BioQuakes

AP Biology class blog for discussing current research in Biology

Page 5 of 83

Is COVID-19 Linked to Diabetes?

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On January 15, 2024

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COVID-19 Virus diabetesToday’s children are being born into a world much different than what we once knew. The new reality of our world involves grappling with the effects of COVID-19. However, it seems that some children are experiencing greater effects than we could have imagined. As it was recently discovered, after a child is infected with COVID, he or she may have a heightened risk of developing Type 1 Diabetes. This adds another complicated layer to the pandemic that we thought we had mostly seen the end of. This article will detail the facts of the research while also providing insight from my AP Biology studies.

Over the past three years, we have become all too familiar with SARS-CoV-2, known as the virus that causes COVID-19. We have seen its effects in many different ways in our own lives and the lives of those around us. Now, as research improves, new discoveries have been made about COVID’s link to Diabetes in children. This article from NewScientist by Chen Ly highlights these studies. The article mentions that inside the pancreas are these structures called islets of Langerhans. These islets are groups of pancreatic cells that are responsible for producing insulin and glucagon, the two hormones that are crucial for the regulation of our blood sugar. The body can develop an autoimmune response to these islet beta cells and then fight against them with autoantibodies. If enough autoantibodies are created, they can trigger the onset of type 1 diabetes after killing too many islets in the pancreas. In a research study conducted by Annette-Gabriele Ziegler at The Technical University of Munich in Germany, it was concluded that children who had COVID antibodies were twice as likely to develop islet antibodies than those who have not been infected. This information provides insight on the relationship between COVID antibodies and diabetes. If children’s bodies can create these autoantibodies that kill the islets, the insulin production in young children can be weakened by COVID infection.

As stated in this article from the University of Minnesota, diagnoses of Type 1 Diabetes increased as a result of documented COVID infections. The incidence rate of T1D was 29.9 from January 2020 to December 2021. This was a jump up from the 19.5 incidence rate recorded in 2018 and 2019. This jump suggests that COVID infection is correlated to an observed increase in T1D. In an article by the CDC, it was reported that people under the age of 18 were more likely to receive a diabetes diagnosis after 30 days from COVID infection. This highlights the importance of COVID prevention strategies in order to additionally prevent other chronic diseases. In addition, this PubMed states that during the pandemic, we observed an increase in cases of hyperglycemia, diabetic ketoacidosis, and new diabetes. Th alludes to the possibility that COVID may trigger or unmask T1D.

Recently in our AP Biology class, we have been learning about the immune system and cell communication. This can be related to the research mentioned above in that we have covered the topic of blood sugar regulation and studied the pathway of insulin and glucagon throughout our bodies. Insulin regulates our blood sugar by helping to store the excess glucose in the liver when there is too much of it in the bloodstream. Glucagon does the inverse of this by taking the stored glucose from the liver and bringing it to the bloodstream when blood sugar levels are low. Both of these hormones seek to maintain homeostasis. In addition, we have focused on how our bodies react to viruses, and the different kinds of cellular responses that are necessary to fight infections. This is related to my research for this article because it dives deeper into the concepts of immune responses and blood sugar regulation. Getting to read about these topics in relation to the COVID-19 pandemic has further enhanced my understanding of them. 

I chose to write about this topic because of the impact that both COVID-19 and Diabetes has had on my family, which helps me to connect with these topics and heightens my curiosity. I welcome any comments regarding these topics and how they may have affected you or someone you know. What are your thoughts on these findings?

Oxygen, Aliens, and Technosignatures: The Extraterrestrial Quest for Advanced Technology

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On January 8, 2024

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Do YOU believe in aliens? Well if you do, get excited because the article, Is oxygen the cosmic key to alien technology? discusses how researchers are expanding the search parameters for extraterrestrial life. To do this, they are considering biological markers as well as technological ones. In a study published in Nature Astronomy, scientists Adam Frank and Amedeo Balbi explore the connection between atmospheric oxygen and the possible growth of advanced technology on different planets. 

Atmospheric oxygen pertains to the presence of O2 in the atmosphere, particularly within the troposphere, which facilitates the flourishing of life. It is deemed a necessity for humans, surpassing even the importance of food. 

Atmospheric oxygen is also crucial for Cellular Respiration specifically in the Krebs cycle (known as the Citric Acid cycle) and during Oxidative Phosphorylation.

CellRespiration

In my AP Biology class, I learned that during the Krebs cycle, acetyl CoA molecules enter the mitochondria and are oxidized, producing high-energy electrons. In the subsequent electron transport chain, these electrons combine with oxygen to form water, facilitating the regeneration of molecules for continued energy production. Without sufficient atmospheric oxygen, this process is impaired, disrupting cellular respiration and the creation of ATP.

Now… back to the aliens, researchers introduce the concept of “technospheres,” expansive realms of advanced technology that emit detectable signs known as “technosignatures.” Technosignatures are essentially evidence of advanced life. This aids in the research as technosignatures extend the scope of conventional biological markers in the search for extraterrestrial life. Researchers can investigate the potential of highly developed civilizations displaying indications of sophisticated technology by considering technological evidence. This broadening of the search parameters expands the research’s scope beyond traditional methods.

Technosignatures
Moreover, it is stated that high oxygen concentrations are necessary for the development of advanced technospheres, as oxygen is crucial for processes like open-air combustion, a key component of technological civilizations. The research proposes the “oxygen bottleneck,” indicating that high oxygen levels are essential for the emergence of technological species.

The discussion of oxygen levels ties back to Earth’s atmosphere. It prompts reflection on environmental issues and the importance of maintaining a balanced atmosphere for the well-being of our planet. An issue that I think about daily is climate change and while the immediate focus of the research is on oxygen and technology, it prompts the reader to consider the broader environmental challenges we face, including those related to climate change.

Returning to the study, the findings emphasize the importance of prioritizing planets with high oxygen levels in the search for extraterrestrial technosignatures with the intention of expanding space search parameters. 

After reading this article and doing outside research I believe this study to be highly important because it contributes to our understanding of the conditions necessary for advanced technology beyond Earth. As someone who has always been fascinated by outer space and extraterritorial beings, it is valuable for me to be educated on advancements in technology and science. So … aliens, real or not? Let me know what you think in the comments! 

Next-Gen Therapeutics!

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On January 8, 2024

In Student Post

Scientists at St. Jude Children’s Research Hospital have launched a massive mission to confront the escalating challenge of antibiotic resistance in Mycobacterium abscessus (Mab), a pathogen naturally resistant to antibiotics. The urgency of this is emphasized by the increasing threat of Mab infections in healthcare settings, mainly those with compromised lung function or weakened immune systems. In response to the need for innovative therapeutics, the researchers at St. Jude undertook a careful approach, which focused on redesigning the antibiotic spectinomycin to generate new versions capable of overcoming the primary driver of resistance, which is something called efflux (the process cells use to remove drugs). The findings of their work, published in Proceedings of the National Academy of Science, discovered the development of structurally distinct N-ethylene linked aminomethyl spectinomycins (eAmSPCs), outperforming standard spectinomycin by up to 64 times in power against Mycobacterium abscessus.

Antibody

Connecting to class, this work underscores the significance of antibodies (Unfortunate Ned), which are proteins produced by B cells in response to specific pathogens. The development of this variant against Mab links to the antibody-mediated immune response. Engineering more potent antibiotics against Mab shows a real-world application of understanding and manipulating the immune system’s humoral response, highlighting the importance of B cells in providing long-term protection against infections.

Humoral Response Drawing

Overall, the significance of this breakthrough is not only in the efficiency of eAmSPCs, but also in solving their course of action. By explaining how these compounds avoid efflux, the researchers have paved the way for a shift in antimicrobial therapy. The researchers discovered that eAmSPCs show compatibility with various classes of antibiotics used to treat Mab, while retaining their effectiveness against other mycobacterial strains. This adaptable characteristic leads eAmSPCs to be the potential future of therapeutics, offering hope for patients struggling with limited or nonexistent treatment options.

 

(Post Includes Edits Made Through Grammarly)

Tardigrades: Tiny Survivors in Denmark

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On January 8, 2024

In Student Post

What happened to the Tardigrade when it was bit by a zombie…? The tardigrade went into cryptobiosis,  half-dead state! 
Waterbear

The University of Copenhagen’s research reveals the widespread presence of microscopic water bears, or tardigrades, in Denmark’s diverse environments. Previously associated with extreme locations like Mount Everest and deep seas, tardigrades were found in soil, moss, and rain gutters across the country. Using environmental DNA analysis, scientists identified 96 unique tardigrade DNA sequences, indicating a diverse and previously underestimated population.

Tardigrades, resembling chubby teddy bears, exhibit unparalleled resilience, surviving freezing temperatures, desiccation, extreme radiation, and even the vacuum of outer space. Tardigrades, with unique genomic features enabling resilience in these harsh environments, intrigue scientists exploring the genetic mechanisms behind their remarkable adaptability. The study, the first of its kind in over 50 years, highlights the importance of tardigrades in local ecosystems and their unique ability to enter cryptobiosis, a state where metabolic activities are suspended. This extraordinary survival mechanism sparks interest in various scientific fields, including biomedicine and space research, as researchers explore the potential applications of tardigrade abilities in enhancing the resilience of other organisms. According to the article ‘Once-in-a generation’ tardigrade fossil discovery reveals new species in 16-million-year-old amber, discovering rare tardigrade fossils, like Pdo. chronocaribbeus, can help scientists learn more about the changes that happened during important events in tardigrade evolution. This includes understanding how they became some of Earth’s tiniest animals with legs.

In AP Bio’s Unit 3 on Cell Communication, we explored the world of Tardigrades very vaguely, but I was intrigued to know more. As part of the learning experience, I took the opportunity to complete an extra credit creative project about Tardigrades. I discovered so many captivating and cool facts about these water bugs. Although labeled as aquatic due to their dependence on water to prevent dehydration, Tardigrades possess a remarkable capacity to withstand extremely dry and harsh conditions. A key player in this resilience is the Tardigrade-specific Intrinsically Disordered Protein (TDP). When tardigrades experience dehydration, TDP replaces intracellular water, forming a glass-like substance. This unique mechanism preserves the integrity of their cellular structures, contributing to their ability to endure hostile environments.

In my creative Tardigrade project, I reimagined Tyler, the Creator’s “Flower Boy” album cover by replacing the bees with tardigrades. As I explored the connection between tardigrades and the album’s meaning, I discovered their remarkable ability to endure extreme environments, mirroring the metaphorical journey depicted in “Flower Boy.” Much like tardigrades thriving in harsh habitats, Tyler, the Creator explores the resilience needed to navigate life’s extremes. The album’s aquatic imagery aligns with tardigrades’ dependence on water for survival, fittingly nicknamed “water bears.” Water, symbolizing life and change, parallels the exploration of fluctuating experiences and emotions in “Flower Boy,” echoing the dynamic environments where tardigrades thrive. 

The University of Copenhagen’s research highlights the widespread presence and remarkable resilience of tardigrades in Denmark. From genetic studies to creative projects, the exploration emphasizes the significance of these tiny creatures in scientific understanding and survival strategies. What’s your take on the incredible resilience of tardigrades? Share your thoughts or any interesting facts you know!

Fighting the Flu: Why Kids Need More Influenza Antivirals

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On January 8, 2024

In Student Post

Influenza Virus

Influenza, otherwise known as the flu, is a very well known disease, that is unfortunately still very common. Given its commonality, there are many different ways to try and treat or mitigate the virus. Despite this fact, we can see discrepancies between guidelines and actual prescription practices for flu treatment among children, thanks to the study “Trends in Outpatient Influenza Antiviral Use Among Children and Adolescents in the United States.” 

The lead author, James Antoon, a professor and doctor at Vanderbilt, emphasizes that antiviral treatment, especially when administered early, significantly improves health outcomes in influenza cases among children. However, the study reveals that a significant proportion of children, particularly those under the age of 5 and especially those under 2, are not receiving the recommended antiviral treatments. In fact, only about 40% of children studied were treated with antivirals, despite guidelines suggesting that all of them should receive this treatment.

Interestingly, the study reveals a notable disparity in the geographic use of influenza antivirals, showing a significant difference in prescription rates across different regions, independent of flu cases.

The reasons behind the under prescription of antivirals in children is likely due to various factors, including differing perceptions about effectiveness, variations in the interpretation of diagnostic testing, misunderstanding of national guidelines, and concerns about potential adverse drug events associated with certain antivirals, such as oseltamivir.

Additionally, the study mentions a previous investigation led by Antoon that explored neuropsychiatric side effects in children diagnosed with influenza. While these events are relatively infrequent, the study observed that they occurred in both treated and untreated children.

The research emphasizes the importance of improving flu management among vulnerable children in the United States, highlighting the need for better following of guidelines regarding antiviral use in pediatric flu cases.

This study connects to a few things we’ve learned this year in our AP Biology class. The way oseltamivir works, is that once inside, your body metabolizes it, which activates the oseltamivir. Once activated, it binds to and inhibits the active sites of the enzymes responsible for spreading the flu throughout a host’s body. As we learned in AP Biology, it doesn’t completely stop the spread of the virus, but it definitely slows it down, allowing your white blood cells to eradicate the virus.

Do you think the underuse of antiviral medications in children with influenza is a widespread issue? How might this research impact pediatric healthcare practices in managing flu cases more effectively?

(Post Includes suggestions made by ChatGPT)

Miracle Drug for Drugs?

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On January 7, 2024

In Student Post

A fascinating new drug called CSX-1004 may be the cure to the fentanyl epidemic. Scientists who have recently discovered the drug have been conducting experiments on monkeys to fully grasp the effects of the drug before they begin their human trials. If the drug is found effective, there could be a revolution in the fight against drugs.

 Understanding Fentanyl Addiction

Fentanyl is a highly addictive synthetic drug that is nearly 50 times more potent than heroin and 100 times more potent than morphine. Fentanyl binds to the body’s opioid receptors, receptors responsible for pain reduction, emotions, and breathing regulation. Opioid receptors are G-coupled receptors. As we learned in AP Biology, the G protein receptor is first activated by a ligand, triggering the G protein to activate. The activated G protein causes GDP to turn into GTP. Then, the G protein binds with adenylyl cyclase, triggering ATP to become cAMP. The cAMP triggers the activation on Protein Kinase A, finally, triggering a response. In the case of fentanyl, fentanyl is the ligand. Typical responses of the drug include a feeling of euphoria, drowsiness, nausea, respiratory depression, confusion, and unconsciousness. The drug targets parts of the brain that control reward, causing users to take more of the drug. As abuse continues, the brain is no longer able to naturally produce dopamine, the neurotransmitter that binds to the opioid receptors. An addict quickly becomes reliant on drugs to give them the happiness and pain regulation that they once naturally had.

Antibody IgG1 surface

CSX-1004

CSX-1004 is an antibody that binds to fentanyl in the blood, stopping a great majority of it from reaching target receptors in the brain. As we also learned in AP Biology, antibodies are part of the humoral response and fight against infections. B-Plasma cells, which patrol the plasma, secretes antibodies. These antibodies bind to and neutralize the pathogen until a macrophage engulfs and destroys an antibody-coated pathogen. In conclusion, if CSX-1004 can bind to and neutralize fentanyl, it can potentially be killed or weakened before reaching receptors in the brain!

The Study

Scientists gathered groups of squirrel monkeys and began by giving them increasing doses of fentanyl over 28 days. They found extreme respiratory conflicts at the higher doses. They then repeated the experiment for another month. This time, they treated the monkeys with one dose of CSX-1004. They found that the dose decreased respiratory harm by 15% at all doses of fentanyl.

Timeline. Drug overdose death rates by sex, United States

The Future

If CSX-1004 is found effective and safe for humans, we could be looking at a decline in fentanyl addiction and deaths. Scientist Andrew Bennet stated that “If we can block the high produced by fentanyl, gradually people will stop using it as they realize it is not doing anything”. Fentanyl has been named the most dangerous illegal drug and was responsible for 28.8% drug related deaths in 2018. Drugs have a higher mortality rate than gunshots and automobile accidents. Does this statistic shock you? This is why drugs like CSX-1004 are so important to be in the works. CSX-1004 could be the key needed to prevent more lives lost at the hands of fentanyl.

1.78 Billion Year Old Bacteria: the Origins of Photosynthesis

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On January 7, 2024

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E. coli Bacteria (7316101966)

Pretty music everyone is aware of the term photosynthesis. We identify photosynthesis as the process plants take to make food by utilizing the sun’s energy. New findings take us back in time to the earliest signs of this process. The article published on January 3 2024 reveals that bacteria fossils hold some of the oldest signs of machinery required for photosynthesis. Cyanobacterias’s invention of photosynthesis is responsible for the oxygen in Earth’s atmosphere which is a large sum of information derived from fossils. 

The bacteria fossils are compression of carbon that don’t contain any mineralized structures such as bone or shells. The fossils also revealed that there are complex structures inside of the microscopic bacteria such as thylakoids which are located inside of the chloroplast and allow photosynthesis to take place. It is exciting to see such old thylakoids inside of the bacteria fossils but it is not unheard of as some researchers believe that thylakoids may have evolved before the Great Oxidation Event which occurred around 2.4 billion years ago and marked a significant increase in Earth’s oxygen levels.

During the period that the bacteria fossils lived in, oxygen levels in Earth’s atmosphere were at a fraction of today’s levels which helps explain why the fossils hint that there may have been small pockets where oxygen was abundant, possibly allowing the evolution of the ancestors of plants and animals. Most of the rocks that scientists believe may harbor fossils similar to the ones discovered have been compressed destroying intracellular structures like thylakoids which makes the findings even more rousing. 

A similar article published the following day identifies the bacteria fossils to be between 1.73 and 1.78 billion years old. Furthermore, the article points out that prior to this discovery, the presence of thylakoids in cyanobacteria was traced back to only around 600 million years ago, but now the earliest evidence of thylakoids in cyanobacteria is 1.2 billion years older. The fossils are also defined as Navifusa Majensis, a presumed type of cyanobacteria. N. majensis fossils add a vital data point in the timeline that aims to discover the exact timing of oxygenic photosynthesis’s evolution.

A second article published on the same day explains that the bacteria fossils “were laid down in mud and squeezed as the mud was transformed into shale over time.” The intriguing part, though, is that the internal structures of the cells were preserved throughout this process. 

To help further explain the job of thylakoids in plant cells, in AP Biology class, we learned about the specifics of the chloroplast, the organelle in plant cells that is responsible for photosynthesis and plants green color. Furthermore, we learned that grana, located below the inner membrane of the chloroplast, are stacks of thylakoids. A large surface area of thylakoid disks results in better productivity in the cell. In the article linked in the previous paragraph, astrobiologist Emmanuelle Javaux is referenced as speaking about “dark lines stacked through tiny sausage-shaped cells” that they believe represent thylakoids. An image in the Cells Notes Packet displays the same description that Javaux is providing with dark rectangles being spread across an image of the chloroplast. 

I believe that these new findings are a great advancement in the mystery that is the evolution of photosynthesis in plants. These findings are one of the first steps of discovering the exact timing of oxygenic photosynthesis’s evolution. I look forward to seeing if more fossils are discovered with thylakoids and other complex structures still intact, what do you think?

 

The Fountain of Youth for Muscles: Targeting 15-PGDH to Halt Age-Related Weakness

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On January 7, 2024

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Eventually, everybody ages. While some good things come with age, aspects of aging, such as muscle weakness, can now potentially be stopped. For a long time, scientists have wondered why muscles start to weaken as humans age, but now, due to a recent ScienceNews article, we may be able to answer and solve muscle weakness!

Muscle Tissue: Cross Section Whole Skeletal Muscle

In the article, scientists discovered that inhibition of an an enzyme called 15-hydroxyprostaglandin dehydrogenase, or 15-PGDH for short, can help with strength and more muscle mass in older humans. 15-PGDH breaks down a signaling compound called prostaglandin E2, which activates the production of muscle cells that regenerate damaged muscles. Though it may seem confusing why 15-PGDH breaks down prostaglandin, the enzyme is a tumor suppressor. The enzyme inhibits proliferation so that cancer and other cells can be differentiated. In younger muscle tissue, 15-PGDH was found at reduced and relatively little abundance, but in older muscle fibers, it was found in great abundance, which caused relatively minor muscle repair. In the study, 15-PGDH was inhibited by gene knockout. However, studies show that the enzyme has potential effectors that cause an induced closure of the enzyme’s active site, which inhibits 15-PGDH. This would be an allosteric interaction in which the effector works by binding to the enzyme and changing the shape of the active site so that it can no longer work.

Silence of the Genes

Eventually, everybody ages, so this discovery is important to me. Being able to have optimal strength and energy while being old may be possible, according to the findings made by scientists. Hopefully, by the time I age, these findings can help allow older humans to continue to have peak performance. If you guys have any other studies relating to human muscle deterioration, I would love it if you shared them in the comments!

 

Is Diet Soda a Scam?

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On January 7, 2024

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If you are like me and your favorite drink is Diet Coke, then you are no stranger to the people around judging your choice and claiming that you are drinking chemicals. “It’s just as bad as the real thing,” they all say. I genuinely think the diet and regular versions of soda taste different, and when it comes to Coke, I just prefer the diet version. However, some people drink it as an alternative to the high levels of sugar in regular sodas.

Recently, studies have come out to prove that the sugar substitutes in diet sodas are just as bad for you as the cane sugar in regular soda. So, is the impression that Diet Coke is healthier than regular Coke a scam?

Drink it in a Coke

First, you need to understand what mimics the sweetness of regular sodas in diet ones. The chemicals that people are referring to are the sweeteners used in replacement of the almost 40g of sugar in a regular coke. The main sweetener is aspartame, which is a dipeptide composed of two amino acids; phenylalanine and aspartic acid. The other is acesulfamm potassium. Acesulfame Potassium, also known as Ace-K, is a potassium salt that is roughly 200 times sweeter than sucrose. Both of these sugar substitutes are synthetic products.

So, are these sugar substitutes better or the same as the real thing?

In a study done by the Research Ethics Committee of the Federal University of São Paulo, 15 healthy participants participated in a blindfolded trial including a Diet soft drink, Regular soft drink, water with sweeteners, water with a low sucrose content, and regular water, in 5 days. The goal of the experiment was to study the aspartame excretion in saliva and the salivary insulin, in response to the ingestion of the beverages. Each day, their saliva was collected when fasted, 15, 30, 60, and 120 minutes after drink intake, to check for the levels of salivary aspartame and insulin levels. The researchers found that insulin levels increased 1 hour after both regular and soft drink digestion. Therefore, the study found that although diet soda is sugar and calorie free, it still influences insulin levels, like regular sodas. So, by avoiding the regular version of a soft drink, you are not avoiding the insulin spike. However, the research only included a 15 participants, so an experiment with a larger sample size would need to be conducted to reach a final conclusion. But, the idea that “no sugar” soft drinks are that much healthier than the real thing, isn’t exactly true.

This connects to what we have been learning in AP Bio because we learned about insulin and glucose levels and how they maintain homeostasis in our bodies. Insulin is a hormone produced in the pancreas that regulates blood glucose levels. Insulin helps blood sugar enter the cells of our body so it can be used for energy along with sending signals to the liver in order to store glucose for later use. However, when insulin levels rise too high, it can cause the cells in our bodies to absorb too much glucose from the blood, and the liver to release less glucose. This causes dangerously low glucose levels in the blood. If this becomes chronic, and there is constantly high insulin levels, it can lead to prediabetes and Type 2 Diabetes.

Do you still think your diet soda is better for you than the regular one, or will you opt for a regular coke next time?

 

 

 

 

Individual Cells Move Differently When They Are Together

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On January 7, 2024

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In a groundbreaking study, researchers have unveiled that a protein crucial for powering movement in individual cells operates distinctly when cells collaborate in groups. Cells engage in intricate pushing and pulling interactions with each other and surrounding tissues during processes such as embryonic organ formation, wound healing, pathogen pursuit, and cancer dissemination. The investigation, led by researchers at NYU Grossman School of Medicine, focused on a cluster of 140 cells known as the primordium, observing how these cells generate forces while adhering to each other during movement in zebrafish embryos—a model organism highly valued for its transparency and shared cellular mechanisms with humans.

The study reveals the role of a protein called RhoA, a primary structured protein, in propelling the group forward during embryonic development. As cells strive to move, they extend protrusions and utilize them to anchor onto nearby tissues before retracting them, a process analogized to the casting out and hauling in of an anchor.

Blood Anemia.jpg

In AP Biology, delving into the intricacies of the RhoA protein offers a compelling view of the relationship between structure and function in molecular biology. The distinct domains within RhoA, such as the GTPase domain, Switch I and II regions, insert region, and C-terminal hypervariable region, serve as structural modules that underpin its role as a molecular switch in cellular signaling. The GTPase domain’s proficiency in binding and hydrolyzing GTP is pivotal, causing RhoA’s influence on the cytoskeleton and, consequently, cellular processes like shape modulation, adhesion, and motility. The activation and inactivation, regulated by proteins like guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs), displays these cell signaling pathways. RhoA’s dysregulation is a key player in diseases, displaying its integral contribution to maintaining cellular homeostasis. RhoA protein is a monomeric protein, meaning it does not have a quaternary structure.

Senior study author Holger Knaut, PhD, an associate professor in the Department of Cell Biology at NYU Langone Health, expressed surprise at the finding, stating, “This finding surprised us because we had no reason to suspect that the RhoA machinery required to move groups of cells would be different from that used by single cells.”

Prior research had indicated that single cells move forward by activating RhoA at their rear ends, initiating a process involving the motor protein non-muscle myosin II, resulting in cell constriction and detachment from the underlying surface.

Contrary to this, the current study revealed that cells in the primordium activate RhoA in pulses at the front of the cells, where it performs a dual role. At the front tip, RhoA stimulates the outward growth of the cell skeleton (actin meshwork), forming protrusions that grip the surface. Simultaneously, at the base of these protrusions, RhoA triggers non-muscle myosin II to pull on the actin meshwork, retracting the protrusions. This coordinated action propels the cell group forward, akin to the movement of a banana slug along the ground.

Dr. Knaut emphasized, “Our findings suggest that RhoA-induced actin flow on the basal sides of cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies the movement of many cell groups.” He added that while the machinery suggests similarities in the movement of single cells and cell groups, RhoA contributes differently in each case.

Dr. Knaut also noted that a deeper understanding of the mechanisms by which cell groups move holds potential in halting the spread of cancer. He remarked, “The machinery suggests that the movement of single cells and groups of cells is similar, but that RhoA contributes to that machinery differently in each case. Within moving cell groups, RhoA generates actin flow directed toward the rear to propel the group forward.” The study’s findings could guide the design of treatments aiming to block the action of proteins implicated in the spread of cancer.

I personally never knew, especially before taking AP Biology, that cells move together. I did know that they always work together, but not necessarily that they coordinate their movements as a collective entity. It’s fascinating to learn about the intricate processes that govern cellular behavior.

I’ve been particularly intrigued by the role of proteins in these cellular functions. For instance, considering the RhoA protein, what would happen if it misfolded or denatured within our bodies? How would our body react to such a disruption? My assumption is that the consequences could be severe, possibly even leading to a breakdown in essential cellular activities. Could it be so detrimental that it might result in death? I’m curious to hear your thoughts on this matter.

I’ve been contemplating the impact of extreme heat on protein structure. If the RhoA protein were to misfold or denature due to high temperatures, it seems logical that our cells might struggle to move effectively within the body. The idea that external factors like heat could influence such fundamental cellular processes is both intriguing and concerning.

I’m curious about the specific gene responsible for coding the RhoA protein. Are there any specific diseases associated with mutations in this gene? It seems like understanding the genetic aspect could provide further insights into potential health implications.

 

 

Breaking the Resistance: Texas A&M’s groundbreaking Polymers kill Antibiotic-Resistant Bacteria

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On January 7, 2024

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As the threat of antibiotic-resistant bacteria becomes a bigger threat, the production of new antibiotics is necessary. The Texas A&M-led collaboration, consisting of many different scientists and organizations, is doing just that. The group has created a polymer capable of “killing bacteria without inducing antibiotic resistance by disrupting the membrane of these microorganisms.” The polymers work in a way that does not allow bacteria to resist. The polymer was made by designing “a positively charged molecule that can be stitched many times to form a large molecule made of the same repeating charged motif using a carefully selected catalyst called AquaMet.” The catalyst AquaMet is quite a feat, as it has to withstand high concentrations of charges and remain water-soluble. After synthesizing the polymer, the team began testing it on human red blood cells and antibiotic-resistant bacteria, such as E. coli. The Texas A&M-led group of scientists believes testing human blood cells is pertinent to their discoveries, as many current antibiotics cannot differentiate between the bacteria being targeted and other cells. This inability to differentiate bacteria from other cells is the cause of gut health issues as a result of antibiotics, which is why the scientific collaboration wishes to find a balance between controlling the harmful bacteria and attacking other cells.

Single Polymer Chains AFM

Image of a single polymer chain:

In AP Biology, I have learned about polymers and catalysts. Polymers, composed of multiple monomers linked by covalent bonds, are the foundational long-chain molecules in organic compounds. Monomers are the most basic structures in organic compounds. For example, the monomer for carbohydrates is a monosaccharide, and the polymers for carbohydrates are disaccharides and polysaccharides. Secondly, catalysts are any substances that speed up the rate of reactions. Organically, catalysts are found as enzymes. Usually, they work by lowering the amount of activation energy required for a specific reaction. AquaMet, which is the key to creating the polymer, is a catalyst. Having a foundational understanding of polymers and catalysts made the discussed article much more comprehensive, as the antibiotic in trial is an artificial polymer created using a specific catalyst. The topic discussed is very appealing to me because of how important it is. New antibiotics that work against antibiotic-resistant bacteria are incredibly important to human safety. The idea of sickness caused by bacteria without an antibiotic to help you is a scary one, and I am happy to learn of the antibiotic frontier! 

What do you think? What role does the Catalyst specifically play in creating the polymer? Do you think this will lead to large scale production and eventually be used to treat antibiotic resistant bacterial infections?

From Individual to Environmental: COVID-19 Antigen Testing Expands

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On January 7, 2024

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Until recently, testing for COVID-19 has focused on the individual rather than on the environment. However, newly introduced technology promises to expand the scope of COVID-19 detection. Researchers at Washington University in St. Louis have developed an apparatus to detect the presence of the covert virus in SARS-CoV-2 without backgroundenvironmental settings. Previous attempts at this technology have been limited by the volume of air tested. Without adequate air quantity, the sensitivity of the technology is negatively impacted. The current system, however, is capable of concentrating up to 1000 m³ of air per minute, compared to the two to eight cubic meters assessed in previous attempts. The result is a system that increases viral detection sensitivity while maintaining specificity.

The newly introduced apparatus functions by using centrifugal force to approximate viral particles to a liquid matrix adherent to the wall of the test chamber. Within the matrix are found nanobodies, bioengineered antibody fragments derived from llama antibodies. As we discussed in class, the human immune system is composed of humoral and self-mediated factors. Antibodies fall into the humoral category. While human antibodies consist of a light chain and a heavy chain, llama antibodies are composed of two heavy chains. By isolating heavy chain llama antibody fragments sensitized to the COVID-19 spike protein and then splicing multiple sensitized heavy chains together, researchers were able to amplify the viral signal, in a manner similar to PCR.

While the device has yet to be approved, cleared, or authorized by the FDA, it holds promise for meaningful real-world application. For example, prior to a large public event, indoor spaces could be screened for the presence of COVID-19. If the virus were detected, remediation could be performed and the environment retested prior to the public event. In doing so, countless potential COVID-19 infections could be avoided.

This novel technology diverges from current efforts at viral detection in that it does not rely on the existence of an infected individual but rather focuses on environmental detection thereby constituting primary prevention. In the future, the technology could be applied to prevention of other infectious diseases, both viral and bacterial. Further work is needed to explore the potential application of this method.

I urge readers to respond to the above and offer opinions.

The Great Disappearance of the Alaskan Snow Crab

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On January 7, 2024

In Student Post

Have you ever indulged in the scrumptious cuisine that is Alaskan Snow Crab? Any such meal is one to remember. However, there is a threat to this dish, and to the ChSnow crab legs and old bay seasoningionoecetes opilio species as a whole: the crabs are cannibalizing each other. Or so, scientists think.

The snow crab population was once rapidly expanding in the eastern Bering Sea, reaching its highest recorded abundance in 2018 at 11.7 billion. The population then rapidly declined to an all-time low of 940 million in 2021. At least 10.76 billion crabs disappeared within the course of 3 years. But where did they go? Chionoecetes opilio 31353372

Researchers have proposed various theories to account for the decline in population. The first obstacle was determining whether the crabs had died off, or merely relocated. After surveying the surrounding habitats and observing no significant influx of snow crabs, the researchers were able to conclude that the crabs had indeed passed on.

With the cause of the crab disappearance isolated, theories were proposed for the cause of death. Temperature, predation, fishery, disease, and cannibalism were all considered. As far as temperature, snow crabs typically exist in cold environments—hence their name. An increase of temperature in their habitats could potentially have accelerated the crabs’ metabolic rates, and consequently expended calories at a rapid rate. With regard to predation, snow crabs are a component of the Pacific cod diet. Relative changes in abundance and distribution of the cod species could have affected the rate of snow crab death. Fisheries provided yet another possibility, as trawling rates are dependent on consumer demand. Disease was also a consideration. Snow crabs are susceptible to Bitter Crab Syndrome, a disease caused by the dinoflagellate parasite Hematodinium perezi, a single-celled eukaryote. Single-celled eukaryotes are organisms comprised of a single cell, as discussed in class. Finally, cannibalism could have been at play. Large snow crabs have been observed to cannibalize smaller snow crabs as a source of food.

Researchers were able to rule out predation and fishery as potential causes of the snow crab population decline. Disease and cannibalism were also eliminated. Through the use of various models, researchers determined that environmental temperature and population density correlated positively with crab mortality, Global Warming In The Worldparticularly in mature crabs. Therefore, increased caloric expenditure as a result of increased environmental temperature was identified as the likely culprit of the crabs’ disappearance. Accordingly, a clear link exists between declines in snow crab population and climate change. Further work is necessary to clarify the exact association between the two phenomena.

I invite comments and potential solutions to this serious challenge.

With the Same COVID Variant, Why Doesn’t Everyone Show the Same Symptoms? Genetic Variations Could Give Us the Answer

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On January 7, 2024

In Student Post

Have you ever wondered why you display less or more severe symptoms when you catch COVID compared to your friends even though it was the same variant? When I was infected with COVID, I couldn’t help but wonder why I had a more severe fever than some of my friends although we caught it around the same time, and I never understood why. In the medical community, this has always been a mystery as well until a study that was published in July that unveiled a possible explanation – genetic variants that are present in some people but not others. 

 

In the study, after analyzing the genetic data of 30,000 who carried the COVID virus, the researchers found that those the people with a specific gene variant – HLA-B15:01- were more than twice as likely to remain asymptomatic, and individuals with two copies of the variant showed a eightfold greater likelihood of being asymptomatic. This reveals that this could be the key gene that influences whether an individual is likely to display certain symptoms after catching COVID. Those participants who were found to not have this particular gene then displayed the common COVID symptoms such as fever, shortness of breath, and cough.

 

This study underscores the significance of variations in the human leukocyte antigen (HLA) complex, a set of genes that is crucial for the immune system’s ability to detect disease causing organisms. Further study conducted by the researchers revealed that this gene variant’s protective effect is due to its ability to tap into the body’s immune system against common viruses like the flu or cold. By analyzing T cells (white blood cells that play crucial roles in the body’s immune system) collected before the pandemic from individuals carrying the HLA-B15:01 variant, researchers discovered that these cells exhibited reactivity not only to a protein fragment from SARS-CoV-2 but also to similar fragments from seasonal viruses. This suggests that individuals with the HLA-B15:01 variant may have immune cells primed for the virus from exposure to seasonal viruses, contributing to their asymptomatic reaction to COVID.

 

In our AP Biology class, we learned about the specific mechanisms and functions of T cells, which is important in this case to understand why the genetic variation is able to prevent certain symptoms from occurring. T cells are type of white blood cells in the body’s immune system that recognize antigens presented by dendritic cells (Helper T Cells), stimulate other immune cells such as B cells to produce antibodies, as well as attack cells infected with the virus (cytotoxic T cells). In this case, those individuals who have the HLA-B15:01 variant would already have primed T cells from seasonal viruses that prepare their bodies against the actual COVID virus, leading to the lack of symptoms displayed. 

 

Looking ahead, this study suggests that these findings and observations could help inform and design the next generation of vaccines, offering potential solutions to prevent symptoms in those infected with viruses. After reading this article, how do you think this finding regarding the impact of genetic variation on COVID symptoms will influence the future of vaccines?



The ghost of COVID: COVID-19’s affect on people years after they contracted it

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On January 7, 2024

In Student Post

In early 2020, the entire world suddenly stopped due to COVID-19. Even as time passed and the deadly rampage of the disease slowly died down, its effects could still be felt. In 2021, Jayson Tatum, a star basketball player for the Boston Celtics, admitted that COVID caused him to use an inhaler before games so he could open up his lungs, even months after he actually had it. Being a big Jayson Tatum fan, I wondered what caused that, but there wasn’t much research on the long-term effects of COVID at the time. Now, a recent ScienceNews article shows that even 2-3 years later, COVID-19 can affect those who contracted it during the height of the pandemic. This phenomenon, called long COVID, could lead to fatigue, blood clots, and even heart disease.Jayson Tatum

The study shown in the article used the health records of 140,000 veterans who were infected with COVID-19 during the height of the pandemic and compared it to about 6 million people who were not reportedly affected by COVID-19. The researchers in the study found that people with past battles with COVID were more at risk of contracting other diseases or having health complications. Though research on why this happens isn’t conclusive yet, recent researchers have discovered that people who experience long COVID tend to have traces of the Sars-CoV-2 in their poop even months after having the virus, which suggests that some of the virus still remains in their guts. This triggers the immune system to act, specifically the innate cellular defenses, which (in this case) is unnecessarily activated due to the detection of the strains of COVID-19 in the gut. This may explain the symptoms felt due to long COVID because as the immune system works, histamine is released, which causes expansion of blood vessels and swelling of fluid/inflammation, explaining many of the symptoms of long COVID, such as trouble breathing, are related to inflammation in the body. On top of this, the strains of Sars-Cov-2 lead to long COVID because the interferons, which are another part of the innate cellular defense, reduce the absorption of an amino acid called tryptophan. Without tryptophan, the body can’t make neurotransmitters like serotonin; the lack of serotonin and other neurotransmitters is what scientists currently believe causes long COVID symptoms.

Novel Coronavirus SARS-CoV-2

Long COVID is a severe problem that has affected billions worldwide. As of now, there is no way to cure it, so it’s essential to try your best to avoid getting COVID-19. People who have underlying health conditions, have been seriously harmed by COVID-19, or don’t have any vaccinations against COVID-19 are the most likely to contract long-term COVID. Another way to avoid long COVID is to stay up-to-date on COVID vaccinations. Many people don’t even know what long-term COVID is. Did you know about long COVID? If not, write about what you learned in the comments.

The “Slow but Steady” Increase of yet Another COVID-19 Variant: What are the Implications?

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On January 7, 2024

In Student Post

“Globally, there has been a slow but steady increase in the proportion of BA.2.86 reported, with its global prevalence at 8.9% in epidemiological week 44” (WHO)

Another variant? Since the beginning of the epidemic, we have seen a few strains of COVID-19 arise, notably the Omicron, Delta, and Alpha variants. You may ask, how do these mutations keep on materializing?

Like all viruses, SARS-CoV-2 — the virus responsible for COVID-19 — goes under, and will continue to go under, several mutations.

File:SARS-CoV-2 without background.pngAs a coronavirus, SARS-CoV-2 uses protein spikes (visualization on right) that fit into cellular receptors, in order to infiltrate our cells. Upon entry of the virus, the invaded cell begins to translate the viral RNA into viral proteins, which leads to the production of new viral genomes. According to Akiko Awasaki, PhD, this is where mutations often arise, stating that, “When viruses enter the host cells and replicate and make copies of their genomes, they inevitably introduce some errors into the code.” While these introduced errors may be inconsequential, they can also be of benefit to the virus, increasing contagiousness. These successful mutations may change how the virus behaves in the future, becoming the foundations of new evolutionary steps.

As we learned in AP Bio, the sequence of amino acids plays a heavy role in the primary structure of the spike protein. When the sequence is altered, hydrogen bonds will be corrupted or created, affecting the stability of the secondary structures like alpha helices and beta pleated sheets. This changes will in turn affect the tertiary structure, ultimately morphing the three-dimensional shape of the spike protein.

Given this knowledge of how SARS-CoV-2 invades cells, and how it may lead to evolution and mutation, what is the significance of this newest variant, and how can it be fought?

BA.2.86 was discovered over the summer with cases from Denmark, Israel, the United Kingdom, and the United States. Later on, it spread to various countries all over the globe, being discovered in wastewater in countries such as Spain and Thailand. As weeks passed, the new strain did not seem to pose a threat compared to its predecessors. However, months later, BA.2.86 on the rise. On November 11th, the CDC estimated that 3.0% of cases came from BA.2.86. November 28th’s estimate, 8.9%, is shockingly almost triple of the earlier estimate just two weeks prior. This is apparently garnering the strain some sort of reputation, now being labelled a “variant of interest” by the World Health Organization.

While the percentage may seem scary, the rise of the strain has not brought a disproportionate growth in infections or hospitalizations. Rather than posing new or threatening danger, it seems to be much better adept to escaping our bodies’ defense systems. The improved ability to slip past antibodies, compared to previous variants, likely comes from its large number of mutations, 30, on its spike protein. Antibodies, which serve to fight these invaders, may find difficulty recognizing and defeating the new strain.

Due to the strain only taking the notice of researchers recently, there are still many things to be uncovered. Some researchers have affirmed their support in newer vaccines against BA.2.86 and future variants. As always, it is best to wear masks when necessary, wash your hands, quarantine if you are experiencing symptoms, and receive the latest vaccine.

File:Janssen COVID-19 vaccine (2021) K.jpg

 

 

 

 

Unveiling the Nobel-Worthy Breakthrough: The mRNA Pioneers Behind Life-Saving Vaccines

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On January 7, 2024

In Student Post

 

Solo-mrna-vaccine-3

In a historic announcement, the Nobel Prize in Physiology or Medicine for 2023 has been awarded to biochemist Katalin Karikó and Drew Weissman, recognizing their groundbreaking contributions to mRNA research. Their work laid the foundation for what has become one of the most influential medical advancements of our time: the development of mRNA vaccines against COVID-19.

Karikó, currently at the University of Szeged in Hungary, and Weissman from the University of Pennsylvania, received this prestigious honor for their pioneering research on modifying mRNA. These modifications were crucial in making the first COVID-19 vaccines possible, notably those produced by Pfizer/BioNTech and Moderna.

Revolutionizing Vaccines

Traditional vaccines typically use weakened or killed viruses, bacteria, or proteins from pathogens to stimulate the immune system. However, mRNA vaccines work differently. They contain genetic instructions for building viral proteins. When administered, these instructions prompt cells to temporarily produce the viral protein, triggering an immune response. The immune system then builds defenses, providing protection if the person is later exposed to the actual virus. This may sound familiar, as AP Bio has taught about immune response and cells. We learned that memory T cells are a crucial component of the immune system, formed after the body encounters a pathogen like a virus or bacteria. These specialized cells “remember” the specific characteristics of the invader, allowing for a rapid and targeted response upon subsequent exposures, effectively combating and neutralizing the illness. Memory B cells, a crucial component of the adaptive immune system, exhibit remarkable specificity and functionality. During the primary immune response, these cells undergo affinity maturation, producing high-affinity antibodies with increased binding capacity to pathogen-specific antigens. Notably long-lived, memory B cells persist in the body, ensuring prolonged immunity. Upon re-exposure, they swiftly differentiate into Plasma B cells, which serve as antibody factories, producing copious amounts of antibodies tailored to the familiar pathogen. On the other hand, memory T cells, including cytotoxic and helper T cells, play distinct yet coordinated roles. Cytotoxic T cells retain the capacity to directly eliminate infected cells, preventing pathogen spread, while helper T cells release cytokines that stimulate antibody production by B cells and enhance cytotoxic T cell activity. With immunological memory, memory T cells provide rapid and targeted responses upon reinfection, actively surveilling for cells displaying specific antigens associated with previously encountered pathogens. Together, these memory cells form a sophisticated and enduring defense mechanism, contributing to the immune system’s ability to combat and neutralize pathogens efficiently.

The technology behind mRNA vaccines has proven immensely effective in combating the COVID-19 pandemic. As of September 2023, over 13.5 billion COVID-19 vaccine doses, including mRNA vaccines and other types, have been administered globally. These vaccines are estimated to have saved nearly 20 million lives worldwide in the year following their introduction.

Modified mRNA and Its Potential

RNA, the lesser-known cousin of DNA, serves as the genetic instruction manual for cells. Messenger RNA (mRNA) copies genetic instructions from DNA and is crucial for protein synthesis. Karikó and Weissman’s pivotal contribution was modifying mRNA building blocks to overcome challenges in early trials.

Traditional mRNA injection would trigger adverse immune reactions, leading to inflammation. By swapping the RNA building block uridine for modified versions, the researchers found a solution. Pseudouridine and later N1-methylpseudouridine proved effective in dampening harmful immune responses. This breakthrough, dating back to 2005, enabled the safe delivery of mRNA to cells.

“The messenger RNA has to hide and go unnoticed by our bodies,” explains Kizzmekia Corbett-Helaire, a viral immunologist at the Harvard T. H. Chan School of Public Health. The modifications developed by Karikó and Weissman were fundamental, allowing mRNA therapeutics to hide while being beneficial to the body.

This technology extends beyond COVID-19, with potential applications against other infectious diseases, cancer, and even rare genetic disorders. Clinical trials are underway for these applications, though results may take several years to emerge.

A Journey Decades in the Making

The road to this groundbreaking achievement was not without obstacles. In 1997, Karikó and Weissman, working in separate buildings, collaborated to address a fundamental problem that could have derailed mRNA vaccines. Initial setbacks, including failed clinical trials in the early 90’s, led many researchers to abandon mRNA as a viable therapeutic approach.

Undeterred, Karikó and Weissman persisted. “We would sit together in 1997 and talk about all the things that we thought RNA could do,” Weissman reflected. The duo’s resilience led to the formation of RNARx in 2006, a company dedicated to developing mRNA-based treatments and vaccines.

Despite the groundbreaking nature of their work, Karikó’s contributions were initially overlooked. Ten years ago, she faced termination from her job and had to move to Germany without her family to secure another position. The Nobel recognition sheds light on her unwavering commitment to mRNA therapeutics.

The Nobel Committee’s decision to acknowledge this achievement swiftly, a mere three years after the vaccines demonstrated their medical importance, highlights the urgency and impact of mRNA technology. Emmanuelle Charpentier and Jennifer Doudna’s Nobel Prize for Chemistry in 2020, awarded eight years after the description of CRISPR/Cas 9, reflects a similar trend of more current acknowledgments.

In a press conference at the University of Pennsylvania, Weissman expressed his surprise at the recognition. “I never expected in my entire life to get the Nobel Prize,” he confessed. The laureates will share the prize of 11 million Swedish kronor, approximately $1 million.

A Nobel-Worthy Legacy and a Glimpse into the Future

The timely recognition of Katalin Karikó and Drew Weissman emphasizes the transformative potential of mRNA therapeutics, extending far beyond the current success against COVID-19. As we celebrate this Nobel-worthy legacy, it opens a new chapter in medical science, offering hope for innovative solutions to combat various diseases and improve human health.

The journey from a meeting in 1997 to the global impact of mRNA vaccines in 2023 showcases the power of perseverance, collaboration, and the pursuit of groundbreaking ideas. 

What do you think about mRNA vaccines? Did/Will you receive one?



Astronomy tools used to detect COVID-19 !?

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On December 15, 2023

In Student Post

Would you ever expect a laser designed for outer space to analyze your health? If you answered yes, get ready to learn why! If not, pay close attention because what you’re about to learn is incredible! This laser is called an “optical frequency comb.” These lasers emit light waves, initially for researching outer space and accurate timekeeping. Because of the COVID outbreak, researchers have found a more promising use of this frequency mechanism. 

The Optical Frequency Comb received its name from the way it functions. These FrequencyComb-measurement
rapid bursts happen in a specific order across different colors of light, ranging from infrared to ultraviolet. When these frequencies are on a graph, it creates peaks that are said to look like the “teeth” of a comb. Now, researchers are exploring the possibility of utilizing this tool to identify specific molecules associated with COVID, and the comb can potentially identify these molecules by recognizing the absorbed colors. It would make most sense that the laser seeks out particular proteins on the virus. As evaluated in our AP Biology class, we know proteins are extremely important in terms of viruses. Proteins in viruses play a vital role by building the virus’s structure and helping it interact with the host’s cells. They enable the virus to enter cells, replicate, and avoid the host’s immune response. Viral proteins also manipulate the host’s cellular functions/processes, ensuring the virus’s survival and spread in the host organism.

Because specific molecules absorb distinct colors of light. The comb can recognize certain molecules in an air sample by identifying the absorbed colors. Because of the severe global pandemic, scientists have found a way to utilize this tool to diagnose patients with COVID in a less “nosy” technique (literally)! Rather than sticking a swab up your nose, all you have to do is exhale. Easy!

Researcher Qizhong Liang mentions that it is best to take the typical PCR test for a more precise result. Because this new COVID testing method is new and still under evaluation, it is best to double-check the test results. Nevertheless, this researchSARS-CoV-2 without background offers a promising future for detecting diseases, such as COVID-19, in a quicker, less effortless way! I find it incredibly fascinating how a group of scientists could take an astronomy tool and use it medically to help diagnose patients. Would you trust this method to diagnose you?

What is the difference between the Pfizer, Moderna and Novavax vaccines?

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On December 15, 2023

In Student Post

After the COVID-19 outbreak, various vaccines were developed to fortify our immune response against the virus. However, questions have arisen regarding the distinctions among the three prominent vaccines: Pfizer, Moderna, and Novavax. Despite the emergence and spread of new COVID-19 variants, these vaccines continue to be recognized as effective measures in preventing severe disease.

The Pfizer vaccine is a messenger RNA (mRNA) vaccine, meaning that a small piece of mRNA will instruct the host cell to produce copies of the spike protein

Novel Coronavirus SARS-CoV-2from a harmless version of the COVID-19 virus. The immune system will then identify the viral protein and will begin to produce antibodies that will attach to and mark the pathogens for destruction. Isn’t the immune system so amazing! The immune system then deploys B memory cells to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future. Common side effects of the Pfizer vaccine include pain, redness, and swelling at the injection site, as well as tiredness, headache, muscle pain, chills, fever, or nausea throughout the body.

Similarly, the Moderna vaccine employs mRNA technology. It instructs host cells to replicate the spike protein, leading to the immune system generating antibodies that identify and target the foreign viral protein. B memory cells are then employed to prevent reinfection by remembering the antigen which allows your immune system to quickly fight it in the future. The side effects of using the Moderna vaccine are also pain, redness, swelling in the area where the shot was administered, and tiredness, headache, muscle pain, chills, fever, or nausea throughout the body. The key distinction between the Pfizer vaccine and the Moderna vaccine lies in storage requirement.  Pfizer vaccine needs to be shipped in a special freezer that reaches very cold temperatures compared to Moderna that can survive in less extreme conditions.

In contrast, Novavax is the only non-mRNA vaccine available in the United States. It is a protein adjuvant vaccine. A protein adjuvant vaccine contains pieces of a harmless version of the COVID-19 spike proteins and pieces of an adjuvant. The immune system identifies the spike proteins as foreign bodies and the adjuvant aids in antibody production and activation of other immune cells to combat the spike proteins. The B memory cells are then used to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future.

Isn’t the way our bodies are able to fight off infection really amazing. Feel free to leave a comment and one fun fact you learned from this blog post!

Covid Brain Fog

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On December 15, 2023

In Student Post

COVID BRAIN? That’s a thing? Yes. Within the metaphorical shadow of an ice sheet, “brain fog” has evolved into a comprehensive label, encompassing the intricate cognitive, psychological, and emotional struggles intertwined with long COVID.3D medical animation coronavirus structure

The referenced article shares the story of Kenton Kaplan, a senior in the Edmund A. Walsh School of Foreign Service at Georgetown University, showing signs of COVID-related brain symptoms. Ken’s year-long battle with severe memory loss, extreme fatigue, and immunosuppression highlights the diverse experiences enclosed by this term. Despite its recognition as a federally acknowledged disability, individuals reporting “brain fog” face disbelief, hindering their access to necessary accommodations. 

Emily Mendenhall, a medical anthropologist, explored the varied manifestations of long COVID symptoms beyond the popular definition of mild forgetfulness. Interviews with 22 sufferers revealed debilitating episodes, with individuals describing struggles with daily tasks during “brain fog” episodes. These individuals spoke of debilitating days where routine tasks became overwhelming: chronic nerve pain, severe headaches, episodes of dizziness, nausea, and fainting. The disparity between how healthcare professionals perceive “brain fog” and the actual experiences of those affected emphasizes the necessity for clear categorizations that can more effectively address the range and intensity of symptoms. 

Faced with difficulties in securing accommodations, Ken’s ongoing struggles with sporadic memory loss emphasize the importance of acknowledging the complexity of a cloudy consciousness. Clearer names and understanding the various aspects of symptoms could help make medical leave and accommodations more accepted. This support would be beneficial for those dealing with the continued effects of long COVID in their everyday lives.

When the immune system encounters specific pathogens, such as the COVID-19 virus, it relies on the binding action of B cell antigen receptors or antibodies to epitopes on the pathogen for recognition. This recognition serves as a trigger, setting off a cascade of events that activate B cells and stimulate the production of antibodies. These antibodies play a crucial role in safeguarding the body against the virus. This shows how important a strong immune system is in dealing with complicated conditions like long COVID, especially when it comes to cognitive challenges like “brain fog.”

A couple of weeks ago, my mom tested positive for COVID, marking the first time she had ever faced the virus since the beginning of the pandemic. Despite being up to date on all her vaccines, including mRNA shots, which introduce genetic material into cells to prompt the production of viral proteins and trigger the immune system, she still experienced a severe case. Unfortunately, COVID hit her hard, unleashing a wave of symptoms ranging from chills and fever to body aches, a runny nose, and a persistent cough. As if that wasn’t challenging enough, she started experiencing heightened anxiety as she struggled with memory lapses, struggling to recall the day she tested positive, losing track of time, and questioning how long she had been in quarantine. It was a tough period for her, navigating not only the physical toll of the illness but also the mental strain of uncertainty. So, how can we collectively raise awareness about the diverse experiences encapsulated by the term “brain fog” and advocate for better understanding and support?

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