Editorial Board: VolumE X
editor-in-Chief
Audrey Cheng ’25
exeCutive editor
Jenny Zhao ’25
direCtor of ProduCtion
Aileen Ryu ’25
senior assoCiate editors
Mahika Kasarabada ’26
Ava Martoma ’25
design editor
Gloria Yu ’26
subMission editors
Clare Pei ’26
Ainsley Walters ’27
Ethan Zhu ’26
Henry Tsai ’26
Alice Xie ’26
Cancer is a devastating disease that not only impacts those diagnosed, but also their loved ones. Many have encountered this troubling disease, either experiencing it personally or supporting someone who has. Those fortunate to overcome cancer often describe it as one of the most challenging times of their life, riddled with suffering, pain, and grief. While most people understand cancer as a deadly incurable disease, few truly understand the complexities behind the mechanics of it and why it’s so hard to treat.
The development of cancer in the body starts with a deoxyribonucleic acid (DNA) (Koeffler et al., 1991). The mutation causes an imbalance in cell proliferation, causing the cancer cells to multiply without restriction and ignore signals that call for apoptosis (cell death) or ceasing of division. As the equilibrium between cell division and death is disrupted, many systems halt function, which leads to life threatening effects for the host (Kashyap & Dubey, 2022). Cancer can form in any cell of the body, at any time, even while in the womb. Risk of cancer can be passed down through the family if the mutation is present in a parent’s egg or sperm cell; up to ten percent of cancer results from inherited genetic alterations. For instance, Hereditary Cancer Syndrome, an uncommon disorder in which blood relations have higher risk of obtaining the same types of cancer, is due to certain cancer-related gene variants continually being inherited. Common epigenetic or environmental factors may also cause family members to develop the same disease, such as tobacco use or polluted drinking water. A common misconception is that cancer itself is passed from parent to child. Neither genetic changes in tumor cells nor cancer can be directly bequeathed, but a specific genetic mutation that raises the risk of cancer advancement may be. Furthermore, receiving a cancer-related gene variation does not necessarily imply the existence of cancer, although it considerably increases the holder’s chances (National Cancer Institute, 2024).
However, not just any genetic change leads to cancer. The accumulation of specific mutations or just an unfortunate one can lead to normal cells making the transition to cancerous cells. There are also certain types of genetic modifications sorted into categories that commonly induce cancer. Some mutations, such as the point mutation, may affect a single DNA nucleotide. The mutation may remove or even replace it with a different nucleotide, bringing about major damage. An example of a point mutation is the replacement of a single nucleotide base in the Kirsten Rat Sarcoma Virus (KRAS) gene (National Cancer Institute, 2024). This simple change leads to the abnormal increase of K-Ras protein that promotes the development and advancement of tumors by activating proteins at the cell surface which signals cells to continually reproduce. The KRAS gene point mutation is especially potent in those who have or currently smoke. Another type of genetic mutation is when segments of DNA are reordered, copied, or eliminated. This type of change is called chromosomal rearrangement. An example of a chromosomal rearrangement is Chronic Myelogenous Leukemia, a type of blood cancer caused by the placement of the Breakment Cluster Region (BCR) gene next to the Abelson Murine Leukemia (ABL) gene (National Cancer Institute, 2024). This causes an irregular protein to form, called BCR-ABL, that stimulates leukemia cell growth in bone marrow and prevents apoptosis. However, not all cancerous variants happen in the DNA; some cancer-causing mutations affect DNA segments that act like the activation switch for other genes. A particular instance of this are some brain cancer cells that have many triggered switches next to other genes to promote cell growth. Another DNA change classified as epigenetic changes or epimutations can also lead to cancer. Epigenetic changes can be revocable and do not actually affect the DNA code. Instead, epimutations alter how DNA is arranged in the nucleus of a cell, which influences the amount of protein a particular gene creates. Epigenetic
changes can also be caused by specific environments and substances, such as heavy metals like lead and arsenic, smoke from cigarettes and vapes, and viruses like the Epstein-Barr virus, a common contagious virus spread through saliva that attaches to white blood cells, making it hard to fight infections (National Cancer Institute, 2024). Exposure to radiation and carcinogens from bad lifestyle choices such as smoking and bad diet can also lead to the appearance of cancer (Davey, 2020). A common case of this is skin cancer, which is caused by too much ultra-violet (UV) radiation from unprotected exposure to the sun.
For some cancers, as cancer cells grow, a clump of tissue called a tumor develops. While the tumor enlarges, the cancer cells push on and enter surrounding tissues and lymph nodes, which allows the tumor’s passage to other organs and vital systems (Wein, 2024). The cancer cells, called local invasion or invasive cancer, also secrete enzymes that break down nearby tissues and normal cells as they grow, aiding its exploit to the rest of the body. Some invasive cancers can progress to become metastatic (Canadian Cancer Society, n.d.). Once the metastatic cancer successfully expands its region, it forms new tumors, which further advances the growth of the cancer. The cancer then effectively spreads from its primary organ to the entirety of the body, leading to fatal damage from which most people cannot recover. The metastasis process is what usually makes cancer lethal to one’s life. When a cancer metastasizes, it usually becomes classified to be stage IV cancer, which is notoriously hard to overcome (Metastatic Cancer, 2025a). Patients suffering from metastatic cancer have significantly lower survival rates than those ailing from localized cancer. Over ninety percent of cancer-related deaths are caused by metastatic disease. Therefore, it is highly beneficial to remove cancer before it becomes metastatic, as once it develops as such, death does not follow far (Seyfried and Huysentruyt, 2013).
Despite major advancements in cancer technology, prominent issues with cancer still persist in relation to resistance to treatment (Chakraborty & Rahman, 2012). Cancer is caused by genetic mutations, and as time progresses, additional new mutations develop and accumulate in the body, leading to various sets of mutations throughout. Within a single tumor, the cancer cells are not identical as the cells contain different sets of mutations, each
requiring a distinct treatment in order to be removed. As a result, identifying the correct medications and utilizing accurate treatment plans becomes tedious work. In fact, cells that survive the treatments may repeatedly multiply in numbers, increasing the severity of the cancer, and can even develop new mutations which give potential into spreading and surviving in other bloodstreams of the body (Worldwide Cancer Research, n.d.). This poses a critical concern for patients as several costly treatments are administered without the proper guarantee that all cancer cells will be destroyed.
Cancer stem-cells, or cells that hold stem-cell like properties, are hard to target during treatment. During usage, many drugs have been found to have benefits towards the regression of a tumor but fail to remove the stem cells. Gleevec, a notable drug used to treat Chronic Myelogenous Leukemia, is a striking example of this conclusion. It works by targeting the ATP binding site in BCRABL proteins and aims to stop tyrosinase activity. While the drug itself holds promising effects, cancer stem cells are shown to withstand Gleevec, leading to recurrences of cancer tumors upon discontinuation (Chakraborty & Rahman, 2012).
Many cancer treatments also rely on complex mechanisms between the drug and the proteins within the body in order to be activated. Thus, in order for cancer cells to prevent the effectiveness of these drugs, deactivation is necessary. Cancer cells perform this action by producing proteins and enzymes that inhibit the activation of the drug. One key example of this is demonstrated by the relationship with cancer and the drug AraC, which uses phosphorylation reactions to activate and treat acute myeloid leukemia. AraC is not designed to have an immediate impact among cancer cells, but when phosphorylated with enzymes deoxycytidine kinase, uridine and cytidine monophosphate kinase, and nucleoside diphosphate kinase, it becomes lethal to cancer cells. However, cancer-produced proteins and enzymes included in the activation process may emerge with mutations, causing the activity of AraC to become reduced. Cancer cells become drug-resistant and as a result AraC provides no efficient use to treatment (Mansoori, September 2017).
Cancer is a deadly disease and all for a good reason. While many treatments have been made to withstand
the series of mutations, much research is needed in order to ensure a guaranteed cure for patients. Still, technology and other developments are on the rise to maximize the number of improved outcomes for cancer, and with a collective effort from medical professionals, scientists, and researchers, the world can hope for a more effective remedy in the near future.
Canadian Cancer Society / Société canadienne du cancer. (n.d.). How cancer starts, grows and spreads. Canadian Cancer Society. https://cancer.ca/en/cancer-information/what-is-cancer/how-cancer-starts-growsand-spreads
Chakraborty, S., & Rahman, T. (2012, November 14).
The difficulties in cancer treatment. Ecancermedicalscience. https://pmc.ncbi.nlm.nih.gov/articles/ PMC4024849/
Coelho, M. A., Strauss, M. E., Watterson, A., Cooper, S., Bhosle, S., Illuzzi, G., Karakoc, E., Dinçer, C., Vieira, S. F., Sharma, M., Moullet, M., Conticelli, D., Koeppel, J., McCarten, K., Cattaneo, C. M., Veninga, V., Picco, G., Parts, L., Forment, J. V., … Garnett, M. J. (2024, October 18). Base editing screens define the genetic landscape of cancer drug resistance mechanisms. Nature News. https://www. nature.com/articles/s41588-024-01948-8
Davey, R. (2020, December 14). Investigating the molecular mechanisms of cancer. News. https:// www.news-medical.net/life-sciences/Investigating-the-Molecular-Mechanisms-of-Cancer.aspx
The Genetics of Cancer. NCI. (2024, August 8). https:// www.cancer.gov/about-cancer/causes-prevention/ genetics
Kashyap, A. K., & Dubey, S. K. (2022, January 21). Molecular mechanisms in cancer development. https:// www.sciencedirect.com/science/article/abs/pii/ B9780323998833000160
Koeffler, H. P., McCormick, F., & Denny, C. (1991, November). Molecular mechanisms of cancer. The Western journal of medicine. https://pmc.ncbi.nlm. nih.gov/articles/PMC1003063/
Mansoori, B., Mohammadi, A., Davudian, S., Shirjang, S., & Baradaran, B. (2017, September). The different mechanisms of cancer drug resistance: A brief review. Advanced pharmaceutical bulletin. https:// pmc.ncbi.nlm.nih.gov/articles/PMC5651054/
Metastatic cancer: When cancer spreads. NCI. (2025a, January 17). https://www.cancer.gov/types/metastatic-cancer
National Cancer Institute. (2024, August 8). The genetics of cancer. National Cancer Institute. https://www. cancer.gov/about-cancer/causes-prevention/genetics
Seyfried, T. N., & Huysentruyt, L. C. (2013). On the origin of cancer metastasis. Critical Reviews in Oncogenesis, 18(1-2), 43–73. https://doi.org/10.1615/critrevoncog.v18.i1-2.40
Wein, H. (Ed.). (2024, June 17). How cancer cells spread in the body. National Institutes of Health. https:// newsinhealth.nih.gov/2017/04/how-cancer-cellsspread-body.
Worldwide Cancer Research. (n.d.). Why is cancer so hard to cure?. Why Is Cancer So Hard To Cure? https://www.worldwidecancerresearch.org/information-and-impact/cancer-myths-and-questions/whyis-cancer-so-hard-to-cure/.
Wu, Y., Song, Y., Wang, R., & Wang, T. (2023, June 15).
Molecular mechanisms of tumor resistance to radiotherapy - molecular cancer. BioMed Central. https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-023-01801-2
Nicole Li ’27
In 1987, psychologist Ole Ivar Lovaas from the University of Los Angeles created a program to conduct a study using Applied Behavioral Analysis (ABA), and treated 19 children with autism (Carpenter, 2015). Lovaas announced that nearly half of the children who participated in the program “recovered” from autism, no longer displaying any symptoms (Carpenter, 2015). However, his report has been scrutinized heavily for its ambiguity and lack of specificity, as it was most likely over exaggerated. The study was unsuccessful in demonstrating that all autism symptoms had vanished, prompting skepticism to the plausibility of a “cure” to autism. Today, most clinicians and experts still agree that autism is a lifelong condition.
The Autism Spectrum Disorder (ASD) is a complex neurological condition characterized by difficulties in social interactions, communication, and repetitive and unusual behaviors (Webb & Jones, 2009). Symptoms in early childhood include lack of eye contact, limited language and speech development, and difficulty in using or understanding body language. Because autism manifests differently across individuals, ranging from mild difficulties to significant impairments, autism is considered a spectrum disorder. The condition is often misunderstood and has several myths circulating around it, such as that autism is a disease.
Over the decades, significant research has focused on understanding the complexities of ASD. While Lovaas’ study certainly opened doors to exploration in the “recovery” of autism, a study published in the Journal of Child Psychology and Psychiatry further delved into this complex phenomenon (Fein et al., 2013). The research compared three groups: 34 optimal outcome (OO) individuals, 34 typically developing (TD) individuals, and 44 individuals with high-functioning autism (HFA) (Fein et al., 2013). The participants ranged from 8 to 21 years old to ensure a thorough examination of developmental changes (Fein et al., 2013). To further develop findings from previous research on the reduction of symptoms in
autism, the goal of the study was to determine whether OO individuals, people who initially were diagnosed with autism and eventually lost the diagnosis, had truly “recovered” from ASD or if they still had small residual symptoms left. Researchers explored subtle differences between OO and TD individuals by examining specific communication, social interaction, and language behaviors. The study used a variety of tests to measure its participants such as the Autism Diagnostic Observation Schedule (ADOS) and the Reysen Likability Scale (Fein et al., 2013). The ADOS was a major assessment used to diagnose Autism Spectrum Disorder. It involved direct observation of the individual and assessed communication and social interactions. The clinician would mainly observe the participant’s conversing, eye contact, engaging in play, and response to social clues. They desired to discover all the social and communication impairments in the OO group, rather than generalize that the OO individuals had completely lost all symptoms (Fein et al., 2013). Using the specific tests available to the researchers and heavy analysis, the study determined that overall, OO individuals displayed no significant differences from their TD peers in domains of communication, language, facial recognition, or socialization. In most cases, they were perceived as even more approachable and friendly than TD individuals. Despite these similarities, OO individuals showed mild abnormalities in understanding social relationships, with 35% displaying some difficulties (Fein et al., 2013). They also reported less mature friendships compared to TD peers, indicating possible residual attentional and self regulatory challenges. However, in comparison to individuals with HFA, OO individuals demonstrated significantly milder social symptoms. Unlike those with HFA, who scored poorly in communication aspects and repetitive behaviors, the test results of OO participants more frequently aligned with the patterns of TD individuals (Fein et al., 2013). In addition, this ground-breaking study highlighted differences across life stages, from childhood to early adolescence,
and young adulthood. In early childhood, OO individuals often exhibited mild ASD symptoms. Over time, researchers notice that the symptoms seem to evolve into subtler attentional, self-control, and immaturity difficulties, which were the most major differences between the OO and the TD group. Specifically, the study provided evidence that some individuals diagnosed with ASD in early childhood later showed attention-related deficits associated with ADHD after they lost their ASD diagnosis. Overall, OO participants clearly lost their ASD diagnosis and displayed few differences from their TD peers.
Despite the impact of the study done by Fein et al., the notion of “recovery” and finding a “cure” from autism still remains divisive and controversial. Critics argue that using such hurtful words frames autism as a condition to be “overcome,” stigmatizing individuals with autism (Sarris, 2016). Instead, many advocate for the acceptance, appreciation, and accommodation that enable individuals with ASD to thrive without losing their unique characteristics. In fact, Fein’s use of the term “optimal outcome” instead of “recovery” reflects this belief, emphasizing the importance of acknowledging individual strengths and overcoming challenges (Sarris, 2016). Having autism does not indicate that there is something “wrong” with the individual, but rather that they are different and unique.
The findings from Fein’s research support the existence of optimal outcomes in a small minority of individuals previously diagnosed with autism. While they no longer meet the diagnostic criteria for autism anymore, they may still face subtle difficulties and challenges in social relationships and self-regulation. The possible lingering effects on OO individuals underscores the complexity of the autism spectrum and highlights the importance of further discovery and support of ASD. Fein suggests that future research should focus on comparing OO individuals with individuals with ADHD, as her study showed a possible correlation between a reduction of ASD symptoms and attention deficit (Fein et al., 2013). However, as research advances, a main goal should still remain fostering environments that celebrate neurodiversity and provide accessible and specialized interventions and treatments for all individuals with ASD.
Autism. (2024, October 1). Cleveland Clinic. Retrieved December 25, 2024, from https://my.clevelandclinic.org/health/articles/autism
Carpenter, S. (2015). The children who leave autism behind. Spectrum. https://doi.org/10.53053/koyo9875
Fein, D., Barton, M., Eigsti, I.-M., Kelley, E., Naigles, L., Schultz, R.T., Stevens, M., Helt, M., Orinstein, A., Rosenthal, M., Troyb, E. and Tyson, K. (2013), Optimal outcome in individuals with a history of autism. Journal of Child Psychology and Psychiatry, 54: 195-205. https://doi.org/10.1111/jcpp.12037
Sarris, M. (2016, January 27). Road to “Recovery”: What Does it Mean to Lose an Autism Diagnosis? Kennedy Krieger. Retrieved January 3, 2025, from https:// www.kennedykrieger.org/stories/interactive-autism-network-ian/recovery-losing-autism-diagnosis
Webb, S. J., & Jones, E. J. (2009). Early Identification of Autism: Early Characteristics, Onset of Symptoms, and Diagnostic Stability. Infants and young children, 22(2), 100–118. https://doi.org/10.1097/ IYC.0b013e3181a02f7f
Ruben Lee ’28
The growing consumption of fast food and other unhealthy diets has increased concerns of fatty liver disease as well as type 2 diabetes in the general population. The enticing factor of cheap and tasty food has people eating from a high caloric and unhealthy fat source with an excessive carbohydrate intake. The devastating truths about consistent fast food consumption are often hidden well under corporate marketing. However, research shows that there is a health risk people are taking to enjoy their fast meals. Fortunately, recent evidence shows how the effects of overeating fast food are reversible and innovation of possible alternatives is on the horizon.
Fast food has become a major industry and an essential part of life for many individuals, especially in the United States. Meals that are prepared quickly, easy to access, cheap, and delicious are an enticing choice in comparison to a meal from home or at a full-service restaurant. There is a clear upward trajectory in the development of the fast food industry as almost 37% of adults indulge in fast food every day (CDC, 2018). Comparing numbers from the late 1970s to now, fast food consumption has almost tripled, having increased from 5.92% of total food consumption to 16.26% in just 50 years (U.S. Department of Agriculture, 2024). The market has exploded in popularity in recent years, measuring to be worth 595.93 billion USD in 2021, and is estimated to grow at a compound rate of 5.0% from 2022 to 2029 (Grand View Research, 2021). However, recent studies show that eating fast food just twice per week is linked to damage to the liver and other internal organs, in addition to weight gain and insulin resistance.
The possible dangers of fast food, a diet high in fat and sugar, was shown in a study done by the University of Minnesota in 2005 where data was collected on 3,031 young adults over the course of 15 years. The CARDIA (Coronary Artery Risk Development in Young Adults) study started recording data in 1985-86, where there would be frequent dietary checkups to measure the
correlation between the frequency of visits to fast food restaurants and the changes in body weight and the homeostasis model (HOMA) for insulin resistance. With the help of linear regression models, data was gathered on persons who consumed fast food more than twice a week and was compared to those who consumed fast food less than once a week. The data demonstrated that people who consumed fast food more frequently had gained, on average, 10 additional pounds and had an insulin resistance that doubled, which increased their risk of type II diabetes and heart disease (NIH, 2005). Mark Pereira, an assistant professor of epidemiology at the University of Minnesota remarked, given the “extreme difficult[y] [of] eat[ing] in a healthy way at a fast-food restaurant…people need to evaluate how often they eat meals at fast-food restaurants and think about cutting back” (NIH, 2005). Especially with the introduction of food delivery apps such as Uber Eats, DoorDash, and Grubhub, and the rise of new fast food establishments, access to a high-fat and sugar diet has risen exponentially.
In addition to the possibilities of weight gain and insulin resistance, a past study done in Europe revealed that fast food consumption is closely related to damage to the liver. Brent Tetri, M.D., a professor of internal medicine at the Saint Louis University, explains that a fast-food type of diet has been strongly linked to causing significant damage to the liver and having serious consequences to one’s health (Saint Louis University Medical Center, 2008). In 2007, Tetri conducted an experiment with mice that were placed on an average fast-food diet. Data was collected on mice that were fed food consisting of 40 percent fat and high-fructose corn syrup (a sweetener commonly found in soda and some juices) and were kept sedentary, recreating the lifestyle of an average American. After 4 weeks, the mice had an increased amount of liver enzymes, a key indicator of liver damage and the beginnings of glucose intolerance, which is a marker for type II diabetes (Saint Louis University Medical Center,
2008). Thankfully, most of the population is safe within the boundaries of ‘reversible damage’. A simple change in diet and keeping physically active can effectively supplement the unhealthy lifestyle of fast food consumption. Tetri explains, “The big issue is caloric content...the [main] harm comes from eating too many calories and too much fat and sugar” (Saint Louis University Medical Center, 2008).
There is strong evidence that also proves a correlation between fast food intake and fatty liver disease. Keck Medicine of USC offered data that stated, “The association between liver steatosis and a 20% diet of fast food held steady for both the general population and those with obesity or diabetes even after data was adjusted for multiple other factors such as age, sex, race, ethnicity, alcohol use, and physical activity” (Keck Medicine of USC, 2023). Fatty liver disease is often caused by a build-up of fat in the liver and could lead to diabetes, high blood pressure, and kidney disease (NHS, 2024). Healthline suggests avoiding harmful fat sources such as saturated or trans fats, an excessive carbohydrate intake (e.g. excess sugar), and eating beverages that contain simple sugars such as fructose (e.g. sugar-sweetened beverages and packaged sweets), all of which can be found in a fast food diet, to fight against developing fatty liver disease even beginning the potential reversal of it (Soliman, 2024).
As of now, the best solution to any of the problems fast food causes is simply to refrain from eating it in the first place. However, there are new advancements in food innovation that are opening doors to healthier ways of enjoying fast food. One popular option is a plant-based diet, which is more sustainable and reduces the risk of developing diseases (Seitz, 2022). The diet is also lower in saturated fat and sodium while providing additional nutrients such as fiber, and contains similar amounts of protein (Seitz, 2022). Another way scientists are paving a path for a healthier fast food culture is to invest in cell-cultured meat. Cellular agriculture is producing a meat or plant product without having to grow the full organism. By taking a part of the organism’s tissue or cell, biotechnologists work to create meat without having to raise farm animals (Science Direct, 2023). Cultured meat is another strong alternative to processed meats that is more sustainable, nutritious, and conscious of animal welfare (Science Di-
rect, 2023).
Everyone loves fast food. It is impossible to resist the temptation of a large McDonald’s fries or a Popeyes drumstick. However, there is strong evidence that eating fast food too many times could lead to possibly drastic and detrimental changes to the body, particularly to the liver. So until people can turn plants into meat, make meat available without heavy processing, or miraculously alter the unhealthy side effects of fast food, think twice before “lovin’ it”.
15-year Study Shows Strong Link Between Fast Food, Obesity And Insulin Resistance. (n.d.). ScienceDaily. https://www.sciencedaily.com/releases/2005/01/050111152135.htm
Fast Food Market Size, Share & Trends Analysis Report by product (Burgers/Sandwich, Asian/Latin American), by end users (Fast Casual Restaurants, QSRs), by region (North America, APAC), and segment Forecasts, 2022 - 2029. (n.d.). https://www.grandviewresearch.com/industry-analysis/ fast-food-market#:~:text=Report%20Overview,factors%20driving%20the%20market%20growth Food consumption and nutrient intake trends emerge over past four decades | Economic Research Service. (n.d.). https://www.ers.usda.gov/amber-waves/2024/august/food-consumption-and-nutrient-intake-trends-emerge-over-past-four-decades Grand view research. (2020). Fast Food Market Size, Share, Segmentation | Industry Report, 2020 Grandviewresearch.com. https://www.grandviewresearch.com/industry-analysis/fast-food-market
Products - Data Briefs - Number 320 - September 2018 (n.d.). https://www.cdc.gov/nchs/products/databriefs/db322.htm
Pereira, M. A., Kartashov, A. I., Ebbeling, C. B., Van Horn, L., Slattery, M. L., Jacobs, D. R., & Ludwig, D. S. (2005). Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. The Lancet, 365(9453), 36–42. https://doi.org/10.1016/s0140-6736(04)17663-0
Saint Louis University Medical Center. (2008, May 2). Fast-Food Liver Damage Can Be Reversed, Experts Say. ScienceDaily. Retrieved January 17, 2025 from www.sciencedaily.com/releases/2008/04/080430204519.htm
Consumption of fast food linked to liver disease. (2023, January 19). Keck Medicine of USC. https:// medresources.keckmedicine.org/news/consumption-of-fast-food-linked-to-liver-disease#:~:text=Potential%20surge%20in%20fatty%20liver,alcohol%20use%20and%20physical%20activity
Website, N. (2024, December 20). Non-alcoholic fatty liver disease (NAFLD). nhs.uk. https://www.nhs.uk/ conditions/non-alcoholic-fatty-liver-disease/#:~:text=Non%2Dalcoholic%20fatty%20liver%20disease%20(NAFLD)%20is%20the%20term,cirrhosis%2C%20if%20it%20gets%20worse
Crna, R. N. M. (2024, August 28). Diet and lifestyle tips to reverse nonalcoholic fatty liver Disease. Healthline. https://www.healthline.com/health/how-to-clean-afatty-liver#diet
Rd, L. P. M. (2022b, January 4). Incorporating PlantBased Meat Alternatives into Your Healthy Diet Healthline. https://www.healthline.com/nutrition/isplant-based-meat-healthy#benefits
Jahir, N. R., Ramakrishna, S., Abdullah, A. A. A., & Vigneswari, S. (2023, April 28). Cultured meat in cellular agriculture: Advantages, applications and challenges. Food Bioscience. https:// www.sciencedirect.com/science/article/abs/pii/ S2212429223002651#:~:text=Cultured%20 meat%20is%20a%20good,production%20 (Orzechowski%2C%202015)
George Cavanna ’27
Unbeknownst to most people there exists a small hidden world invisible to the naked eye. Bacteria thrives almost everywhere: in food, on the papers people read, and in the human body. Another microbe that we cannot see but is very well known is viruses. Viruses are infectious microbes that want to make more of themselves. The concept of the virus was created in 1957 by André Lwoff, who described them as having small genomes with a limited number of genes. (Beklizs et al. 2016). Viruses can enter cells and, using their limited number of genes, make copies of themselves and then spread to other living cells. For example, Covid-19 is a respiratory virus with about 16 genes (Naqvi, A et al. 2020). Scientists all over the world are still debating whether viruses are alive or not. This is because those who say they are not alive define life as being independent or having the ability to replicate without a host cell. The people who argue they are alive emphasize that many other organisms rely on their host cells for support, just like a virus. Most biologists would argue that viruses are nonliving. They cannot produce without a host nor have a metabolism, thought, or self-propulsion (Brown, 2016).
A new recent discovery may blur our understanding of viruses. In 2003, scientists discovered a large bacteria, a strange anomaly later named the giant virus. Giant viruses are about 0.4 micrometers (µm), whereas typical viruses are about 5-300 nanometers (Kaiser, n.d). In truth, the size of these microbes is not what puzzles scientists; it is the number of genes these giant viruses have. Giant viruses have a larger genome than bacteria (Brown, 2016). One of the first giant viruses discovered was the acanthamoeba polyphaga mimivirus (APMV), also known as mimivirus, in 2003 (Brandes and Linial 2019). This giant virus has more genes than a bacterium, and shares genes similar to those of archaea, bacteria, and eukaryotes. Some scientists argue that these genes reinforce the idea that these giant viruses are like other viruses (Brown, 2016). Another giant virus that has genes that constitute
life is the cafeteria roenbergensis virus (CroV), residing in plankton in the Gulf of Mexico. Its genes consist of 45% eukaryotic sequences and 22% bacteria sequences; the rest are from other viruses. These gene sequences are similar to other strains of mimivirus (Colson et al., 2019). Additionally, most of the genes in giant viruses are unidentified; uncharacterized proteins often reach 65-85% (Brandes and Linial, 2019). In other words, scientists have little to no idea what these proteins do. Thus, while giant viruses share many characteristics with viruses and other microbes, its uncharacterized elements distinguish it as a new class of microbe.
Another giant virus is the pandoravirus, the third largest known physical virus. According to an article published in the American Society for Microbiology, “93% of the Pandoravirus genes could not be assigned to known functions, many new details on this unique group of organisms are expected in future studies” (Antwerpen et al. 2015). Some genes encode for metabolism in a giant virus, but they do not work (Brown, 2016). Again, the larger genome is unique to giant viruses. Furthermore, giant viruses acquired a new family recognized by the International Committee on Taxonomy of Viruses, also known as ICTV, named Mimiviridae (Bekliz et al. 2016).
Another unique concept of a giant virus is virophages. The concept of a “virophage as a parasitic agent that depends on and predates the replicative cycle of a host mimivirus dates back to 2008 when La Scola et al. observed the presence of small virions of approximately 50 nm” (Rolland, C, et al. 2019).≥. In other words, when virophage infection happens, virophages infect a giant virus, which infects a cell. When the giant virus is replicating, the virophages infect the factories and cause them to make virophages. One example of a virophage is Sputnik. Sputnik infects a giant virus and waits for it to infect a cell. When the giant virus enters a cell and releases its genes and proteins, Sputnik infects the giant virus’s protein-making facilities. This forces the giant vi-
rus to make Sputnik virophages. Some giant viruses are created during the infection but most are impaired. This was the case with the viral factory of Acanthamoeba castellanii mamavirus infected with Sputnik (Rolland, C, et al. 2019). There are other virophages related to Sputnik. All of them share similar genomes of around 20 genes. The only difference is the size and prey preference of the virophage (Bekliz, M, et al. 2016).
This puts into perspective how something that might be nonliving can be hunted by something that is also nonliving. Giant viruses obscure the barrier between a living organism and a nonliving material. All giant viruses contain genes that constitute life. Giant viruses can lead to a deeper understanding of the virus’s origin. Many scientists wonder how something considered nonliving came to be in the first place. Currently, they still do not know the origin of viruses. Also, giant viruses have some of the most puzzling genomes in biology. Although, like any regular virus, giant viruses require a host cell to replicate, which would technically make them not alive, they may need a new classification for life because of their uniqueness. About 70% of all giant virus genes are unidentified (Bisio, et al. 2023). There is a high possibility that these genes will be unciphered. The new genes could look into viruses’ origins and maybe utterly new gene functions. There are still searches for new giant viruses every day. These hidden giants may look like significant microbes, but in reality, they are giant replication factories. Studies on giant virus genes are happening today, and there are possible discoveries in the future that could tell us more about what constitutes life, viruses as a whole, and what these new genes mean. So keep an eye out for any news about giant viruses, whether a new virus discovery or a massive discovery on the origin of viruses. Giant viruses offer us a look into the past, present, and future.
Antwerpen, M.H.; Georgi, E.; Zoeller, L.; Woelfel, R.; Stoecker, K.; Scheid, P. Whole-genome sequencing of a pandoravirus isolated from keratitis-inducing acanthamoeba. Genome Announc. 2015, 3. https://journals.asm.org/doi/full/10.1128/genomea.00136-15
Bekliz, M., Colson, P., & La Scola, B. (2016). The Expanding Family of Virophages. Viruses, 8(11), 317. https://doi.org/10.3390/v8110317
Bisio, H., Legendre, M., Giry, C. et al. Evolution of giant pandoravirus revealed by CRISPR/Cas9. Nat Commun 14, 428 (2023). https://doi.org/10.1038/ s41467-023-36145-4
Brandes, N.; Linial, M. Giant Viruses—Big Surprises. Viruses 2019, 11, 404. https://doi.org/10.3390/ v11050404
Brown, N. ARE VIRUSES ALIVE? https://microbiologysociety.org/publication/past-issues/what-is-life/ article/are-viruses-alive-what-is-life.html
Colson, P.; La Scola, B.; Levasseur, A.; Caetano-Anolles, G.; Raoult, D. Mimivirus: Leading the way in the discovery of giant viruses of amoebae. Nat. Rev. Microbiol. 2017, 15, 243–254. https://www.nature. com/articles/nrmicro.2016.197
Kaiser, G, Sizes, and shapes of Viruses (n.d). https:// bio.libretexts.org/Bookshelves/Microbiology/ Microbiology_(Kaiser)/Unit_4%3A_Eukaryotic_Microorganisms_and_Viruses/10%3A_Viruses/10.02%3A_Size_and_Shapes_of_Viruses
Naqvi, A. A. T., Fatima, K., Mohammad, T., Fatima, U., Singh, I. K., Singh, A., Atif, S. M., Hariprasad, G., Hasan, G. M., & Hassan, M. I. (2020). Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: Structural genomics approach. Biochimica et biophysica acta. Molecular basis of disease, 1866(10), 165878. https://doi. org/10.1016/j.bbadis.2020.165878
Rolland, C., Andreani, J., Louazani, A. C., Aherfi, S., Francis, R., Rodrigues, R., Silva, L. S., Sahmi, D., Mougari, S., Chelkha, N., Bekliz, M., Silva, L., Assis, F., Dornas, F., Khalil, J. Y. B., Pagnier, I., Desnues, C., Levasseur, A., Colson, P., Abrahão, J., … La Scola, B. (2019). Discovery and Further Studies on Giant Viruses at the IHU Mediterranee Infection That Modified the Perception of the Virosphere. Viruses, 11(4), 312. https://doi.org/10.3390/ v11040312
Size and shapes of viruses. (2016, March 8). Biology LibreTexts. https://bio.libretexts.org/Bookshelves/Microbiology/Microbiology_(Kaiser)/
Unit_4%3A_Eukaryotic_Microorganisms_and_ Viruses/10%3A_Viruses/10.02%3A_Size_and_ Shapes_of_Viruses
Scientists have known for a while that bacteria are capable of producing electricity from atmospheric hydrogen. The ability to generate electricity from ‘thin air’ is not only an important biological mystery but also a potential path for future energy generation and power sources for small devices. Scientists have long been puzzled by how these bacteria extract hydrogen from the air at such low concentrations (hydrogen is estimated to take up roughly 0.00005% of the atmosphere) (Thomas Jefferson National Accelerator Facility, n.d.). A recent discovery unveils the enzyme that is responsible for that reaction: “Huc” (pronounced “Huck”), which is a hydrogenase enzyme. Hydrogenase extracts hydrogen H2 from the surrounding atmosphere and breaks apart the two bonded atoms. When the chemical bonds between the electrons are broken, the electrons are released, flowing into the bacterium’s electron transport chain, which in turn provides the cell with the energy needed to sustain itself (Greening et al., 2023). The energy generated from this extraction can then be used to fuel the bacteria’s chemical processes during times of low food sources.
A team of researchers, led by Monash University’s Dr. Rhys Grinter, set out to discover how Huc generates electricity on its own. They first isolated the enzyme from a chosen bacterium Mycobacterium smegmatis, commonly found in soil, by adding a sequence into the genes responsible for creating this enzyme, which allowed the team to gain a closer look at a purified and isolated sample of Huc. The resulting purified enzyme was able to withstand temperature changes from 80℃ to -80℃ (176℉ to -112℉) (Greening et al., 2023).
Notably, whereas oxygen usually prevents the function of hydrogen-extracting catalysts, Huc appears to be nearly unaffected by oxygen particles. This trait allows it to retain a stable performance, one that is extremely useful for using these biocatalysts in other areas of energy generation. Huc was identified as an O2-insensitive enzyme, compared to others, such as O2-tolerant and O2-sensitive.
Looking into the structure of Huc’s gas channels leading to its active site, the researchers discovered that the channels are much narrower than tolerant or sensitive enzymes. Through simulations, they concluded that the constricted channels permit the passage of H2 molecules but prevent larger O2 molecules from entering the active site and hindering energy conversion. The channel serves as a bottleneck that blocks the passage of O2 and other larger molecules. To confirm this result, simulations where mutations of Huc excluded this bottleneck characteristic showed that O2 molecules indeed entered the active site at a much higher rate (Grinter et al., 2023).
The team also discovered that Huc, different from other biocatalysts that extract hydrogen from the air, can isolate H2 particles at extremely low concentrations. The team showed that Huc was capable of oxidizing H2 at concentrations even below the limit of the team’s gas chromatograph, which is a method used to detect a particle’s presence or absence in a substance (Grinter et al., 2023). Huc’s high affinity to H2 proves to be very different from other hydrogenase enzymes, especially O2-sensitive enzymes that react faster but have low affinity. The environments of their active sites show no significant divergences, suggesting that the difference in affinity is a result of other regions in the enzyme. Specifically, researchers speculate that the previously mentioned gas channels may specifically single out H2 molecules to bring to its active site, resulting in Huc’s lower rate of conversion and high affinity (Grinter et al., 2023).
These characteristics make Huc an invaluable biocatalyst. In terms of scientific research, this discovery greatly improves our understanding of how nature sustains itself. Nearly 60 to 80% of bacteria found in soil, particularly nutrient-deprived soil, display usage of Huclike enzymes. These bacteria absorb nearly 70 million tonnes of hydrogen from the air each year, reshaping the composition of our atmosphere and contributing to an extended understanding of how we can regulate our
environment to balance the climate (Monash University, 2023).
In terms of clean energy generation, Huc’s extremely high affinity gives it the potential to outperform current hydrogen sensors. As the hydrogen industry is becoming an increasingly eye-catching source of clean energy, a Huc-powered hydrogen sensor could detect faint leaks in devices and infrastructure before any current technology (Greening et al., 2023). Additionally, unlike other clean energy resources at the moment, Huc is a very stable and nearly limitless source of electricity as it absorbs hydrogen from the atmosphere. However, since hydrogen is only a minute percentage of our atmosphere, the electric current generated by Huc is considerably weaker than other clean energy sources. Nevertheless, Huc still has the potential to replace solar power as a battery source for small, air-powered devices, such as biometric monitors, simple computers, and clocks (Greening et al., 2023).
The role of Huc in enzyme biofuel cells (EBFCs), which are devices that use enzymes rather than traditional convert energy into electricity, is particularly interesting. EBFCs have multiple advantages over current fuel cells. For instance, EBFCs do not require rare materials or precious metals, and their oxidation processes are inhibited by a much smaller number of molecules than traditional fuel cells. However, the current EBFCs are less effective than traditional fuel cell technologies due to reasons such as long-term stability. However, the discovery of Huc, coupled with further research into its abilities in energy conversion, could advance the state of the field. Primarily, Huc’s insensitivity to oxygen as an inhibitor broadens the width of EBFCs’ feedstock from purified hydrogen flows to waste gas mixtures, which would likely result in positive economic and environmental impacts. Secondly, Huc’s high affinity allows it to extract energy from extremely diluted feedstock sources (Portland Press Ltd, 2023).
Huc has incredible potential as a breakthrough in scientific studies of biochemical catalysts and clean energy generation. To harness its full capability, the current and most weighty challenges are improving its yield, stability, and scale of manufacturing and commercialization. As we continue researching the science behind its nature, Huc will contribute to an increasing portion of the clean energy industry, provide insights to stabilize the climate,
and more.
Greening, C., Kropp, A., Grinter, R. (2023, March 22). Electricity from Thin Air: An enzyme from bacteria can extract energy from hydrogen in the atmosphere. SAEF. https://arcsaef.com/story/electricity-fromthin-air-an-enzyme-from-bacteria-can-extract-energy-from-hydrogen-in-the-atmosphere/
Grinter, R., Kropp, A., Venugopal, H., Senger, M., Badley, J., Cabotaje, P. R., Jia, R., Duan, Z., Huang, P., Stripp, S. T., Barlow, C. K., Belousoff, M., Shafaat, H. S., Cook, G. M., Schittenhelm, R. B., Vincent, K. A., Khalid, S., Berggren, G., & Greening, C. (2023, March 8). Structural basis for bacterial energy extraction from atmospheric hydrogen. Nature News. https://www.nature.com/articles/s41586023-05781-7
Monash University. (2023, March 9). The enzyme that could make energy dreams come true. Monash Lens. https://lens.monash.edu/@medicine-health/2023/03/09/1385541/the-enzyme-thatcould-help-make-energy-dreams-come-true
Portland Press Ltd. (2023, September 23). Developing high-affinity, oxygen-insensitive [nife]-hydrogenases as biocatalysts for energy conversion | biochemical society transactions | Portland press. Biochemical Society Transactions. https://portlandpress.com/ biochemsoctrans/article/51/5/1921/233544/Developing-high-affinity-oxygen-insensitive-NiFe
Thomas Jefferson National Accelerator Facility - Office of Science Education. Composition of the Earth’s Atmosphere. JLab Science Education. education. jlab.org/glossary/abund_atmos.html
Anika Amin ’27
A combination of factors, including climate change, the COVID pandemic, and geopolitical conflicts, have led to an alarming increase in global hunger and food insecurity in recent years. Currently, malnutrition affects roughly 195 million children worldwide under the age of five years old (Fontaine et al., 2023). While such issues are inherently crucial as humanitarian concerns, addressing them becomes particularly important as they remain barriers to sustainable development. The United Nations’ second Sustainable Development Goal that calls for ending hunger, achieving food security, and improving nutrition recognizes this significance (United Nations, 2022). Severe malnutrition appears in three primary forms: wasting, which refers to being too thin for one’s height; stunting, which refers to being too short for one’s age; and being underweight.
Traditionally, malnutrition is categorized into two main categories: moderate acute and severe acute. Children who have severe acute malnutrition commonly exhibit symptoms, including fever related to infection, diarrhea, anemia, and extreme emaciation. Malnutrition treatment has focused primarily on providing calories and replenishing essential vitamins and nutrients. For children suffering from malnutrition in places where food insecurity is common, the traditional treatment for these conditions involve ready-to-use therapeutic or supplementary foods (RUFs) (Pennisi, 2024). This type of fortified spread is rich in lipids and is a hygienic paste. It does not support the growth of bacteria since it does not contain water. Peanut butter is a typical lipid base. Milk powder, which is rich in proteins, is embedded in the paste to add adequate protein and micronutrient content (Manary and Sandige, 2008).
However, recent research shows a promising complementary strategy to combat the most severe cases of malnutrition in children that centers around nourishing the gut microbiome, which refers to the diverse community of microorganisms residing primarily in the human
gastrointestinal tract, including bacteria, viruses, fungi, and archaea. This complex ecosystem plays a crucial role in digestion, nutrient absorption, immune system regulation, and host metabolism. Malnourished individuals often have an impaired microbial balance, which can weaken immune responses, impair nutrient absorption, and increase susceptibility to infections and metabolic disorders. By restoring a healthy gut microbiome, malnutrition treatment should, in theory, become more effective (Iddrisu et al., 2021).
Prior research has shown that the gut microbiome can be altered through fecal microbiota transplantation. In an experiment, one group of “germ-free” mice with no intestinal flora (naturally occurring bacteria in the gut) was given microbiomes from malnourished children, while another group of mice in similar conditions was given microbiomes from healthy children. Unlike the latter group, the mice with microbiomes from malnourished children were unable to generate immune systems to function properly (Fontaine et al., 2023). These findings support the hypothesis that repairing malnourished children’s microbiomes may also strengthen their immune systems, improving their overall recovery.
Building on those findings, a recent study was conducted in Bangladesh, its results highlighting the benefits of “microbiome-directed” supplements for severely malnourished children, not only for moderately malnourished children which had been previously documented. This study by Jeffrey Gordon and Tahmeed Ahmed, published in October 2024, is the first to focus on children suffering from severe malnutrition, which is a more challenging condition to treat than its moderate form. In the study, 124 children ages 12 to 18 months in Bangladeshi urban and rural hospitals were treated for infections and diarrhea, stabilized from severe to moderate malnutrition, and divided into two groups. One group received the RUFs for three months, while the other was given the microbiome-directed supplement. The second group showed
faster weight gain and higher concentrations of proteins associated with the skeleton, muscles, and brain (Pennisi, 2024). This breakthrough study could have important implications on future methods used by health professionals to treat severely malnourished children. More significantly, the research also sheds light on the mechanisms underlying the treatment’s success.
To better understand how the treatment works, the scientists studied fecal samples that were collected. By sequencing DNA and RNA, they could track changes in the composition of the children’s gut microbiome. They observed how 75 microbial species became more abundant as the children’s health improved. One species, Prevotella copri, stood out for its role in breaking down complex carbohydrates in the supplement into simpler forms, which can then be used by other helpful bacteria and intestinal cells (Pennisi, 2024).
While these findings are encouraging, more research is needed amongst a larger data set to help validate the results. The World Health Organization, together with the Bill and Melinda Gates Foundation, are running a larger scale study to investigate whether microbiome-directed supplements are as effective across different regions with different diets, microbiomes, and cultural practices (Strait, 2023). The trial is expected to include more than 6,000 children, ages six months to two years old living in Bangladesh, India, Pakistan, Mali, and Tanzania and is expected to conclude by the end of 2025 (Pennisi, 2024).
It is unclear if therapies that help malnourished children restore their gut health and catch up physically also help them catch up with cognitive development, as the first three years of life are critical for brain development. Studies using animal models indicate that interventions targeting the gut microbiome may help reverse cognitive deficits caused by malnutrition. However, further research is required to explore the long-term effects and potential implications for humans (Shennon, 2024).
Even with the promising evidence that microbiome-directed supplements could help improve health for children suffering from malnutrition, several challenges remain before fully embracing and implementing this treatment. For one, it is uncertain if these benefits can be reproduced across other populations around the world. It is also important to consider cultural sensitivities around ingredients and dietary practices. Communities and regions must also be educated about the benefits of microbiome
supplements to ensure acceptance, especially those accustomed to traditional RUFs. Additionally, work needs to be done to address logistical challenges associated with scaling the production and distribution of the supplements in a cost-effective manner (Fontaine et al., 2023). While the scientific community still needs to assess the viability of adopting microbiome-directed supplements to treat malnutrition, the latest data is very promising and could be a game changer in impacting millions of children’s lives.
Fontaine, F., Turjeman, S., Callens, K., & Koren, O. (2023). The intersection of undernutrition, microbiome, and child development in the first years of life. Nature Communications, 14(1), 3554. https://doi. org/10.1038/s41467-023-39285-9
Iddrisu, I., Monteagudo-Mera, A., Poveda, C., Pyle, S., Shahzad, M., Andrews, S., & Walton, G. E. (2021). Malnutrition and Gut Microbiota in Children. Nutrients, 13(8), 2727. https://doi.org/10.3390/ nu13082727
Manary, M. J., & Sandige, H. L. (2008). Management of acute moderate and severe childhood malnutrition. BMJ, 337(nov13 1). https://doi.org/10.1136/bmj. a2180
Pennisi, E. (2024). Microbiome-based treatment helps ease severe malnutrition. Science, 386(6717), 14–15. https://doi.org/10.1126/science.adt5693
Shennon I, Wilson BC, Behling AH, Portlock T, Haque R, Forrester T, Nelson CA, O’Sullivan JM; M4EFaD consortium. The infant gut microbiome and cognitive development in malnutrition. Clin Nutr. 2024 May;43(5):1181-1189. doi: 10.1016/j. clnu.2024.03.029. Epub 2024 Apr 4. PMID: 38608404.
Strait, J. E. (2023, December 13). Gut bacteria of malnourished children benefit from key elements in therapeutic food | WashU Medicine. WashU Medicine. https://medicine.washu.edu/news/gut-bacteria-of-malnourished-children-benefit-from-key-elements-in-therapeutic-food/
United Nations. (2023). Goal 2: Zero Hunger - United Nations Sustainable Development. United Nations Sustainable Development; United Nations. https://www. un.org/sustainabledevelopment/hunger/
Blair Bartlett ’27
Music has been around for longer than historians can track, informing, entertaining, and connecting groups of people and cultures together. Each year, Americans pour over 200 billion dollars into supporting the music industry as countless people make and listen to music. The social and emotional benefits that music delivers go well beyond the surface level of a song. Muriel Zaatar, Kenda Alhakim, Mohammad Enayeh, and Ribal Tamer worked together to create a comprehensive literary review to “explore the intricate relationship between music and the brain” (Zaatar et al., 2024).
Highlighting the transformative powers of music, the Zaatar et al. review from 2024 emphasized that music leads to increased neuroplasticity by reshaping neural networks. Neuroplasticity is the process in the brain through which functional and structural modifications take place following events such as injury (Zaatar et al., 2024). In short, neuroplasticity is our brain’s ability to adapt to change, and music has the power to influence neuroplasticity. Listening to preferred music can lead to brain network oscillations, which are important because they stand as the method of communication between specific regions of the brain responsible for cognitive processes and states (Zaatar et al., 2024). The accumulation of grey matter in specific areas of the brain influences how musicians’ brains adapt in response to their training, resulting in a differing brain connectivity than non-musicians (Zaatar et al., 2024). Because of its positive correlation with neuroplasticity, listening to music is linked to increasing cognitive resilience and protection.
Not only does music influence our brain’s flexibility, but it also affects full-scale intelligence quotient (FSIQ) and working memory. In a 2015 study, the corpus callosum was found to be larger in musicians, correlating with years of musical work and training (Reybrouck and Brattico, 2015). This finding is significant because a larger corpus callosum improves connectivity between the two hemispheres of the brain, which thus enhances
adult attentiveness and engagement (Westerhausen et al., 2017). In addition, the hippocampus was found to have increased grey matter volume in professional musicians compared to non-musicians, resulting in more vivid memories associated with music (Zaatar et al., 2024). Increased grey matter volume in the brain has been shown to be positively correlated with FSIQ intelligence, and is responsible for synapses in the brain critical for connectivity (Narr et al., 2007). Receiving benefits from music is not limited to the professionals. People involved with music for both long and short term showed an increased verbal memory, quicker neural response to speech, and better performance in specific auditory tasks (Zaatar et al, 2024).
According to the Wan and Schlaug 2010 study, musicians were “less sensitive to age-related degeneration in the brain,” meaning that the regular practice of music can actually slow down the process of aging. Participants over 75 years old in the study who played an instrument were less likely to develop dementia than non-musicians (Wan and Schlaug, 2010). Playing an instrument resulted in greater protection against the decrease in volume and activity in specific brain regions often correlated with aging, in comparison to other cognitive tasks such as reading or solving a crossword puzzle (Zaatar et al, 2024). In general, musicians who practiced often were less susceptible to age-related cognitive degeneration in comparison to non-musicians (Wan and Schlaug, 2010). For patients already suffering from dementia, music has the ability to improve quality of life by triggering memories and increasing positive mood (Zaatar et al, 2024).
In addition to music’s ability to help slow the process of aging, music’s positive effects on our emotional state have physical benefits in the brain and body. A Ferreri and Rodriguez-Fornells 2017 study revealed a connection between participants’ music preference, the release of dopamine in the brain, and a stronger, more enhanced memory. Positive feelings from listening to
music promote physical health and pain management, and can therefore improve rehabilitation outcomes (Zaatar et al, 2024). Because of music’s healing potential, music therapy is increasingly used by therapists, doctors, and clinicians to treat a range of diseases. In a study featured in Translational Psychiatry, the placement of young children with autism in music group therapies positively correlated with the children’s improvements in communication and brain connectivity (Sharda et al, 2018; Zaatar et al, 2024). Moreover, music is closely linked to social activity. When people sang or played instruments in groups, their stress and endorphin levels fell, while their pain threshold increased (Zataar et al 2024).
Beyond the medical implications of music, Zataar et al emphasizes its effect on cognitive and emotional function in addition to its use in promoting physical well-being (Zataar et al, 2024). Many studies referenced by Zataar et al found a connection between musicianship and cognition. Not only did music enhance working memory processes, but it also improved attention span, underscoring its capability to improve cognitive ability (Zataar et al, 2024). A study featured in a Neurobiology of Learning and Memory issue, emphasized the powerful effect of classical music, specifically on short-term memory, when listened to during sleep and study (Gao et al, 2020). Music’s benefits go beyond working memory, and attention span; in fact, music provides therapeutic benefits by reducing stress, anxiety, and depression.
In the future, research could delve into the neuroplastic effects of other art forms in addition to music, to provide important information supporting both physical and emotional health for a wider variety of people (Zaatar et al, 2024). Further, to expand the use of music as a therapeutic tool in the future, Zataar et al encourages doctors to look for ways to create music interventions specific to different conditions, while taking into account individual background and preference. Music affects humans throughout their lifespan, and when optimized, could be used as a tool to treat diseases and promote overall health in addition to promoting positive culture (Zataar et al, 2024).
Caire, M. J., Varacallo, M., & Reddy, V. (2023, March 27). Physiology, Synapse. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK526047/
Ferreri, L., & Rodriguez-Fornells, A. (2017). Music-related reward responses predict episodic memory performance. Experimental Brain Research, 235(12), 3721–3731. https://doi.org/10.1007/s00221-0175095-0
Gao, C., Fillmore, P., & Scullin, M. K. (2020). Classical music, educational learning, and slow wave sleep: A targeted memory reactivation experiment. Neurobiology of Learning and Memory, 171(1074-7427), 107206. https://doi.org/10.1016/j.nlm.2020.107206
Narr, K. L., Woods, R. P., Thompson, P. M., Szeszko, P., Robinson, D., Dimtcheva, T., Gurbani, M., Toga, A. W., & Bilder, R. M. (2006). Relationships between IQ and Regional Cortical Gray Matter Thickness in Healthy Adults. Cerebral Cortex, 17(9), 2163–2171. https://doi.org/10.1093/cercor/bhl125
Reybrouck, M., & Brattico, E. (2015). Neuroplasticity beyond Sounds: Neural Adaptations Following LongTerm Musical Aesthetic Experiences. Brain Sciences, 5(1), 69–91. https://doi.org/10.3390/brainsci5010069
Sharda, M., Tuerk, C., Chowdhury, R., Jamey, K., Foster, N., Custo-Blanch, M., Tan, M., Nadig, A., & Hyde, K. (2018). Music improves social communication and auditory–motor connectivity in children with autism. Translational Psychiatry, 8(1). https://doi. org/10.1038/s41398-018-0287-3
Trimble, M., & Hesdorffer, D. (2017). Music and the brain: the neuroscience of music and musical appreciation. BJPsych International, 14(2), 28–31. https://doi. org/10.1192/s2056474000001720
T Zaatar, M., Alhakim, K., Enayeh, M., & Tamer, R. (2023). The transformative power of music: Insights into neuroplasticity, health, and disease. Brain, behavior, & immunity - health, 35, 100716. https://doi. org/10.1016/j.bbih.2023.10071
Wan CY, Schlaug G. Music Making as a Tool for Promoting Brain Plasticity across the Life Span. The Neuroscientist. 2010;16(5):566-577. doi:10.1177/1073858410377805
Westerhausen, R., Friesen, C.-M., Rohani, D. A., Krogsrud, S. K., Tamnes, C. K., Skranes, J. S., Håberg, A. K., Fjell, A. M., & Walhovd, K. B. (2017). The corpus callosum as anatomical marker of intelligence? A critical examination in a large-scale developmental study. Brain Structure and Function, 223(1), 285–296. https://doi.org/10.1007/s00429-017-1493-0
Mila B. Cooper ’26
Nearly one in ten people worldwide suffer from autoimmune diseases—conditions where the body’s immune cells attack healthy cells and tissues. Weakening the body and causing possibly life-threatening organ dysfunction, conditions included under this wide umbrella term range from type I diabetes and celiac disease to multiple sclerosis, rheumatoid arthritis, and lupus (Gordon, 2024). Although genetic predispositions and environmental factors are likely to contribute to the onset of autoimmune disorders, their causes remain largely unknown, and cures and therapies have proven extraordinarily difficult to develop (“Autoimmune Diseases,” n.d.).
The human immune system consists of two parts: the innate and the adaptive systems. Considered the less specific immune response, the innate immune system contains cells and molecules in the skin, gut, lungs, and nose, acting as the first line of defense against bacteria and viruses. Cytokines, proteins produced by immune cells, link the immune system to the rest of the body, activating or inhibiting immune responses (“Immune cells,” 2014). As the name suggests, the adaptive immune system, on the other hand, reacts differently to each type of germ affecting the body. In a healthy immune system, adaptive white blood cells called T cells and B cells— also known as T and B lymphocytes—kill pathogens and infected cells. Cytotoxic T cells recognize and remove infected cells, and T ‘helper cells’ produce molecules that alert other cells of an infection, coordinating an immune response (“Immune cells,” 2014). These helper cells can also activate B cells, which cause the B cells to copy themselves into plasma cells that secrete large amounts of antibodies targeting a specific pathogen (Institute for Quality and Efficiency in Health Care (IQWiG, 2023).
Autoimmune diseases, however, are characterized by the autoreactive activation of these adaptive cells, meaning the T cells and antibodies created by B cells target the body’s own cells, known as autoantigens (Johns Hopkins University, n.d.). Antigens can be exogenous,
meaning they are introduced to the body from outside, or endogenous, meaning they are created inside the body. Exogenous antigens are broken down and surrounded by proteins by antigen-presenting cells (APCs), which are then presented to T cells to be killed or left alone. Endogenous antigens are produced by normal cell metabolism, and the immune system’s tolerance mechanism destroys autoreactive T cells before they can kill these ‘normal’ cells. In autoimmune diseases, this tolerance mechanism goes awry, and the immune system loses its ability to ‘tolerate’ antigens that belong in the body while attacking those that do not (Willyard, 2024).
Depending on the disease, different cells in the body can be targeted, but the cause of each specific condition remains obscure. In multiple sclerosis, for example, autoreactive (self-attacking) T cells are activated in the central nervous system (CNS), crossing the blood-brain barrier into the brain by binding to adhesion molecules. They then attack the myelin sheath—a layer of fat covering neuronal axons—in the CNS, and myelin-reactive T cells induce greater inflammatory responses in the CNS (Song et al., 2024). By contrast, in type I diabetes, T cells infiltrate groups of cells in the insulin-producing pancreas, where they produce inflammatory cytokines and activate B cells that secrete antibodies, attacking autoantigens. This “immune infiltration” causes reduced pancreatic volume and the degrading of its function (Song et al., 2024). In each condition, however, the general idea remains the same: the immune system’s tolerance breaks down, causing its attack on antigens of its own cells.
Current methods of treating autoimmune diseases include immunosuppressants, which curb the body’s general immune response. Steroids, for example, deplete T and B cells and prevent the body from producing cytokines, broadly blocking inflammation (“Immunosuppressive,” n.d.). These medications, however, are not only limited in their treatment effects, but also weaken the immune system’s ability to combat actual external patho-
gens. New research has looked into targeting and bioengineering T cells to rebuild the immune system’s tolerance.
A team led by immunologist Pere Santamaria at the Canadian University of Calgary has been researching a possible new way to target type I diabetes, as well as autoimmune diseases more generally. Santamaria hypothesized that they could use iron oxide nanoparticles to build up a damaged immune system’s tolerance. Antigen-presenting cells (APCs) normally surround antigens with proteins to indicate to T cells whether to kill or ignore the antigen (Garber, 2014). In autoimmune diseases, this process fails. The process of desensitization, or administering increasing quantities of the problematic antigen to non-damaged parts of the immune system in an attempt to ‘teach tolerance,’ has sparked research into “antigen-specific therapy” (Willyard, 2024). Santamaria’s nanoparticles are surrounded by proteins called major histocompatibility complexes that spike out of the particles, mimicking APCs (Willyard, 2024). In response to the antigen-carrying nanoparticle, T cells mutate into regulatory T cells, antigen-specific T cells essential to maintaining peripheral immune system tolerance. These regulatory T cells can then travel to the site of inflammation, where they deactivate APCs corresponding to the antigen they now recognize from the nanoparticle (Garber, 2014). Since every autoimmune disease deals with varying antigens, picking the correct one(s) to target is a difficult task. Although a control in one of Santamaria’s studies of a mouse model for type I diabetes introduced only one known antigen, while the experimental trial presented eight, both the control and the experimental subjects showed a reversal of diabetes symptoms (Willyard, 2024). This surprising result suggests that these nanoparticles may induce a larger reaction to a plethora of APCs carrying various antigens related to type I diabetes. This ‘master-switch’ strategy began testing in its first human trial in 2024.
On the other side of the globe in China, a trial led by Xu Huji, a rheumatologist at the Naval Medical University in Shanghai has focused on CAR-T therapy (Mallapaty, 2024). A technique initially used for precise tumor treatment, chimeric antigen receptor T cells (CAR-T) are engineered by connecting CAR molecules to the surface of T cells (Song et al., 2024). The CAR molecules include chains of ligands of antibodies that will target specific an-
tigens (Song et al., 2024). The CAR-T cells can thus target and eliminate autoreactive B cells. CAR-Treg cells have also been engineered to target specific antigens, which could help build the immune system’s tolerance. With his team, Huji used CRISPR to create CAR-T cells from donated immune cells. The three patients in the study have all gone into remission, with the woman’s autoantibodies falling to undetectable levels, and the two men seeing significant declines in theirs (Mallapaty, 2024). Researchers remain cautiously optimistic about how long the effects will last, and how the practice will work in a larger study. Previously, these bioengineered cells had only been made from the cells of each individual patient. Having a donor pool could make the treatment accessible to more autoimmune disease patients.
Furthermore, in the search for causes and cures, many scientists are only beginning to include female cell lines in research. Up to four out of five autoimmune diseases patients are women. For lupus, the ratio of femaleto-male patients is 9:1; for Sjogren’s syndrome, it is 19:1 (Goldman, 2024). Only recently have researchers been discovering why. A molecule called Xist, present in women to avoid the overproduction of proteins by their two X chromosomes, generates additional RNA-protein-DNA complexes in the inactivated X chromosome (Goldman, 2024). Anti-Xist-complex antibodies are now believed to be linked to an increased autoimmune response. Each cell in a female’s body produces Xist, but male cell lines have been used as the standard of reference for decades (Goldman, 2024). Female anti-Xist-complex antibodies have thus gone unresearched, leaving out a large part of women’s susceptibility to autoimmune diseases and hampering the development of therapies that could target these types of autoantibodies. Continued research on both female and male cell lines into the markers of autoimmunity and a focus on bioengineering treatment development could one day lead to cures for these often-touted ‘incurable’ diseases.
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The three-dimensional structure of DNA was first discovered in 1953 by Watson and Crick. Since then, progress has been made in understanding the structure and arrangement of the human genome, though initially at a slow rate. After the initial breakthrough of the double helical structure of DNA, it took 11 years to decipher the triplet code for amino acids. It then took another 15 years to recognize that eukaryotic genes are disrupted by introns separating exons. Although it eventually became apparent that protein coding genes are only occasional charms on a long bracelet, the reason behind why these long stretches of non-coding introns existed was unknown (Boland, 2017). Researchers are still trying to understand all the crucial roles that these non-coding regions play in gene regulation, genome stability, and other evolutionary processes.
In the 1980’s, the identification and isolation of the first human genes through positional cloning, a complicated and tedious process, led DNA scientists to focus on the sequencing of the entire human genome. The Human Genome Project (HGP) marked the world’s largest collaborative scientific project to date, and was recognized as “unique and remarkable for the enormity of its effort” (Collins et al., 1995). By 2001, the first draft of the human genome was completed, and by 2004, 99% of the project was completed (Collins et al., 1995). It came as a major surprise, even to some of the field’s top scientists, that only about 1.5% of the human genome encodes approximately 21,000 distinct protein-coding genes (Green, 2025). This raised the question: Is the rest of the DNA just packaging material? The non-coding DNA was initially referred to as “junk”; however, it was discovered that these non-coding sequences were repetitive and transferable sections that facilitate gene rearrangement and were of evolutionary importance (Anguera, 2023). Approximately 45% of our genome consists of tandemly-repeated DNA elements such as long terminal repeats (LTRs), long and short interspersed nuclear elements (LINEs and
SINEs), and around another 25% consists of shorter tandem repeats, such as satellites, minisatellites, and microsatellites (Boland, 2017). Despite 98.5% of the human genome consisting of non-protein coding DNA sequences, most of the human genome is transcribed into RNA. At least 98% of the RNA are non-coding RNAs (ncRNAs), such as long non-coding RNAs (lncRNAs), short interfering RNAs (siRNAs), Piwi-interacting RNAs, small nucleolar RNAs (snoRNAs), and microRNAs (Mattick, 2013).
These findings of the existence of many different kinds of RNA sequences provoked many questions, especially regarding what each of their individual roles are. From a structural perspective, the structure of RNA appeared rather unorganized and insubstantial (Boland, 2017). However, more recently, scientists have begun recognizing how these expressed RNAs can regulate cellular functions and behavior. For example, long non-coding RNAs and microRNAs regulate the transcription of mRNAs, short interfering RNAs prevent gene expression, Piwi-interacting RNAs determine gene silencing, and small nucleolar RNAs interact with proteins (Zhang et al., 2019). Most of these non-coding transcripts regulate the amount and form each gene is transcribed and translated into a protein. Furthermore, there are distinct patterns of non-coding RNA expression connected to various diseases, including cancer where they can affect its progression and development (Boland, 2017). More research continues to be conducted in this promising field.
Furthermore, since cancer is a genetic disease, evidence of mutated DNA in the blood, stool, urine, and other tissues or body fluids of patients can be traced and used to detect cancer. Each cell has only two DNA copies of each gene, which can make it hard to detect the abnormal DNA samples of cancers. However, when DNA is transcribed into RNA, the number of copies of potentially cancerous genes may increase, with some RNA released by the cell. This has led to many researchers observing RNA species
in various clinical settings due to their surprising stability in blood and even stool (Maio et al., 2014). Consequently, various RNAs are being explored as possible biomarkers in the diagnosis of cancer and have shown more promise than DNA tests.
Additionally, RNA has also been found to have therapeutic uses that could delay or entirely prevent cancer progression. For example, miRNAs can target oncogenes, specific groups of genetic mutations that can cause cancer, and lncRNAs have the possibility to act as tumor oppressors (Uppaluri et al., 2023). H19 is one of the first lncRNAs found to be overexpressed in various cancer types, including colorectal cancer and breast cancer. It is a paternally imprinted gene that was initially discovered as expressed in embryonic tissues during mouse development, but it becomes silenced due to issues that occur at birth. The loss of H19 imprinting leads to H19 re-expression, and eventual overexpression, which triggers the formation of tumors in mice and human cell samples (Arun et al., 2018). However, the overexpression of H19 lncRNAs has also led to decreased tumorigenicity of human tumor cell lines, resulting in very divergent outcomes regarding whether H19 acts as an oncogene or as a tumor suppressor. Several different pathways have been explored to understand how H19 affects tumor progression. H19 can serve as a precursor for microRNA, which targets the tumor suppressor retinoblastoma (RB) protein in colorectal cancer (Arun et al., 2018). Increased levels of H19 lead to a decreased expression of RB, therefore promoting cell proliferation in colorectal cancer cells. Increased levels of H19 are observed in various cancers and contribute to cancer cell proliferations and tumor growth. However, the H19 gene may also be capable of acting as a tumor suppressor and will continue to be a target for future therapeutic approaches.
The scientific community is just beginning to understand the complex relationships among RNA species. One particularly exciting development is the use of CRISPR mediated genome editing approaches to explore lncRNA functions on a wider genome scale. Some scientists have made genome-scale systematic attempts to prevent lncRNA expression in cancer cells and pluripotent stem cells (iPSCs - stem cells capable of developing) in order to find a functional outcome. Results from these projects could help in discovering possible cures
and new methods of diagnosis for diseases such as cancer. Non-protein-coding RNA sequences are full of potential for cancer biomarkers and new cellular behaviors that could greatly push the known boundaries of human health. This is only the beginning of discovering all the structures and possible applications of the human genome, and so far, non-coding RNA is greatly contributing to the effort.
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Planarians are a type of marine flatworm that can regenerate body parts, such as eyes or tails, and even split into two new planarians when cut in half. Their abilities depend upon a robust system involving pluripotent stem cells, positional information, and precise cellular organization.
The standard response to injury for most animals is to seal off the open wound and repair the immediate area, and trigger the healing process (Friar, 2022). However, for planarians, the healing process transitions to regeneration, restoring any lost parts. This regeneration process is triggered by the equinox gene, which is present in the skin that grows to cover the wound site in planarians (Friar, 2022). In addition, planarians maintain guidepost cells, to help direct axons (in the nerve cells) as well as position control genes (PCGs) that determine where body parts regrow (Friar, 2022). Over 200 PCGs are activated post-injury, including Follistatin, which is responsible for the speed of regeneration (Ge et al., 2022).
Planarians possess a stem cell population called neoblasts, which includes pluripotent and fate-specified cells, crucial for the regenerative abilities of the species. Neoblasts account for 20-30% of planarian cells, and can be identified by unique structures called chromatoid bodies (Agata et al., 2008). They are characterized by their pluripotency, or ability to differentiate into various cell types, making them essential for damaged or lost tissues. Upon injury, neoblasts proliferate and migrate to the wound site, where they contribute to the formation of new somatic tissues (Reddien, 2013). Neoblasts regulate tissue proportions during growth and degrowth in response to nutrient availability and replace damaged and aged cells, both of which are guided by conserved genetic networks and pathways (Aboobaker, 2011). Neoblasts also exhibit morphological plasticity, allowing planarians to shrink or grow based on food availability by adjusting cell numbers through proliferation and cell death (Cebria et al., 2011). There are two main types of neoblasts: pluripotent neo-
blasts, stem cells capable of developing into all cell types, and specialized neoblasts, fate-specific subpopulations (Reddien, 2018). Each is dedicated to regenerating specific tissues. Neoblast specialization occurs in a spatially coarse pattern and is influenced by positional information (Reddien, 2018). This specialization also allows planarians to regenerate complex structures more efficiently by deploying pre-determined progenitors rather than relying solely on pluripotent stem cells (Scimone et al., 2014). Furthermore, regeneration begins with a broad proliferation of neoblasts, followed by localized replacement of missing tissues and formation of regenerative blastemas, which are masses of undifferentiated cells that develop into organs (Aboobaker, 2011). Neoblasts migrate to injury sites, differentiate into tissue-specific progenitor cells, and form a blastema, which acts as a hub for new tissue production (Ge et al., 2022). Positional information, primarily stored in muscle tissue through the expression of PCGs, guides this neoblast activity and tissue regeneration to ensure appropriate restoration. One important type of PCG is Wnt signaling molecules and their inhibitors, such as WntP-1 and notum, that regulate anterior-posterior (AP) polarity, essentially determining whether the head or tail is formed during development (Reddien 2018). WntP-1 plays a pivotal role in tail regeneration and its depletion results in head regeneration instead (De Robertis, 2010). Planarians display a unique regenerative ability where Wnt transcription is activated by wounding through a β-catenin-independent mechanism. Hedgehog (Hh) and Bone Morphogenetic Protein (BMP), two kinds of genes, signaling play a crucial role in this process, promoting tail regeneration by activating Wnt transcription at wound sites (De Robertis, 2010). Wnt is expressed in all types of wounds initially, which suggests that there exists a complex regulatory mechanism, exhibited through the inhibitor molecule, which causes the generation of the head (De Robertis, 2010). WntP-1 molecules interact with other pathways like Hh
and BMP, which also regulate tissue growth and polarity during regeneration (De Robertis, 2010). Aside from WntP-1, the interactions between epithelial and mesenchymal tissues, as well as gap junction communication, play significant roles in defining AP regeneration (Cebria et al. 2007). Along with the AP polarity which helps in determining the location of the head and the tail,, BMP signaling controls the dorsal-ventral axis organization, whereas Slit and wnt5 signaling regulate the medial-lateral (ML) axis, maintaining body symmetry (Forsthoefel et al., 2009; Reddien, 2018).
Another interesting ability of planarians is their capacity to regenerate their central nervous system (CNS), including their brain and ventral nerve cords, within a week after amputation (Cebria et al. 2011). This process involves three main stages: formation of brain rudiments, growth of neural networks, and functional recovery (Cebria et al. 2011). It involves conserved axon guidance cues like netrins,which can attract or repel growing axons, and Robo receptors, which mediate repulsive guidance (Cebria et al. 2011). Neural connectivity is essential for proper tissue patterning, and the ability to regenerate the CNS is crucial to the survival of the planarians even after experiencing significant injury (Cebria et al. 2007)
Ultimately, research into planarian regeneration holds significant potential for advancing regenerative medicine and applying those methods to human health and healing (Friar, 2022). Additionally, the regenerative processes of planarians share molecular mechanisms with cancer biology, which could provide greater insight into both fields (Aboobaker, 2011). Future studies in planarian regeneration could explore the underlying molecular mechanisms behind regeneration, the evolutionary aspects of regenerative abilities across species, and their practical applications in regenerative medicine.
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Sonia Shum ’27
In the modern age, space exploration has been a consistent frontier in the world of science, regularly providing scientists with new perspectives on the fundamental laws of our universe. As one of mankind’s greatest mysteries, outer space is a primary target of scientists nowadays.
The recent solar eclipse on April 8, 2024, was a dramatic event for astronomers and physicists. Solar eclipses occur when the sun and moon line up from Earth’s perspective, casting a shadow over the Earth. They allow for studies of the sun’s corona, the Earth’s ionosphere, and other space weather events. The sun’s atmosphere is a major study point during solar eclipses because the obscuring of solar light reveals hidden atmospheric features. The atmosphere comprises three main levels: the photosphere, chromosphere, and corona. The photosphere is the innermost ‘surface’ of the sun and where most of the sun’s brightness comes from. Photons produced from nuclear fusion travel thousands of years from the sun’s core, repeatedly absorbed and emitted by surrounding atoms until they reach the photosphere. This relatively thin layer allows the photons to stream out in billions, giving the sun its harsh brightness (Fox, 2012). Outside the photosphere is the chromosphere, which emits a reddish glow from the heated hydrogen burning off and conducts heat outward from the photosphere to the corona (Sharp, 2022). The corona, the outer layer of the sun’s atmosphere, emits light as white streams or plumes of ionised gas produced when gas particles are energised to the point where they lose electrons and become plasma, a super-heated mixture of positively charged ions and negatively charged electrons. The ionised gas flows outward into space and becomes solar wind as it cools. The photosphere usually overpowers the corona’s light, making the corona invisible to human instruments. However, this layer intrigues scientists because it is mysteriously much hotter than the photosphere which is closer to the sun’s burning core. During a solar eclipse, the moon blocks the blinding light
of the photosphere and reveals the corona’s white plumes of gas, providing scientists with the perfect investigation opportunity. The corona is also a major source of bursts of charged particles that cause geomagnetic storms around Earth, which may damage electronic systems that humanity relies heavily on.
The ionosphere is a charged layer in Earth’s upper atmosphere. Extreme Ultraviolet (EUV) and X-ray solar radiation ionise atoms and molecules by exciting atoms’ electrons past the maximum energy they can possess while remaining a part of their atom. This causes the electrons to be ejected out of the atoms, creating a layer of free-roaming electrons essential for long-range radio communications (Ionosphere, n.d.). As radio waves are sent out into the Earth’s atmosphere, they hit the electrons in the ionosphere and are reflected back to Earth. Under normal circumstances, high-frequency radio waves are more effective for long-range communication as they can travel further out into the Earth’s atmosphere before being radiated back to Earth (Skybrary, n.d.). The ionisation of the ionosphere is largely dependent on solar irradiance and phenomena, such as solar flares, wind, and geomagnetic storms. Thus, solar eclipses greatly affect the ionosphere’s charges.
The 2024 solar eclipse was particularly special due to its long time frame, large path of totality, and the sun’s being near its solar maximum in its 11-year activity cycle. The eclipse lasted about four and a half minutes with the moon at a point in its orbit comparatively close to Earth, making it appear larger. The path of totality, regions on Earth where solar light is completely obscured by the moon, passed within the observing range of three radars in the worldwide Super Dual Auroral Radar network, which monitors ionosphere activity by sending pulses of high-frequency electromagnetic waves. With a more disturbed magnetic field of the sun leading to a high rate of solar activity, scientists also expected more plasma streams from the corona and an increased chance of coro-
nal mass ejections. If satellites happened to lie in the path of an ejection, solar material could be collected and analysed, providing great insights into the sun’s atmosphere and how solar activity may disrupt communications and power grids on Earth or threaten satellites and astronauts in orbit (Riordon, 2024).
To study the solar eclipse, scientists flew jet planes along the path of totality, such as the WB-57F planes used in the solar eclipse in 2017, equipped with improved cameras and spectrometers to capture detailed views of the corona and detect different wavelengths of light that can help identify the corona’s temperature and structure (Gramling, 2024). In addition, ground-based observations were conducted with telescopes and cameras by community participants involved in the Citizen Continental-America Telescopic Eclipse experiment (CATE). While cloudy weather along the path of totality from Texas to Maine slightly affected image collection on the ground, observing teams still captured over 47,000 images that showed different parts of the corona (Gramling, 2024). The project also aimed to bond scientists with their communities and inspire public interest and appreciation for the sun’s mysteries.
Another experiment that scientists conducted was the Nationwide Eclipse Ballooning Project, which gathered more than 800 students to launch weather balloons into the sky to measure waves of pressure in the Earth’s atmosphere. Scientists suspected that the sudden cooling caused by the moon’s shadow during solar eclipses would alter the atmosphere’s equilibrium and create gravity waves, similar to the effect seen every day at sunset. However, this experiment was impeded by cloudy weather. Still, past data from the 2023 October eclipse showed evidence of gravity ripples in the atmosphere during the eclipse (Gramling, 2024).
Further, an event organised by HAMsci joined the ham radio community with space scientists to investigate the Earth’s ionosphere’s height, density, and structure during solar eclipses. With volunteers transmitting over 52 million signals at high frequencies, ranging from 1-30 megahertz, they saw a drop in communications when the moon’s shadow passed, suggesting a dip in electron density that allowed more radio waves to escape into space. As a result, low-frequency radio waves briefly became
more effective as the ionosphere’s ionisation changed. Moreover, the height of the ionosphere shrunk as the base of the layer rose in altitude during the eclipse before returning to normal thereafter, revealing relationships between space and the Earth’s upper atmosphere (Gramling, 2024).
While phenomena in outer space may seem far, insignificant, and disconnected from humanity on Earth, scientists see space exploration as a crucial step to understanding the universe, preserving life on Earth, and pushing the limits and fascination of the human mind. There is currently limited data on the Sun’s atmosphere, such as its temperature, density, outflow, magnetic structure, and evolution. From Earth, the sun appears as a two-dimensional structure, making inferences and predictions difficult because the fuller three-dimensional picture is hidden (Mann, 2024). As a result, scientists struggle with forecasting space weather events which deal with blasted radiation and charged particles that can damage satellites, communications, and staple electronic equipment on Earth. Developments on the forecasting front are essential for the security of society’s functions as they become increasingly dependent on electronic systems. Moreover, from a scientific perspective, predicting and studying solar eclipses can assure physicists that their underlying physics is correct, confirming that their fundamental understanding of the universe can continue to stand (Mann, 2024). While physically distant from human society, space phenomena, such as solar eclipses, are closely aligned with life on Earth. Hence, scientists are continuously launching investigations to understand this vast, mysterious region of our universe.
Looking ahead at future advancements beyond the scope of natural solar eclipses, space scientists are experimenting with new ways to study the sun’s atmosphere using satellites and coronagraphs, telescopic instruments that block out bright light. The European Space Agency’s PROBO-3 Mission recently launched on December 5, 2024. The mission consists of two small satellites, the Coronagraph and the Occulter spacecraft, that fly in formation, forming a 150-m long solar coronagraph and acting as a “virtual giant satellite” (ESA, n.d.). This marks a big milestone in satellite formation flying, potentially opening the door for future missions to be assembled on
much larger scales. The Coronagraph spacecraft blocks out light from the Sun while the Occulter spacecraft lies in its shadow to study the corona. Scientists hope the satellite’s data will improve predictions for the next total solar eclipse in 2026. Another promising mission is NASA’s Parker Solar Probe, which dipped into the sun’s atmosphere and reached within 6.1 million kilometers of its surface on December 24, 2024. The probe seeks the source of solar winds, aiming to bring back information about how to predict and gauge the implications of these mysterious winds. Looking further, space scientists plan on launching the Vigil spacecraft in 2029, a space weather observatory that can watch potentially hazardous solar activity (ESA, n.d.). The solar phenomena of eclipses provide just a small glimpse into the vast mysteries of the universe that modern-day scientists are continually trying to uncover and understand.
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Gabriel Vermut ’27
Agriculture is confronted with increasing environmental stresses such as drought, salinity, and pest attacks, which have been exacerbated by the changing climate. These are usually challenging to solve with conventional breeding, and the need for newer technologies has arisen. Thus, the CRISPR-Cas9 gene-editing technology has emerged as a promising tool that could help improve crop resilience and ensure food supply. CRISPR-Cas9 enables the precision editing of plant genes, targeting key genes that modulate stress tolerance, yield, and resistance against pests and diseases. CRISPR-Cas9 is developed from a bacterial immune system and functions by inducing targeted double-strand breaks in DNA, which are repaired through the plant’s natural mechanisms (Mahfouz, 2020).
The two main parts in the system are the Cas9 protein, which acts as a restriction enzyme, and a single-guide RNA (sgRNA) that directs the Cas9 to the specific DNA sequence for editing. This method has been widely used in agricultural research because of its efficiency, precision, and flexibility (Doudna, 2024). With CRISPR, the enhancement of genetic traits will surely develop crops that are resistant to any harsh weather conditions, making it a great lead toward sustainable farming. Drought and salinity remain two major stresses that currently have a major limiting effect on crop productivity, and CRISPR-Cas9 has produced promising results over both stresses. For example, rice varieties, after CRISPR is used to edit their OsDREB1A gene, maintain their growth and yield despite stress. Overexpression of the SlMAPK3 gene in tomatoes has increased drought tolerance by helping plants manage oxidative stress better. These advances show that CRISPR can tackle the direct impacts of climate change on agriculture, helping to reduce water usage in crop farming (Mahfouz, 2020). In addition to abiotic stresses, crops are also affected by pests and diseases. CRISPR-Cas9 can create pest-resistant varieties by targeting weak points in the genes. For instance, the removal of the TaMLO gene
provides resistance to wheat against powdery mildew, which is a common fungal disease (Zhang et al., 2018). Such alterations reduce the use of chemical pesticides hence reducing production expenses and other harmful effects on the environment (Zhang et al., 2018). This goes hand in hand with the sustainable agriculture notion wherein environmental health is equally important as the farm’s production. Moreover, CRISPR is being used to improve the nutritional value of crops. Researchers have used this technology to boost the pro-vitamin A content in bananas by editing the MaTMT2 gene. These efforts help address nutrient shortages in regions that rely on specific crops for diets, improving public health. Such applications highlight CRISPR’s versatility in dealing with both agricultural and nutritional challenges (Mahfouz, 2020). Applications of CRISPR-edited crops, however, are still somewhat mired in several important regulatory and ethical concerns. Rules on the book about such gene-edited crops vary across the globe, leading to inconsistencies in how those innovations are accepted and commercialized. In regions that have strict legislation, approval procedures of CRISPR-edited crops can be very long and costly, which hampers their wide diffusion. Additionally, there is a concern about biodiversity and the potential unforeseen effects of genetic modifications. As Doudna said in 2024, policymakers, scientists, and the public have to have frank conversations about the risks and benefits of CRISPR technology. Future agricultural innovation may also be significantly accelerated by the combination of CRISPR-Cas9 with new technologies; for instance, AI will analyze big genomic data sets to find optimal targets for gene editing and further improve the efficiency and accuracy of CRISPR applications. This combination could lead to crop varieties that are better suited to specific environmental conditions, helping address global food security challenges. However, this will require ongoing research funding and the development of appropriate regulations to ensure the responsible use of
this technology (Zhang et al., 2018).
CRISPR-Cas9 is an important tool in the field of plant improvement for growth and stress tolerance by allowing precise genetic modification, hence opening wide possibilities to develop crops which can grow under difficult conditions.
References
Zhang, Y., Massel, K., Godwin, I. D., & Gao, C. (2018). Applications and potential of genome editing in crop improvement. Genome Biology, 19, Article 210.
Doudna, J. (2024). Jennifer Doudna on the brave new world being ushered in by gene editing. The New Yorker. Retrieved from https://www.newyorker. com.
Mahfouz, M. M. (2020). Engineering crops of the future: CRISPR approaches to develop climate-resilient and disease-resistant crops. Genome Biology, 21, Article 289.
