themselves and have the potential to become other kinds of cells. They can be found in the brain, bone marrow, skeletal muscles, and embryo. Mentioning embryos, there are two main types of stem cells. The first is embryonic stem cells. They are created through a process called in vitro fertilization, which, to give you a brief overview, is a process that involves using the totipotent stem cells from an embryo for surgical purposes. Totipotent means that they have total potential to become any other kind of cell. The other predominant cell type is adult stem cells; these are the ones that our body uses when, for example, you get your arm burnt and need extra skin cells to replace the damaged ones. As mentioned previously, in vitro fertilization is the process of creating embryos in the laboratory. To walk you through the process, the sperm fertilizes the egg, and this forms a single, synthesis cell known as the zygote, shown in the image below. Through mitosis, this zygote divides until it forms a blastocyst, which is a cluster of 150-200 cells. In the blastocyst, there is the inner cell mass consisting of totipotent stem cells. These can be taken out through electricity or chemicals. Similar to in vitro fertilization, therapeutic cloning is another way of using embryonic stem cells. It involves taking an egg from a donor and a skin cell from a patient. Then, the doctor/surgeon/scientist can remove the DNA of the egg and replace it with the DNA of the patient’s skin cells. Through chemicals, the embryo dies, but the stem cells survive, which is then inserted into the patient. Earnest McCulloch and James Till were the true pioneers of stem cell research. In the 1960s, they discovered how hematopoietic (blood-making) stem cells were able to convert into any other kind of blood cell. But President Bush, through the Stem Cell Enhancement Act of 2005, banned the funding of cell research by the government. In 2009, this ban was lifted by President Obama. But why did these scientists want to learn more about stem cell therapy? First, stem cell therapy can treat cardiovascular and blood-related diseases by replacing the cells damaged by the disease with new stem cells. One day, this might also help regenerate organs, which is critical since there are not a lot of organ transplants readily available in proportion to those who are sick. Yet, there are many ethical implications to doing this. First, both vitro-fertilization and therapeutic cloning involve destroying a human blastocyst. So, research and development institutions face the difficult question, “When does life begin?” If, according to religion, life begins from conception, then using embryonic stem cells is essentially murder. But is it okay because these embryos are made in the laboratory and are not inserted into a woman’s body? Some pro-lifers support this since they believe conception is also relative to where development occurs. Hence, at the end of the day, religion and politics play a strong influence in answering this question. This is why institutions must provide informed consent and any information about the donors must be kept strictly confidential. To conclude, how does stem cell therapy change our world? First, there is a correlation between aging and the number of stem cells in the body, so this can potentially lead to cures to delay aging. Second, there might no longer be a need for organ donors anymore. But ultimately, stem cell research will influence our generation and those who come after us. It can provide treatments for the diseases that 100 million Americans currently have. So, today, I invite you to look briefly into stem cell research. After all, it could impact you, your family, or your future children one day. Works Cited Brazier, Yvette. “Stem Cells: Sources, Types, and Uses.” MedicalaNewsToday , 19 Oct. 2018, www.medicalnewstoday.com/articles/323343#donating-and-harvesting . Accessed 23 Mar. 2024. Harvard University. “Stem Cells: A Brief History and Outlook.” Science in the News , 3 Jan. 2014, sitn.hms.harvard.edu/flash/2014/stem-cells-a-brief-history-and-outlook-2/ . Accessed 23 Mar. 2024. Lo, Bernard, and Lindsay Parham. “Ethical Issues in Stem Cell Research.” Endocrine Reviews , vol. 30, no. 3, 14 Apr. 2009, pp. 204–213, www.ncbi.nlm.nih.gov/pmc/articles/PMC2726839/ , https://doi.org/10.1210/er.2008-0031 . Accessed 23 Mar. 2024. Moradi, Mike. “Why Stem Cells Could Be the Medical Innovation of the Century.” World Economic Forum , 16 Jan. 2020, www.weforum.org/agenda/2020/01/how-will-stem-cells-impact-the-future-of-medicine/ . Accessed 23 Mar. 2024. White, Deborah. “Arguments for and against Embryonic Stem Cell Research.” ThoughtCo , 24 May 2019, www.thoughtco.com/pros-cons-of-embryonic-stem-cell-research-3325609 . Accessed 23 Mar. 2024. Image Citation Dahal, Prashant. “Zygote- Definition, Examples, Formation, Development, Challenges.” Microbe Notes , 3 Aug. 2023, microbenotes.com/zygote/ . Accessed 23 Mar. 2024. © 2024 Kaylyn K. | All rights reserved  Originally published at themedtales.com

This easy-to-understand study guide strives to give a brief overview of how proteins are produced. OVERVIEW OF PROCESS mRNA (messenger RNA) is produced. The mRNA strand leaves the nucleus and heads for the ribosome/cytoplasm area. The tRNA strands (connected to amino acids) match with the mRNA strand. A long amino-acid chain is produced. Proteins can be formed with these amino-acid chains (AKA polypeptides). KEY TERMS Enzyme: a kind of protein that expedites chemical processes Most enzymes end with the phrase "ase" Example) RNA polymerase, DNA polymerase DNA: deoxyribonucleic acid The genetic information that most of our cells contain in the nucleus Double-helix structure Gene: segments of the DNA that produce a specific protein and, in turn, determine a specific trait Allele: different kinds of genes Example) One gene can code for hair color (broader term), but one allele would code for brown hair (more specific). RNA: ribonucleic acid Typically single-stranded Different kinds) mRNA, tRNA, etc. Protein synthesis: the process in which proteins are produced Central Dogma: a term referring to how information goes from transcription (DNA --> RNA) to translation (RNA --> Amino Acids) Protein: molecules that help organisms survive Amino Acids: the material that the protein is made up of There are 9 essential amino acids that humans need to survive. Promoter: the marker that indicates where the RNA polymerase should attach to the DNA strand Terminator: the marker that indicates where the RNA polymerase should detach from the DNA strand Codons: a system for counting the nucleotide sequences in groups of 3 (triplets) Nucleotide: the material in which nucleic strands are made up of (both DNA and RNA have) DNA: Contains 1 nitrogenous base, 1 deoxyribose sugar, and 1 phosphate RNA: same as DNA, except that it contains a ribose sugar, instead of a deoxyribose one Ribosome: an organelle where protein synthesis takes place Made up of rRNA (ribosomal RNA) Has three sites for the tRNAs to briefly stay and pass on the amino acids Sites A, P, E --> The tRNAs rotate their locations in that respective order FIRST STEP: Transcription KAYLYN TIP #1 Transcript often refers to the written documents of a video, so you can remember transcription as changing one form of something into another form . In this case, DNA turns into mRNA. Location: nucleus DNA is unzipped by the RNA polymerase at the promoter. The RNA polymerase "reads" the DNA's bases and creates complementary pairs. Typically, adenine goes with thymine, but this time, thymine is replaced with a base pair called uracil. Guanine goes with cytosine (and vice versa) This forms an mRNA (messenger RNA) strand. It is then edited and sent out of the nucleus and into the cytoplasm. SECOND STEP: Translation KAYLYN TIP #2 It's all in the name! Translating a speech from one language to another is like translating RNA nucleotides into a chain of amino acids. Location: Cytoplasm/Ribosome The cytoplasm consists of tRNA (transfer RNA) strands that each have an amino acid attached to it. The tRNA strands "read" the mRNA's bases in threes (codons) and bind to the mRNA if they are complementary. EXTRA INFO: Each tRNA strand is called an "anticodon". Translation first starts at the start codon. While the tRNA strand leaves to find another matching codon, the tRNA will leave the amino acids behind, gradually making a long chain of amino acids. This continues until the stop codon indicates that the polypeptide (chain of amino acids) is complete. [NOTE: The following explanation is extremely simplified.] The final step differs for every kind of protein, but it typically requires multiple polypeptides to bond and fold into the shape of a specific kind of protein. Here are the sources I used to make this study guide. Feel free to look at these resources for more information! https://youtu.be/oefAI2x2CQM?feature=shared https://medlineplus.gov/ency/article/002222.htm https://my.clevelandclinic.org/health/articles/21532-enzymes https://www.khanacademy.org/science/ap-biology/heredity/mendelian-genetics-ap/v/alleles-and-genes#:~:text=Genes%20and%20alleles%2C%20two%20fundamental,traits%20such%20as%20eye%20color . https://www.khanacademy.org/science/biology/gene-expression-central-dogma/translation-polypeptides/a/trna-and-ribosomes https://www.genome.gov/genetics-glossary/Nucleotide https://medlineplus.gov/genetics/understanding/howgeneswork/protein/ https://www.cancer.gov/publications/dictionaries/genetics-dictionary/def/nucleotide https://youtu.be/hok2hyED9go?feature=shared Image Credits: https://stock.adobe.com/kr/search?k=dna+transcription https://studymind.co.uk/notes/transfer-rna/ © 2024 Kaylyn K. | All rights reserved  Originally published at themedtales.com