Student Post – Page 4 – BioQuakes

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Cancer-Causing Free Radicals Are the Key to Tardigrade Survival

On February 27, 2024

In Student Post

Many may recognize the resilience of tardigrades, the microscopic water bears that can seemingly endure any and all conditions—researchers have found that tardigrades possess this attribute because of their ability to harness free radicals, the infamous matter that causes cancer in humans.

Tardigrades have survived all five mass extinction events on Earth, and are thought to have been around since before the current eon. They can live through extreme temperature and radiation, and even the vacuum of space. But how are they capable of this immense resilience?

Traditionally, free radicals have been known to promote cancer, causing genetic mutations that allow cells to multiply uncontrollably. First, in mitosis, the mutated cell divides, then its offspring divides, and before long a mass forms. That mass, or tumor, grows uncontrollably, consuming vital nutrients and mechanically interfering with the body’s internal function. If left unchecked, the tumor will eventually overwhelm the body’s ability to survive. However, there’s a flip side to free radicals.

The tardigrade has managed to harness the destructive power of free radicals in its quest for survival. For years, scientists have been baffled by the tardigrade’s ability to undergo drastic transformation in times of extreme stress. The organism’s transformations are a part of cryptobiosis, which consists of (but is not limited to) anhydrobiosis and cryobiosis. In anhydrobiosis, the tardigrade decreases its water content by 99% and its metabolic rate by 99.99%, and remains in a “tun” state for five years or more, only to rehydrate and flourish once environmental conditions are back to normal. In addition, via cryobiosis and other cryptobiosis processes, the tardigrade can survive extreme heat (304° F) and cold (-458° F). And the trigger for all of these survival mechanisms: free radicals, the same extra-electron atoms and molecules that cause human cells to mutate and multiply to form tumors.

Recent research suggests that tardigrades initiate cryptobiosis and protect themselves by releasing intracellular reactive oxygen species (free radicals) that in turn reversibly oxidize cysteine, an amino acid that acts as a sort of regulatory sensor for responses to stressors. The obvious question is: why isn’t the tardigrade harmed by the free radicals? The answer might hold the key to better understanding how to prevent cellular mutation, and cancer, in humans. Additional investigation is needed in this area.

So, what do you think? Are there similar discoveries that may be able to help us combat cancer?

Will Scientists Crack the Impossible Code of Human Anti-Aging?

On February 27, 2024

In Student Post

Have you ever wondered why humans age? Why we can’t stay alive forever? Or is it even possible to? According to a recent article from Scientific American, scientists are actively researching what lifestyle choices and diets can lead to a longer life.

Firstly, before we dive into that, let me explain why the article says we age and what causes cells to lose their ability to regenerate. The article says that cells are constantly being damaged in our body, from UV rays to poor nutrition, which causes them to regenerate to become healthy again. Regenerating cells divide into new healthy ones by making copies of their chromosomes, which contain DNA. But this is where the aging process begins. Each time a cell divides, the end or caps of the chromosome, called telomeres, shrink, and when they become too short, the cells cannot divide further. This cell state is called senescence. This state of the cell is dangerous, so we secrete chemicals to activate our immune system and eliminate them, but when our body does not destroy them, they cause neighboring cells to go into this state as well. If the senescence cells keep spreading to their neighbors, the body and brain work slower, causing our body to deteriorate, become susceptible to disease, and die.

This is where the scientists come in! According to the article, experts often believe in the popular disposable soma theory. This theory indicates that our bodies have limited lifetime energy and that humans use a good amount of it to do reproductive functions. So, if you choose not to reproduce, you could live a longer life. Is that not a hard choice? Children or a longer life? I know I wish there could be a happy medium! But, according to experts, if people try to reach a compromise, they risk mutations and major issues in decedents. Therefore, it is hard to combat the aging of humans from this perspective, not only for ethical reasons but also on the subject of time. In an article by Antonello Lorenzini, he states that time and environmental pressures cause constraints for us to repair damaged cells and reproduce in the limited window we have. Therefore, we as humans must maximize the time and energy we have as it is imperative for our aging process not to slow down at an earlier stage of our lives.

Since this approach did not work, researchers in the article looked at the perspective of targeting short telomeres and preventing cells from entering senescence. Yet, there is a problem in both of these ideas as well. People with long telomeres have more telomerase, which is the enzyme that keeps telomeres long; the problem with this is that cancer cells can use this telomerase to multiply unchecked. As well as this, people with longer telomeres tend to have a more likely chance of getting cancer and brain tumors as well. Is a longer life worth a higher chance of getting cancer? Personally, I do not think so. So researchers also tried to prevent cells from going into a senescent state, but they had a similar problem. The cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells.

Next, researchers looked at ideas for extending our lifespan through caloric restriction. A study from Nature displayed that people who ate 15% fewer calories had less body aging. This is also shown in the research from AARP, which said researchers at the National Institutes of Health found that adults who had 12% less caloric intake over two years opened biological pathways associated with healthy aging. But, back to the original article from Scientific American, it says this must be done carefully. Caloric restriction may extend life span but also may cause side effects, such as decreasing gray matter in the brain. So, as researchers try to find a solution that does not cause any harm to us as a species beyond a balanced diet and exercise, aging will not stop anytime soon. (Very sad, I know.)

Lastly, I want to connect this to something we learned in AP Biology this year. In this unit, we discuss cell division and the cell cycle. This relates to the topic of anti-aging/aging because of the cell reproduction rate and the ability of the cell to replicate. As said above, as the cells are damaged, they must replicate. This process starts with interphase, where the cell will go through the G1, S, and G2 phases or the growing and replicating phases. The cell has normal functions, copies DNA, and doubles its organelles in preparation for mitosis. Next, it will move into mitosis, where it will divide the nucleus through kinetochore and nonkinetochore, and finally go into the stage of cytokinesis, where the cytoplasm is split. This can further relate to the topic through the telomeres and the telomerase. As said above, people with more telomerase can have a higher chance of getting cancer because the cancer can multiply unchecked. They can multiply unchecked because most cancer cells use telomerase to divide indefinitely, as it will continue to replicate and not die, which causes tumors to form. So, suppose our normal cells start to use telomerase. In that case, our cells will act similarly in replication to cancer, and our bodies will not be able to tell the difference.

Most cells only divide when given a chemical signal, but cancer cells do not obey this. They will divide even though they did not receive a chemical signal. In AP Bio, we learned that cancer cells also do not have the signal to stop replicating, which is where the telomerase comes in. Since cancer cells do not receive the signal to stop copying and they have long and reconstructing telomerase that allows them to do this, they will never die.

As well as this, we can link the idea from the senescent state – the cells researchers need to target are the ones that induce aging, but they must avoid the cells benefitting the body, or else it will cause more catastrophe for human cells – to this as well. If genes are damaged when they are targeting aging cells, this can cause oncogenes to form. Oncogenes will cause the cells to divide when no signal is sent. This would lead to tumors because of the rapid cell replication. Similarly, suppose a mutation damages the tumor suppressor in the cell. In that case, there will be nothing stopping the oncogenes from replicating, allowing them to do what cancer does and replicate non-stop. Therefore, the process of anti-aging and cancer remarkably coincide as the very thing that we want to use for anti-aging is something that causes cancer to be able to divide indefinitely. That is pretty amazing and crazy to me! How can something in our bodies allow that to happen? What do you think?

King of the Jungle no more? How an unlikely species have halted Lions in the wild

On February 27, 2024

In Student Post

Everybody has known lions as the ‘Kings of the Jungles.’ For years, they’ve dominated the African Wild and easily maintained their status as most dominant in the African Wild and Jungles. However, recently, a somewhat new and indirect foe has halted the Kings of the Jungle quest. In a recent ScienceNews article, it was discovered that the invasive species Pheidole megacephala, more commonly known as big-headed ants, has indirectly made Lions switch their prey from the preferred zebras to buffalos.

The big-headed ants, seemingly originally imported on produce, prey on the native acacia ants. Although it may seem like a slight difference in an ecosystem, it starts a big chain event. Without acacia ants, who live near whistling thorn trees, elephants can graze on the trees freely. Usually, when acacia ant populations are normal, they stop elephants from grazing on the trees and keep the grassland covered. However, without them, the lions are forced to switch from their primary prey, zebra, to buffalo. Although the lions are still able to successfully hunt, being tertiary consumers, it can potentially be detrimental to their ability to survive. Lions are tertiary consumers, meaning they are at the top of the tropic levels. This indicates that for lions, it’s super hard to get the energy necessary to survive due to the loss of power when transferring from one tropic level to another. Basically, the lions have a super-low availability of energy, and losing the ability to hunt zebras makes this even lower, putting them in even greater danger of going extinct.

For Lions, whose wildlife numbers have dwindled 75% in the past 5 decades, losing a crucial prey could have immense effect. Right now, the impact the introduction of invasive ants will have on Lions is unknown, but since most invasive species come from human trading or shipping, We should feel responsible for helping lions and animals we have exposed to invasive species due to our actions. If you know any other examples of invasive species messing up an ecosystem or how humans impact the introduction of invasive species, let us know in the comments!

Uncovering the Mysteries of Early-Onset Colorectal Cancer: A Growing Concern

By mitochondriadriana

On February 27, 2024

In Student Post

In recent years, an alarming trend has emerged: more and more people under the age of 50 are being diagnosed with colorectal cancer. Once considered primarily a disease affecting older adults, colorectal cancer is now becoming increasingly prevalent among younger and middle-aged individuals. The shift in demographics has puzzled scientists and medical professionals alike, prompting a deep dive into understanding the underlying causes and warning signs of this concerning trend. Normally, colorectal cancer has been associated with older age groups (what is colon cancer?) However, recent studies have shown a significant increase in cases among individuals under 50. This shift in demographics has led to a growing concern within the medical community. As medical professionals try to figure out why this is happening, they notice that it cannot be attributed to a single cause. Researchers are exploring various factors, including obesity, diet, gut microbiome, and even birth cohort effects, to understand the complex interplay contributing to the disease. While the exact causes remain elusive, identifying early warning signs is crucial for timely diagnosis and treatment. Symptoms such as abdominal pain, rectal bleeding, diarrhea, and iron-deficiency anemia have been identified as potential red flags, emphasizing the importance of vigilance and proactive healthcare.

Environmental chemicals crashing our cellular party? It’s like a scene straight out of a sci-fi movie! Who knew our everyday exposures could have such far-reaching effects?

The topic of colon cancer rising in young adults is being explored by many people. The National Cancer Institute shared Doug Dallmann’s story, reflecting the reality faced by many young adults who experience symptoms but may dismiss them due to misconceptions about age-related risk. Dallmann noticed blood in his stool in his early thirties but didn’t think much of it until the bleeding became more frequent and intense. His story underscores the importance of paying attention to symptoms and seeking medical attention promptly, regardless of age.

The article delves into the growing body of research aiming to uncover the root causes of early-onset colorectal cancer. Factors such as obesity, diet, gut microbiome, and environmental exposures are being explored as potential contributors to the rise in cases among younger adults. As we strive to unravel the mysteries surrounding early-onset colorectal cancer, it’s crucial to raise awareness about the importance of vigilance and proactive healthcare. By sharing stories like Doug Dallmann’s we can empower individuals to take charge of their health and advocate for timely screening and intervention. It has become increasingly important to do this.

As someone who enjoys a good Netflix binge, I never thought my TV habits could have anything to do with my colon health. Time to switch to more active hobbies, I guess!

At the core of cellular proliferation lies the tightly regulated process of the cell cycle. This sequence that includes phases such as G1, S, G2, and M, ensures precise DNA replication and distribution of genetic material. Cells progress through this cycle under the watchful eye of intricate signaling pathways and molecular checkpoints. In the context of colorectal cancer, disruptions to these fundamental cellular processes set off a chain reaction culminating in malignant transformation. Mutations in critical regulatory genes, including tumor suppressors like APC and oncogenes such as KRAS, upset the delicate balance of cell cycle control. This imbalance leads to uncontrolled proliferation and the formation of tumors. The article sheds light on the perplexing rise of early-onset colorectal cancer, providing a tangible context to explore these AP Biology concepts. As scientists try to find the root causes of this issue, they consider the interplay between environmental exposures, genetic predisposition, and cellular dynamics. Moreover, the accumulation of mutations, fueled by disrupted DNA repair mechanisms and genomic instability, heightens the risk of malignant progression. Insights drawn from AP Biology concerning DNA repair pathways and genome maintenance offer invaluable perspectives in dissecting the molecular underpinnings of cancer.

As I delved into this topic, I couldn’t help but feel a sense of urgency. The increasing prevalence of colorectal cancer among younger adults serves as a stark reminder of the complex interplay between genetics, lifestyle, and environmental factors in shaping our health outcomes. It’s concerning to think that individuals in their prime years of life are being confronted with such a serious illness, often with delayed diagnosis due to misconceptions about age-related risk.

What are your thoughts on the potential factors contributing to the rise in early-onset colorectal cancer? Have you encountered cases or discussions about this issue in your own communities or healthcare settings? Share your insights and perspectives below! Let’s continue the conversation and raise awareness about this important health concern.

Blueberries: Why They’re Blue

On February 27, 2024

In Student Post

An article published on February 7th 2024 by ScienceNews identifies and reveals why blueberries are blue. Most people reading this article are probably wondering why this is such a big deal and how it relates to science. Spoiler, it does. The secret to a blueberries hue, or color, is in the structure of its wax coat. Many fruits such as grapes, plums, and blueberries have this waxy covering and researchers have identified that it is this waxy coat that makes these fruits appear blue to humans.

Typically, blue is not a common color in nature and although there are some known blue fruits, few of them contain pigments of that shade. For example, blueberries contain large amounts of anthocyanin which is a skin pigment that should give each berry a dark red color, but structures in blueberries waxy outer layers work against anthocyanin creating their own blues.

Rox Middleton, a physicist at the University of Bristol in England and Dresden University of Technology in Germany, conducted an experiment with the help of a few colleagues to better understand what is special about the berries waxy coverings. The group looked at a variety of fruits such as blueberries, Oregon grapes, and Plums under a scanning electron microscope to take a look at the finer details of blue-colored fruit skins. The resulting images revealed nano structures that reflect blue and ultraviolet light and cover up dark red anthocyanin pigments that are found underneath the waxy coating on blueberries skin. Furthermore, wax from the Oregon grapes became transparent when it was dissolved with chloroform.

An article published on the same day through the University of Bristol provides another perspective on blueberries waxy coat. The article identifies that blueberries blue pigment can’t be extracted by squishing the berries because the pigment isn’t located in the juice that can be squeezed from the berry. The article then goes into further detail about the coating stating that it is an “ultra-thin colourant” around two microns thick that reflects UV light well which makes it appear blue as the coating is made up of miniature structures that scatter blue and UV light.

A second article published by dole, helps explains the benefits of anthocyanin. The article states that anthocyanins bind to free radicals therefore protecting against some health disorders that can arise through oxidative processes such as cardiovascular disease and cancer. The pigment is also believed to have a positive effect on inflammation and high blood pressure as well as protecting the gut from bacteria by supporting the digestive system.

To help further explain how pigments work and how we see certain colors, in AP Biology class, we learned that when a plant, for example, appears green, this is because that plant is absorbing all colors available except for green, which it reflects. This is why the rate of photosynthesis in plants is the worst in green light because the plant is unable to absorb the green light which contains the photons it requires to preform photosynthesis. Blueberries also reflect light, but it’s waxy coating instead reflects blue light which is why they appear blue to us.

I believe that these new findings are very exciting as I personally didn’t realize that a waxy coating was responsible for blueberries blue appearance. I look forward to reading about more experiments like Middleton’s that help us further understand why certain fruits and vegetables appear the way they do, what do you think?

Memory Card Plugged in for Future Generations of Bacteria?

By samuelosaurus

On February 27, 2024

In Student Post

Have you ever thought about the ability of being born with knowledge? It sounds like a plot out of a science fiction novel, yet recent research discovered that Escherichia coli (E. coli) bacteria, despite not having a brain, are able to remember past encounters with nutrients and pass this information down to their future offspring. This discovery not only surprises microbial behavior scientists but also reveals the challenge behind the fight against antibiotic resistance.

Swarming of Bacteria
George O’Toole, a microbiologist at Dartmouth College, explains that while “we typically think of microbes as single-celled organisms,” they actually operate in collective units or swarms. Interestingly, when they move in swarms, they become stronger against Antibiotics because there are more of them close together. According to this article from Missouri Department of Health and Senior Services that explain what is Antibiotic resistance, the reason E. coli bacteria become stronger against antibiotics when they are close together in swarms is due to their biological mutations, DNA exchange, and rapid reproductions. Mutations are essential to evolution, they can bring genetic variation (good or bad) to a specie. Because of the vast number of bacteria present and their high reproduction rate, many mutations can occur in a swarm of bacteria. Through random mutations and selection, bacteria can develop defense mechanisms against antibiotics. After some bacteria have developed some anti-antibiotic genes, bacteria will actively swap bits of DNA among both related or unrelated species. Thus, antibiotic-resistant genes will spread rapidly among a swarm of bacteria and can can even be incorporated into other species of bacteria. Finally, given the fast reproduction speed of bacteria, it does not take long for the antibiotic-resistant bacteria to fill up a huge portion of the bacteria population, therefore disabling/nerfing the effects antibiotic drugs.

Collective Memory of E. coli
A team of scientists, as reported in the Proceedings of the National Academy of Sciences USA, found that E. coli bacteria swarms have a form of memory that correspond to their exposure to nutrients. This experiment, led by Souvik Bhattacharyya from the University of Texas at Austin, observed unusual patterns in E. coli colonies. Through deeper examination with his science team, they concluded that these bacteria acted differently because of their previous experiences. Specifically, bacteria from colonies that had swarmed before were more likely to swarm again. This behavior was passed down to their descendants for four generations, suggesting a genetic memory of past actions in the bacteria.

By Cancer Research UK – Original email from CRUK, CC BY-SA 4.0, Link

Genes that are Responsible for this Behavior:
Further investigation was conducted to this phenomenon concluded that two genes responsible for iron uptake and regulation is the keys to bacteria’s memory. Bacteria with lower levels of iron, an essential nutrient for them, are more likely to move collectively(in swarms) to find environments with higher level of iron concentration. In addition to the past research that shown that many bacteria can remember and pass to their offspring of the description of their physical surroundings, this study suggests that bacterial can also remember and pass to their offspring about nutrients’ presence. This ability of bacteria to remember and pass on knowledge about physical surroundings and nutrient existence demonstrates bacteria’s evolution journey.

Purpose?
This research increases our understanding of microbial life, showing that bacteria like E. coli can remember more the physical environments and can also recall the presence of nutrients. These memories will affect their decisions on where to settle and can increase their chances of surviving and fitness. O’Toole believes that this mechanism of bacterial memory is probably not exclusive to E. coli; it can actually be a common mechanism that exists among many different types of bacteria. The insights gained from studying these E. coli at a molecular level can provide valuable context for the development of antibiotics, offering new approaches as traditional antibiotics will eventually lose their effectiveness.

Connection to AP Bio
In AP Biology, we’ve learned about Cell Signaling molecules and mechanisms used by organisms. Bacteria can also communicate amongst them when they are close together through a process called Quorum Sensing. Bacteria will secrete small chemical signaling molecules which will be detected by other bacteria nearby using their receptors. Through Quorum Sensing, bacteria are able communicate with others of their kind, sharing information about bacteria density and adjust gene expression accordingly. In addition, we will also be covering information about DNA, Heredity, and Evolution during this year in AP biology, which are also significant themes in this post. Numerous mutations will occur in swarms of bacteria due to their large number, this mutation of their DNA can occasionally cause significant change. If this change is extremely positive and can do this bacteria good, through natural selection, this gene will be kept and pass on to future generations of bacteria so that more and more bacteria will have this trait. This is the reason behind my antibiotics are slowly losing their functions. More and more bacteria have mutated and can resist the effects of antibiotic drugs.

What are your thoughts?
A couple of years ago, I often watched cartoons that portrays a type of technology that can give knowledge and pass memory to a newborn baby. I thought that it was a fascinating and unrealistic idea. However, during my research, I surprisingly found out that bacteria seemed to have this ability to pass on their memories to their offspring. What are your views about bacteria’s ability to memorize and pass their memories on to future generations? Do you think this experiment is helpful to future development of antibiotics? Feel free to leave a comment below and we can discuss more about this topic! For more information on this post, go to ScientificAmerican.com for the latest research and updates.

How A Lion’s Meal Has Changed Due To An Invasive Ant

By alexoskeleton

On February 27, 2024

In Student Post

In a recent study conducted by wildlife ecologist Jake Goheen and his colleagues at the University of Wyoming and the Ol Pejeta Conservancy in Kenya, the intricate connections within the African savanna’s ecosystem were unveiled. The research focused on the impact of the invasion of big-headed ants (Pheidole megacephala) on the food web, leading to unexpected consequences for the top predator, lions.

Pheidole megacephala commonly known as the big-headed ant, is a globally distributed species recognized for its distinctive characteristics. This ant species exhibits a striking size polymorphism within its colonies, featuring major workers with disproportionately large heads compared to their minor counterparts. This adaptation allows for specialization in various tasks within the colony, with major workers often taking on roles such as defense and foraging. Invasive populations of these ants can outcompete and displace native ant species, altering local ecosystems. Known for their adaptability, Pheidole megacephala colonies can thrive in diverse habitats, from urban areas to forests. Researchers study this species to understand its behavior and biology, aiding in the development of effective management strategies to mitigate its impact on ecosystems where it has become invasive.

The invasion of big-headed ants resulted in the demise of native acacia ants (genus Crematogaster), which played a crucial role in defending whistling thorn trees against hungry elephants. Normally, these acacia ants would swarm up inside an elephant’s nostrils and deter them from damaging the thorn trees. However, with the invasion eliminating these defenders, elephants freely ravaged the thorn trees, transforming the landscape by opening up the grassland.

This alteration in the environment had a cascading effect on the lions’ hunting behavior. The reduction in tree cover made it challenging for lions to pursue their preferred prey, zebras. Instead, the lions shifted their focus to buffalo, a riskier but more accessible target in the changed terrain.

To understand the extent of these changes, the researchers tracked lionesses in the region, collaring them to monitor their activities and kills. They also established experimental plots to observe areas invaded by big-headed ants compared to those where native ants still thrived.

The findings revealed a significant increase in visibility in areas affected by big-headed ants. Lions in these open spaces had a higher chance of spotting prey from a distance. Consequently, the success rate of lion kills on zebras declined when visibility increased.

Over the three-year study period, the lionesses’ diet underwent a transformation. Zebra kills dropped from 67 percent to 42 percent, while buffalo kills rose from zero to 42 percent. Despite the change in prey, the lions faced new challenges, as buffalos are formidable opponents and hunting them posed a greater risk of injury.

This study emphasizes the interconnectedness of species in an ecosystem and highlights the far-reaching consequences of disrupting even seemingly insignificant mutual relationships. It serves as a reminder for ecologists to explore similar relationships in different ecosystems, as the consequences of such disruptions can be unexpected and indirect, ultimately influencing the balance of entire communities.

After studying ecology in AP Biology, I learned how devastating a alter in the food chain/web can be. I learned how interconnected ecosystems are, with each species playing a crucial role in maintaining balance. The concept of trophic levels and the intricate web of energy transfer underscored the importance of even the smallest organisms. The introduction of invasive species, such as Pheidole megacephala, can disrupt these ecological dynamics. Observing the consequences of these disruptions, especially through altered food chains, highlighted the cascading effects on biodiversity and ecosystem stability. Understanding the interconnectedness of species in an ecosystem emphasized the need for conservation efforts and sustainable practices. The lessons from studying ecology in AP Biology not only deepened my appreciation for the complexity of nature but also underscored the responsibility we have in preserving and respecting the delicate balance that sustains life on Earth.

I personally believe that we must take more precautions when traveling to foreign places. I remember when I was in the Galapagos Islands with the school; there were checkpoints at each island and at the airport where they would search your bag for species. You couldn’t even bring a single rock to a different island! As a society, we should take more precautions like these to prevent further damage to ecosystems. We must take care of the places that we stand on. What do you think?

Childhood Stress: Impact on Blood Pressure, Obesity, and Diabetes

On February 27, 2024

In Student Post

Childhood stress can lead to chronic diseases? A study conducted by researchers at the Keck School of Medicine, University of Southern California, emphasizes the importance of comprehending the impact of perceived stress on cardiometabolic health factors, including obesity, Type 2 diabetes, high cholesterol, and high blood pressure. Based on data from the Southern California Children’s Health Study, the study revealed that consistently high levels of perceived stress from adolescence through adulthood were associated with a greater risk for cardiometabolic diseases in young adulthood. Individuals experiencing prolonged stress during this period exhibited worse vascular health, higher total body fat, increased abdominal fat, and a heightened risk of obesity.

The study indicated a general association between higher perceived stress levels and elevated risks of various cardiometabolic health conditions. Those reporting higher stress levels demonstrated poorer vascular health and higher systolic and diastolic blood pressure. The findings suggest that healthcare professionals could benefit from incorporating the Perceived Stress Scale into routine clinic assessments to identify individuals with higher stress levels early, enabling timely intervention and treatment.

While the study provides valuable insights into the long-term impact of stress on cardiometabolic health, it acknowledges the limitation of its relatively small size. The researchers recommend more extensive studies to clarify and validate the associations between perceived stress patterns and various risk factors for cardiometabolic diseases. In a study on adolescents in Louisiana, researchers found that poor diet quality during adolescence is linked to lasting health risks, according to the article Poor diet quality during adolescence is linked to serious health risks. The study focused on physical activity, sleep, and dietary patterns, aiming to improve diet and reduce health risks, including cardiometabolic risks. The findings show that not following dietary guidelines is tied to ongoing health issues in teens over two years. Ensuring adolescents maintain an active lifestyle, adopt a wholesome diet, prioritize quality sleep, and manage stress levels becomes crucial for their overall well-being.

In AP Bio’s Unit 3 on Cell Communication, we explored the endocrine system: a complex network of glands and organs that secrete hormones into the bloodstream to regulate various physiological functions and maintain homeostasis in the body. Perceived stress triggers the activation of the body’s stress response, which involves the release of stress hormones from the endocrine system, primarily cortisol and adrenaline. The prolonged exposure to high levels of stress, as indicated by the study, may lead to dysregulation in the endocrine system. This dysregulation could contribute to disturbances in metabolic processes, potentially explaining the observed associations with cardiometabolic risk factors. My grandfather, Steve, was diagnosed with Type 2 diabetes in 1995. His body’s cells became resistant to the effects of insulin, a hormone produced by the pancreas that helps cells absorb glucose from the bloodstream. As a result, glucose cannot enter cells efficiently, leading to elevated blood sugar levels. As a kid, my grandfather always told me to drink water and get in those daily vegetables with every sweet I ate. As I’ve researched, diets high in refined carbohydrates, sugars, and saturated fats contribute to obesity and insulin resistance. A diet rich in processed foods and poor in fruits, vegetables, and whole grains increases the risk of type 2 diabetes. I would love to hear your thoughts and insights on childhood stress linked to chronic diseases. Please share your comments and join the conversation!

How is Omicron still a problem?

On January 16, 2024

In Student Post

Covid-19 under a microscope

Allow me to take you back to the early days of the Covid-19 pandemic. Alpha, and Delta were the primary variants.

And then Omicron stumbled in, and unlike the others, never left.

Unlike the others, who had viciously ensnared others to their deaths, Omicron was more akin to a hard cold, or the flu. Whilst it shared flagship symptoms like parosmia (loss of smell/taste) and other respiratory symptoms, they resulted in less hospitalizations. In addition, we were going stir crazy and had started to unlock the lockdown.

And Omicron, unlike the others, was a rapidly evolving virus, one variant one second and another the next. The rapid mutations in the epitopes (the spike protein that the immune system uses to distinguish it from other viruses) made vaccines, which are designed to emulate the epitopes so the body can recognize it (hence the potential fever- your body is learning the epitope’s shape so it can catch the real thing faster), next to impossible to settle on. Trying to get a working vaccine for it was like trying to hold a tiny fish in the rain- it just kept slipping away.

And now again, descendants of Omicron are dominant again.

HV.1 is a descendant of Eris (EG.5) but isn’t really that different from Eris. Vaccines that are designed to target XBB (another offshoot) still work on both of them. HV.1 is only dominant for minor mutations, as vaccines still work.

The real worry is BA.2.86, which has been determined to evade the immune system. It, in comparison to say, EG.5.1 or XBB.1.5, resulted in a lower concentration of neutralizing antibodies, meaning one infected would be infected for longer.

Its descendant, JN.1 might be even better at it. It can be transmitted at low levels due to its highly mutated spike protein, and still evades the humoral response more effectively than its predecessor.

I, for one, think that Omicron isn’t going away. It mutates too quickly to truly be caught. But I think a monovalent vaccine is possible per each set of dominant strains. And to that, I mean it will likely become another vaccine to get annually in the fall.

Huntington’s Unveiled: Delving into Delayed Onset and the Fun Side of Therapeutic Possibilities

By mitochondriadriana

On January 15, 2024

In Student Post

Greetings, health explorers! Today, we embark on a riveting exploration into Huntington’s disease, where scientists, spearheaded by the brilliant geneticist Bob Handsaker, have unveiled a compelling clue about its delayed onset in this article.

Picture this: Huntington’s disease stems from a mistakenly repeated segment in the HTT gene. Bucking the conventional belief that these repeats remain constant, the research illuminates their dynamic growth in specific brain cells over time. As these repeats breach a critical threshold, the very activity of numerous genes in the affected brain cells undergoes a dramatic transformation, ultimately leading to cell death. The tantalizing prospect arises – could preventing the expansion of these repeats be the key to halting the development of Huntington’s disease?

But fear not! The study hints at a potential game-changer – curbing the expansion of these repeats might be the key to slamming the brakes on Huntington’s disease development.

Let’s summarize what the article’s main idea was. Scientists, led by geneticist Bob Handsaker, have uncovered a significant clue about the delayed onset of Huntington’s disease. The disease arises from a mistakenly repeated segment in the HTT gene. Contrary to the belief that these repeats remain constant, the research reveals their dynamic growth in specific brain cells over time. Once the repeats surpass a critical point, the activity of numerous genes in the affected brain cells changes drastically, leading to cell death. The study suggests that preventing the expansion of these repeats may offer a way to halt the development of Huntington’s disease.

But let’s not stop there – delve deeper into the intricacies.

Before we move on, let’s pause. Do you know what Huntington’s disease is? Before you move on, read this brief article on Huntington’s disease.

Anyway, let’s continue! A study on the neurological manifestations of Huntington’s disease beckons us, offering insights into the broader impact on the brain. The article, GENETICS AND NEUROPATHOLOGY OF Huntington’s DISEASE, reveals a breakthrough in understanding Huntington’s disease, shedding light on why the fatal brain disorder takes a prolonged time to manifest and suggesting a potential strategy to halt its progression. The key finding is that in some brain cells, the repeats of a gene called HTT, responsible for Huntington’s disease, can grow to hundreds of copies over time. When the number of repeats surpasses a certain threshold, the activity of thousands of other genes in the brain cells changes drastically, leading to cell death.

This discovery is connected to this article about CRISPR technology and its use in treating genetic disorders. The link lies in the common theme of genetic manipulation and its potential role in addressing hereditary diseases. In the case of Huntington’s disease, the research suggests that preventing the expansion of repeats in the HTT gene could stop the development of the disease. This aligns with the broader theme of genetic interventions discussed in the CRISPR article.

Moreover, the article highlights the role of MSH3, a protein involved in DNA repair, in inadvertently adding CAG sequences to the HTT gene. Lowering the levels of this protein may prevent the expansion of repeats. This mechanistic insight provides a potential target for therapeutic intervention, indicating a different approach from current strategies that focus on lowering levels of the huntingtin protein.

In AP Biology class, we covered cell signaling, where cells communicate through molecular signals to regulate various processes. Signaling pathways involve receptors, intracellular messengers, and cellular responses. The Huntington’s disease article reveals that the expansion of CAG repeats in the HTT gene leads to changes in the activity of thousands of genes in brain cells. This alteration in gene activity can be seen as a response to an abnormal signal, impacting cell function. Understanding how abnormal signals lead to cellular dysfunction is crucial to cell communication.

In conclusion, Handsaker’s research cracks the molecular intricacies of Huntington’s disease, providing a deeper understanding of its development and offering potential therapeutic routes. The connection to AP Biology principles underscores the relevance of this study in the broader context of cellular communication and genetic signaling. What are your views on this paradigm shift in Huntington’s research? How might targeting DNA instability revolutionize therapeutic strategies? Please share your thoughts, and let’s engage in a meaningful discussion on this fascinating topic.

Deep Brain Stimulation Offers Promising Results for Traumatic Brain Injury Patients

On January 15, 2024

In Student Post

Traumatic brain injuries can have profound and lasting effects on cognitive functions, impacting memory, attention, and mood regulation. Despite the prevalence of these challenges, there has been a lack of effective therapeutic interventions. However, a recent small-scale study conducted by Nicholas Schiff and his colleagues at Weill Cornell Medical College in New York City offers a glimmer of hope. The study explores the potential benefits of deep brain stimulation in treating cognitive impairment resulting from moderate to severe traumatic brain injuries.

The study focuses on the thalamus, a critical brain region acting as an early stop for sensory information. In the case of traumatic brain injuries, disconnections and cell death can occur, affecting the relay of information to the prefrontal and frontal cortexes responsible for executive function. By surgically implanting electrodes into the thalamus, the researchers sought to restore lost connections and improve cognitive function in individuals with traumatic brain injuries.

The groundbreaking success of deep brain stimulation in treating traumatic brain injuries resonates with the intricacies of cell communication, a topic in AP Biology. At the cellular level, effective communication is vital for maintaining homeostasis and responding to external stimuli. In the context of traumatic brain injuries, where neural connections are disrupted, the restoration of cognitive function through deep brain stimulation mirrors the intricate signaling pathways within cells. In both scenarios, the targeted transmission of signals plays a critical role in orchestrating responses and facilitating recovery.

Deep brain stimulation involves the implantation of electrodes in the brain, powered by a pacemaker, to electrically stimulate targeted regions. This technique has a successful track record in treating conditions such as Parkinson’s disease, epilepsy, obsessive-compulsive disorder, eating disorders, and deep depression. Now, the focus has shifted to traumatic brain injuries, affecting over 5 million people in the United States alone.

Six patients, who had suffered traumatic brain injuries two to eighteen years prior, underwent surgery for electrode implantation. Targeting the central lateral nucleus of the thalamus, the researchers programmed the devices for a 12-hour on/off cycle and optimized them individually over a two-week period. The patients then underwent cognitive tests, such as the Trail Making Test.

The results were surprisingly positive, with five out of six patients showing improvement in attention and information processing. After receiving stimulation for at least three months, the patients demonstrated a significant reduction in the time it took to complete the Trail Making Test. This improvement suggests that deep brain stimulation may be a viable therapeutic option for addressing cognitive impairments caused by traumatic brain injuries.

In a separate publication, the researchers detailed the feedback from participants and their families. Patients reported improvements in everyday activities such as reading, playing video games, and watching television – tasks that had become challenging or impossible due to their injuries. Family members described the treatment as a “miracle,” with one mother expressing joy at having “got my daughter back.”

While the study has shown promising results, Nicholas Schiff plans to conduct larger trials involving more patients and for longer durations to gather more comprehensive data. The potential of deep brain stimulation in treating traumatic brain injuries raises important ethical considerations, as it not only benefits patients but also contributes to our understanding of fundamental questions about human brain function.

How do you feel about this study? How do you think this will affect the future of treating brain trauma?

The groundbreaking study on deep brain stimulation offers a ray of hope for individuals grappling with the lasting effects of traumatic brain injuries. As research advances, deep brain stimulation may emerge as a transformative therapy, offering improved quality of life and a chance for recovery for the millions affected by traumatic brain injuries.

How COVID-19 Robs Us of Our Sense of Smell

By roycellulose

On January 15, 2024

In Student Post

Led by researchers from NYU Grossman School of Medicine and Columbia University, the study with the pandemic virus, SARS-CoV-2, found that the infection caused by SARS indirectly dials down the action of olfactory receptors (OR), proteins on the surfaces of nerve cells in the nose that detect the molecules associated with odors. This new study not only sheds light on the reason for loss of smell, but also sheds light on the effects of Covid-19 on other types of brain cells, and on other lingering neurological effects of COVID-19 like “brain fog”, headaches, and depression.

The study involved analysis of olfactory tissue from human autopsies and experiments on golden hamsters, a species highly reliant on their sense of smell. The researchers observed that the virus triggers an increase of immune cells, which release cytokines altering the genetic activity of olfactory nerve cells. They suggest that that if olfactory gene expression ceases every time the immune system responds in certain ways that disrupts interchromosomal contacts, then the lost of sense of smell may act as an early signal that the COVID-19 virus is damaging brain tissue before other symptoms presents, and suggest new ways to treat it. However, these cells are not infected by the virus directly. These findings could have broader implications than it first seems. The persistence of immune reactions in the nasal cavity may influence cognitive functions and emotions because these olfactory neurons are connected to sensitive brain regions. The team’s next steps include creating treatments to protect the “nuclear architecture” of these cells and prevent long-lasting implications. This study aligns with many core topics in AP Biology, such as proteins, the immune system’s role in disease response, and the immune system’s interaction with neurons. It offers insight into the understanding of how cells communicate and respond to pathogens. It also delves into gene expression which illustrates how factors like viral infections can lead to changes in a cell’s genetic activity. This study represented a significant step in understanding the broader effects of COVID-19 and opens options for new treatment strategies. The Study also provides valuable insights into the functions of the immune system and neurons during a COVID-19 infection. The increase of immune cells and the release of cytokines in response to SARS-CoV-2 can alter the activity of olfactory nerve cells. This not only affects our sense of smell but also has more affects on brain function. The immune reaction in the nasal cavity could impact cognitive functions and emotional states because of the connection of olfactory neurons to sensitive brain regions. This understanding of how COVID-19 effects immune responses and neuronal changes is crucial as it helps scientists find new ways for treating the long term effects of COVID-19. Now this brings the question of if this study gives insight into how to treat patients with long term issues from Covid and how they will be treated.

Is COVID-19 Linked to Diabetes?

On January 15, 2024

In Student Post

Today’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

On January 8, 2024

In Student Post

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.

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.

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!

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.

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.

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

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!

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

On January 8, 2024

In Student Post

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?

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.

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.

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

On January 7, 2024

In Student Post

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

On January 7, 2024

In Student Post

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!

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.

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!

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