AP Biology class blog for discussing current research in Biology

A View into Life Millions of Years Ago

In an obscure geological valley at the very northern tip of Greenland’s large ice sheet, investigators have uncovered scientifically derived evidence of the existence of a lush, ancient ecosystem that was functioning over 2 million years ago. The clues to this ecosystem come from the oldest DNA ever recovered, bits and pieces of genetic material, carefully and tediously extracted from buried sediments representing more than 100 kinds of animals and plants. The investigators painstakingly extracted and “sequenced” the DNA strands and compared them to libraries of existing DNA “reads” from living species today.

DNA double helix horizontal
This is an incredibly impressive example of the power of environmental DNA (eDNA), as it is genetic material collected from the ambient environment and not individual organisms. The investigative team aimed to collect hundreds of samples from different locations within the ancient valley and reconstruct what this ecosystem looked like before the ice age. They found many different types of conifers, including poplars, thujas, and species like black geese and horseshoe crabs, that are now common further south of Greenland, but most of which are no longer found in the Arctic at all.
There are many reasons that I believe this discovery is important, not the least of which is that it may give scientists clues as to how some species were able to adapt to climate change in the past and give us some insight into climate change and evolution as we advance. It may also turn the time-honored discipline of paleontology on its head by driving it from its almost all fieldwork mode into the molecular biology laboratory.

The DNA/RNA biochemical process plays a very important role within the nucleus of each cell which defines the existence and evolutionary success of living plants and animals on the planet. The article which I selected from “Nature” discussed above, really emphasizes importance of these chemical structures regardless of whether we are investigating the past, looking into possible future biological scenarios, or looking to “improve”, correct or modify existing biological systems. Understanding both the future and historic past of the biology of the planet is no longer simply relegated to the desktop microscope, but more appropriately is a function of understanding the complex biochemical reactions at the molecular level, not just the cellular level. The extraction of biological (environmental DNA) material from historic sediments thousands of years old underscores the important changes taking place in this exciting new field and emphasized to me that the study of DNA/RNA biochemistry is very relevant to understanding all living systems, past, present and likely into the future.


A new evolution in cancer metastasis research


Perhaps the greatest fear of any cancer patient is metastasis.  According to Cancer.Net, metastasis is the process by which cancers spread throughout the body.  Furthermore, according to, “Metastatic cancer is notoriously difficult to treat, and it accounts for most cancer deaths.” However, a new study in Nature, as outlined in an article in The Scientist, unearths new truths about how cancer cells metastasize that could perhaps spark a new wave of research.  

As stated in The Scientist, “Previous studies have shown how, counterintuitively, cells pick up the pace as they move through thicker solutions.”  Recent studies have elaborated on this accepted facet of cancer reaction, and have discovered that Cancer cells have the ability to detect, and even memorize the viscosity of their environments.  Researchers noticed that cancer cells initially exposed to viscous environments retained their speedy movement even after they were moved to watery environments, at a level not represented in those constantly in watery solutions, thus indicating a sort of memory of environment in cancer cells.  This phenomenon of “cell memory” is similar to the memorization features seen in T-memory cells we discussed in class during the unit on the immune response.

Breast cancer cell (2)

Later, that same team of scientists released study that aimed to determine how cancer cells are able to move quickly through viscous substances.  According to an article in The Scientist, “cancer cells move by taking up water at the front of the cell and squirting it out the back, propelling themselves like octopuses through narrow spaces.”  Some researchers believe that new drug research could aim to target the ion channel that causes this transportation: TRPV4, but others are not so convinced.  According to Miguel Valverde of Pompeu Fabra University, “Animal knockouts for the TRPV4 channels develop normally,” indicating that the newly discovered transportation mechanism may not be as essential as researchers may believe.

Still, the discovery of a new transportation method for cancer cells explaining its peculiar preference for viscosity is an important breakthrough, that will undoubtedly guide future research in cancer metastasis. 

How “Last-Resort” Antibiotics Kill Bacteria

Polymyxin antibiotics are considered to be “last-resort” antibiotics due to their incredible efficacy, even against otherwise antibiotic-resistant bacteria. However, little was known about exactly how they work – until now. Doxycycline 100mg capsulesResearchers at the University of Basel, Switzerland, have discovered that these antibiotics crystallize the plasma membranes of bacteria.

This crystallization causes the fatty part of a lipopolysaccharide to form a hexagonal structure, which decreases the thickness of the plasma membrane, weakens it, and eventually makes it burst, causing the death of the cell. The lipopolysaccharide normally contributes to the structure and stability of the plasma membrane; if a bacteria is coded without these genes, it will die quickly due to the plasma membrane bursting due to lack of stability. Similarly, the membrane loses much of its structural integrity and collapses when the antibiotic crystallizes it.

This breakthrough is important due to the growing problem of antibiotic resistance: antibiotics are simply less effective than they used to be, as bacteria evolve so that antibiotics no longer kill them. As a result, new antibiotics must be found to maintain efficacy. Now that we know more about why polymyxin antibiotics work, new derivatives can be found to improve public health.

20 VS. 4- A Universal Flu Vaccine

Flu Shot Advertising

20 VS. 4- A Universal Flu Vaccine


Every autumn, it’s the same routine: scientists predict which 4 or 5 strains of influenza will be circulating in the coming months, prepare a vaccine, and those who want it get it; sometimes the predictions are accurate, and people are spared from the virus, but other times it is not. 


As we have learned in AP Biology, the human body has both innate immunity and acquired immunity to protect against diseases; vaccination is a form of artificially acquired immunity, in which a vaccine introduces the immune system to proteins from a virus; this trains the immune system to produce antibodies against the virus, so it knows how to encounter the actual virus later, should it be necessary. Unfortunately, when it comes to the flu vaccine, the antibodies that we are trained to produce from the vaccine are often not a match for the circulating flu strains, which causes the vaccine to be less effective.


But what if there were a way around this? Suppose that, instead of having to play a delicate guessing game as to which flu viruses are circulating more than others, there was a single, comprehensive vaccine that could provide immunity for multiple strains at once. This may be a real possibility in the near future; in November 2022, a research team at the University of Pennsylvania designed an influenza vaccine using mRNA technology, and when tested in mice and ferrets, was discovered to protect against 20 different strains of influenza. 


One may be wondering, how could such a feat be possible? Well, we must look at how this specific vaccine was designed; it was made in a very similar fashion to the COVID-19 Pfizer and Moderna vaccines, using mRNA technology. When a person takes the Pfizer or Moderna vaccine, mRNA is introduced into the person’s body, triggering their cells to recreate a harmless version of the spike protein, causing the person’s immune system to recognize it and therefore learn how to create an efficient immune response against the virus. 


The fact that this has been seen in the COVID-19 vaccine makes it easier to understand why the mRNA vaccine created for influenza was effective in mice. This is very different from the traditional influenza vaccine, which involves injecting an unactivated or weakened version of the virus into the body; while it is a formidable opponent against the influenza when the strains are a match, the design of traditional vaccines have been found to be less protective than mRNA vaccines. 


The experimental 20-strain influenza vaccine has yet to undergo human trials, but it does provide some optimism looking into the future of flu seasons.

Lab-Made Covid-19 Variant?!

COVID-19 has been a part of life for over three years now. Throughout this time, new variants arose from this viral respiratory disease caused by a SARS-associated coronavirus” (WHC 1). This October, scientists at Boston University created a new variant of SARS-CoV-2. They combined different features of pre-existing strains. The lab-made variant reminded people and caused them to question if the original COVID-19 was made in a lab and released or if it was natural. Controversy about this experiment grew, forcing the U.S. government to investigate if what these scientists were doing followed protocol. It turns out that they were trying to figure out how the Omicron BA.1 strain could “escape the protection provided by the immune system and vaccines”(Park 1). They did this by focusing on the Spike Protein, which “is located on the outside of a coronavirus and is how SARS-CoV-2 (the coronavirus) enters human cells”(UNMC 1). They hoped to figure out if the spike protein made Omicron defiant against the vaccine or a different part of the variant. Unfortunately, in the middle of their studies, the scientists accidentally created a very lethal variant to mice, which forced the U.S. Department of Health and Human Services to look into this case. Since the experiment was funded through the university and not the government, it was allowed to continue. This experiment concluded that spike protein in Omicron was the reason it was so resistant to the vaccine. Although what the scientists at Boston University were doing was important, what they created amid the experiment was highly dangerous and not worth the risk. 

Sars cov2Connection to A.P. Biology

The immune system is a very complex space that is supposed to protect the human body from dangerous invaders. There are two types of immunity, Innate and Adaptive. Innate immunity is the body’s first response to foreign substances, and Adaptive develops after exposure to an unknown invader. The scientists questioned why Omicron, a variant of COVID-19, managed to avoid being destroyed in bodies that previously had the vaccine and developed adaptive immunity. But since learning that it was the Spike protein that mutated in Omicron, the human body saw it as a foreign invader, and adaptive immunity was of no use here. 

COVID-19 Puts the AGE in TeenAGEr

A new study from Stanford UnBrain 090407iversity suggests that stress from the COVID-19 pandemic may have changed the brains of teenagers, resulting in their brains appearing years older than the brains of pre-pandemic teenagers. The pandemic resulted in increased anxiety and depression among teenagers, but this new research indicates that the effects may not just stop there.

Scientists know that traumatic childhood experiences can accelerate changes in brain structure. Research conducted by Katie McLaughlin, associate professor of Psychology at Harvard University, and her team led to the conclusion that adversity was connected with reduced cortical thickness. This is a sign of brain aging because as people age, their cortices naturally thin. 

Marjorie Mhoon Fair Professor of Psychology Ian Gotlib originally designed a long-term study to research the effects of depression during puberty. He had been conducting brain scans on 220 children, ages 9-13, but he was not able to continue due to COVID-19. After the pandemic, Gotlib resumed his study, and the results were shocking. Researchers discovered that the deveDiversity of youth in Oslo Norwaylopmental process of cortical thinning had been accelerated for the teenagers compared to normal brain development. According to Gotlib, “Compared to adolescents assessed before the pandemic, adolescents assessed after the pandemic shutdowns not only had more severe internalizing mental health problems, but also had reduced cortical thickness, larger hippocampal and amygdala volume, and more advanced brain age.” It remains unclear to scientists whether or not the teenager’s brain age will eventually catch up to its chronological age.

Scientists speculate that the increased anxiety, depression, and overall mental health issues teenagers are experiencing following the pandemic may be linked to cortical thinning. Researchers speculate that cortical thinning may be linked to the expression of certain patterns of genes associated with different psychiatric disorders. Additionally, from studying children who suffered childhood trauma prior to the pandemic, researchers already know that negative childhood experiences can increase the risk of depression, anxiety, addiction, and other mental illnesses. The risk of physical conditions, such as cancer, diabetes, and heart disease, increases as well. 

Jason Chein, professor of psychology and neuroscience and the director of the Temple University Brain Research & Imaging Center, found the research intriguing, but he cautioned against accepting the conclusion that children’s brains definitely aged faster. “It’s pretty interesting that they observed this change,” he said. “But I’m reluctant to then jump to the conclusion that what it signals to us is that somehow we’ve advanced the maturation of the brains of kids.”


AP Bio Connection 🙂

I chose this topic because I was interested in the effects of the pandemic on people in my age group. This topic connects to AP Bio because brain aging has been linked to increase stress hormones. The stress hormone corticosteroid activates an intracellular receptor which results in the changed gene expression. Due to the fact that corticosteroids activate intracellular receptors, they must be nonpolar molecules in order to enter the cell membrane. Feel free to comment down below if you enjoyed the article!!

Universal cure for all variants of Covid-19?


The main issue with COVID-19 since the beginning of the pandemic has always been the various mutations. Someone could get COVID-19 and develop some sort of immunity, but then a new variant would come around and the immunity would be less effective. Scientists at the Pohang University of Science and Technology are working hard to develop a cure for all variants of COVID-19

COVID-19 is a disease caused by the SARS-CoV-2 virus, which is a member of the coronavirus family. In AP Biology, we learned about viruses and how they infect and replicate within host cells. We learned about how COVID-19 is a prime example of how a virus can cause disease in humans. The SARS-CoV-2 virus enters host cells by binding to a receptor called ACE2, which is found on the surface of cells in the respiratory tract and other organs. Once inside the host cell, the virus uses its own enzymes to replicate and produce more copies of itself. This can lead to the death of the host cell and the release of new virus particles, which can then go on to infect other cells. The immune system plays a crucial role in defending the body against viral infections such as COVID-19. When the body is infected with a virus, the immune system recognizes the virus as foreign and mounts an immune response to try to eliminate it. This can include the production of antibodies, the activation of immune cells such as T cells and B cells, and the release of inflammatory molecules.

The reason COVID-19 has been so infectious and is able to mutate so much is because of the ability of the virus to change structure. This structure change increases the strength of its interaction with hACE2 receptors. An hACE2 receptor is the human version of the Angiotensin-converting enzyme 2, the enzyme that serves as the entry point for SARS-CoV-2. As we learned in AP bio, in order for a virus to enter the body, the antigen must bind to a receptor and then travel into the cell. SARS-CoV-2 binds to hACE2. First, the presence of SARS-CoV-2 produces the protein called, IgG. IgG binds to the spike protein on the SARS-CoV-2 cell and that IgG protein binds with the hACE2 receptors in human cells. This binding of IgG is what allows coronavirus to enter human cells.

Understanding this binding process has been key to developing cures for the virus. Most recently, a research team at Pohang University of Science has developed a revolutionary SARS-CoV-2 neutralizer that can adapt to mutations in the virus. This discovery is groundbreaking in the disease prevention world because the type of technology that is used for this specific example can be spread out across the field and used for other viruses. As Professor Seung Soo Oh described: “It is significant that we have developed the world’s first self-evolving neutralizer-developing platform that shows increasingly better performance with the occurrence of viral mutations.” He added, “We plan to develop it into a core technology that can respond to the next-generation pandemic viruses, such as influenza and Hantavirus.”

This neutralizer works by mimicking the interaction between the virus and the receptor, and than once that reaction is mimicked, its protein fragment and nucleic acids can stick to virus, preventing further interaction with the receptor, which eventually prevents the virus from entering the cells.

In all, a neutralizer that adapts with the virus in order to prevent infection and sickness is a groundbreaking discovery that could potentially change the way COVIS-19 (and viruses as a whole) are looked at.


There’s A Fungus Among Us

Recent discoveries suggest that certain types of fungi that are responsible for severe lung infections have become more widespread in the United States. 

The first type of fungi, Histoplasma, responsible for histoplasmosis infections, was previously only found in the Midwest, and sporadically (no pun intended) found in parts of the East and South. 

Histoplasma pas-d

Medicare records from 2007 through 2016 reflect a serious cause for concern: 47 states and Washington D.C. have now reported a significant amount of cases of histoplasmosis. The second type of fungi, Blastomyces, which is responsible for the lung infection blastomycosis, has followed a similar pattern to Histoplasma

How do these infections occur? People inhale the spores from these harmful fungi, and they attack our immune systems. They do this by attacking B and T cells. The T and B memory cells ultimately remember the pathogen to prevent a repeated infection, and in the meantime, the cytotoxic T cells attempt to destroy the cells that the pathogen has already infected. The infection occurs if the immune system is unable to fight off the pathogens. 

Coccidioidomycosis is the third type of lung infection that has become more widespread. Coccidioides fungi used to only exist in the southwest, but have spread throughout the entire Western region of the United States. 

Letting these lung infections go undiagnosed can be fatal, so scientists hope that these recent discoveries will push doctors to test for fungi more frequently when confronted with patients that have lung infections.

“Secret Doors” Are Not So Secret Anymore! 

In AP Biology class, we learned that an allosteric interaction is when an effector (some other kind of molecule) inhibits or activates an enzyme at its allosteric site. When an allosteric enzyme binds to an effector molecule, a conformational change occurs. The allosteric effects of many mutations that cause diseases, such as cancer drivers, cause them to be pathological. Allosteric sites are very difficult to locate because the rules governing how proteins work at the atomic level are hidden out of sight.


A recent discovery reveals newly discovered “secret doors” that control protein function and which could potentially be targeted in order to improve the conditions of cancer, dementia, and infectious diseases. Proteins play a crucial role in all living organisms by fighting diseases, speeding up reactions, acting as messengers, etc. A protein’s structure is essential to its function, and with one change in its sequence if amino acids could result in devastating consequences to a human’s health. 

Researchers have previously found success in targeting active sites, and now, with this new method, allosteric sites are identifiable as well. Several treatments have been designed that target a protein’s active site; however, active sites of different proteins look very similar, causing medications to bind and inhibit many different proteins at once. This leads to potential side effects. In contrast, allosteric drugs are one of the most effective medications available today due to the specificity of allosteric sites. The new method in targeting allosteric sites has been used to chart the first map ever of these allosteric sites in two of the most common human proteins. This new approach may be a game changer for drug discovery, leading to more effective medications, and enabling researchers to locate and exploit vulnerabilities in any protein—even those previously thought to be untreatable! 

Please feel free to leave your thoughts or questions in the comments! 🙂

Researchers Find Ways To Combat COVID-19

Ever since COVID-19 was discovered scientists had no idea how to stop this virus. After lots of research we were able to know that there were many different variants of  COVID-19. We understood that some variants were stronger than others according to research. There is an article that talks about how they can be able to stop all kinds of COVID-19 viruses and the different variants. In the article, Professor Seung Soo Oh had an idea on how to stop all kinds of variants in one go. He says that the virus can change its structure whenever. It will then bind to the angiotensin-converting enzyme receptor which is a receptor protein. His team developed a hybrid neutralizer that is able to bind to the virus which then cause the virus to not interact with the protein receptor. This neutralizer was able to be about 5 times more effective then what they first had when COVID-19 was discovered.

According to this article, Omicron which was found in November of 2021 in South Africa, is the most dangerous variant of COVID-19. It is a variant of COVID-19 and is one of the strongest variants. In December of 2019, sub-variants of Omicron began to appear. Some of the sub-variants include BA.5, BQ.1, and BQ.1.1. According to the article, the Omicron sub-variants were very effective and was more transmissible then the Delta variant. The neutralizer should be able to stop Omicron and the sub-variants.

According to another article, variants aren’t weakened by covid vaccines that were had a while ago. In order to help stop COVID-19, the article says that getting boosters will be more effective for any new variants that are discovered. This doesn’t mean they will 100% work. With this knowledge, the new neutralizer that was developed should be able to stop all these viruses from mutating and from entering the cell.

This relates to what we have learned in class this year because we have learned cell structure. When COVID enters the cell, it must bind to a receptor. Once it enters the cell the RNA or DNA would then reproduce. This is similar to what we have learned about how other things enter the cell such as glucose and amino acids. In receptor mediated endocytosis, the ligands must bind to the receptor and then enter the cell. This relates to what we have learned in class because we have learned how molecules are able to enter the cell and how receptors work.


SARS-CoV-2 without background


Avian Brain: Proof that Bigger Doesn’t Always Equal Better

There is a common misconception that a bigger brain size always means a smarter living creature or animal. Recent research done by German avian neuroscientist, Kaya von Eugen, from Ruhr University Bochum in Germany, compared neuron activity in the brain of a pigeon to that of other mammals to see if such thought was true.Ruhr University Bochum (37339321200)

Neurons were a substantial part of our learning curriculum in AP Biology. As such, we know their main function to be transmitting impulses and messages from the environment around us, to signal certain body parts to function. This helps us gain a better understanding of von Eugen’s research as it allows us to comprehend the goal of her experiment and how crucial a knowledge of neurons was to it.

Complete neuron cell diagram tr

To aid in her research, von Eugen turned to an experiment conducted in 2016, where scientists injected molecules resembling glucose into pigeons’ veins, and later tracked radioactivity in these pigeons by tracking the “glucose” molecules. By examining both the radioactivity and the blood of the pigeons, scientists were not only able see how much glucose the brain tissue used, but they were also able to calculate how much glucose was used by each neuron every minute.

Von Eugen’s research continued as she compared neuron energy from the pigeon to that of other mammals, and she came to the conclusion that the neuron of a pigeon used around 3 times less energy that the neuron of an average mammal. So, despite the brain size of a bird, or pigeon in this case, being multiple times smaller than the brain size of other animals, it is clear that intelligence and smarts do not depend on brain size.

There Are More Viruses On Earth Than Stars In The Universe. Why do only some infect us?

Scientists have estimated that there are 10 nonillion (10 to the 31st power) viruses currently on our planet. They are everywhere. Many viruses are beneficial for their host, many inflict no harm, but why do so few viruses affect us and even fewer severely affect us? The short answer: “These pathogens are extraordinarily picky about the cells they infect, and only an infinitesimally small fraction of the viruses that surround us actually pose any threat to humans” says virologist Sara Sawyer.

Understanding how certain viruses affect humans is crucial for protecting and preventing future outbreaks. COVID-19, the most recent outbreak that experienced a “spillover event,” was initially spread through interactions with an animal that is a “non-human primate”. This is called zoonosis. Multiple outbreaks have been introduced this way, but not can be started this way. Pathogens can also enter through cuts, scrapes, mosquitoes, ticks, etc. Once a virus has entered, it needs to find a way to get inside the cells and replicate. To do this, it must first attach to the surface of a host cell and then inject its genetic material (RNA) into the cell. The virus’s genetic material then takes over the machinery of the host cell, using it to replicate itself and produce new viruses. Viruses with a lot of genetic flexibility, and particularly those that encode their genomes as RNA rather than DNA, are well-suited to crossing the species divide. The majority of pathogens that have infected the human population in recent decades have been RNA viruses, including Ebola, SARS, MERS, Zika, several influenza viruses, and SARS-CoV-2. The more lethal viruses were found to have been hiding in their hosts for longer periods of time before showing any symptoms. This would allow it to replicate and spread to new species.


Coronavirus. SARS-CoV-2

So the answer is; that a virus has to be incredibly sophisticated for it to cause harm to a human, pandemics are so rare because of precautionary measures such as vaccines, healthcare, and proper sanitation. The continuous study of viruses and their behavior is an important task for the human population and its future as current viruses are continuously mutating and developing with each given day.


The Revolutionary Way Of Detecting Diseases

How it works

Has our way of detecting diseases changed to become more efficient? Well, let’s find out. Scientists at Wenzhou Medical University in China developed a new technique for detecting illness, which uses human tears to identify eye diseases and even early signs of diabetes. The researchers discovered that different types of dry-eye disease produce unique molecular fingerprints in tears and that tears could potentially be used to monitor the progression of diabetes in patients. The technique involves:

  • Collecting tears and adding them to a device with two nano porous membranes.
  • Vibrating the membranes.
  • Sucking the solution through allows small molecules to escape and leaves exosomes behind for analysis.Tears

How it connects to AP bio

The technique for detecting disease using human tears connects to AP Biology in several ways. First, exosomes, small vesicles found in tears, play an essential role in immune system function. Exosomes are involved in the communication between immune cells and can facilitate the transfer of immune-related molecules between cells. Additionally, the mechanism by which exosomes are collected from tears using nano porous membranes is similar to how viruses can latch onto and enter host cells. In this way, the research on exosomes in tears highlights the complex interactions between the immune system and viruses, which is an essential topic in the study of immunity, as we learned in AP Biology.

Stromal lipofuscinosis of the seminal vesicle -- extremely low mag

What can this do for our future?

Ultimately, this efficient method of disease testing using tears has the potential to speed up the diagnostic process and improve patient outcomes significantly. Doctors can make faster and more accurate diagnoses by providing a quick and non-invasive way to gather important information about a patient’s health, potentially leading to earlier treatment and better patient outcomes. Additionally, the ability to test for diseases at home using just a few drops of tears could help to identify and address health issues before they become more serious, potentially saving lives in the long run. But the most important reason is that you will feel no pain because you won’t have to get your blood taken!!!!!!!!


Are Rats Really Interacting With Reef Fish???

A new study has found that the presence of invasive rats on tropical islands is affecting the territorial behavior of fish on surrounding coral reefs. The rats, which arrived on the islands as stowaways on ships in the 1700s, change the behavior of jewel damselfish, a herbivorous species of tropical reef fish that “farm” algae in the branches of corals.Microspathodon chrysurus

The study, which was led by scientists from Lancaster University in the UK and involving researchers from Lakehead University in Canada, was published in Nature Ecology and Evolution and compared five rat-infested and five rat-free islands in a remote archipelago in the Indian Ocean. The rats disrupt an important nutrient cycle by attacking and eating small resident seabirds and their eggs, leading to a drop-off of nutrients in the seas surrounding rat-infested islands. This results in a lower nutrient content of seaweed for herbivorous fish, such as the damselfish. The damselfish around rat-infested islands behave less aggressively and need to have larger territories due to the lower nutrient content of the algae.

Seabirds travel out into the open ocean to feed and return to nest on islands. The seabirds then deposit nutrients, through their droppings, onto the islands, and many of these nutrients are subsequently washed into the seas, fertilizing the surrounding coral reef ecosystems. On islands with invasive rats, the rodent populations decimate the seabirds, leading to seabird densities that are up to 720 times smaller on rat-infested islands. This results in much less nitrogen flowing onto the coral reefs around these islands.

Seabirds LC0141

Around islands with intact seabird populations, the farming damselfish aggressively defend their small patch, typically less than half a square meter, of the reef to protect their food source – turf algae. However, the scientists observed that farming damselfish on reefs adjacent to rat-infested islands were much more likely to have larger territories and were five times more likely to behave less aggressively than those who lived on reefs adjacent to islands without rats. The damselfish around rat-infested islands need to have larger territories because the algae around rat-infested islands is less nutrient-rich due to the missing seabird-derived nutrients.

NSW seabed 1

This behavior change in the damselfish could potentially have wider implications for the spread of different species of coral, the distribution of other reef fish, and the resilience of damselfish over generations due to changes in hereditary traits. Changes in behavior are often the first response of animals to environmental change and can scale up to affect how and when species can live alongside one another. This study is the first to show that invasive rats can change the behavior of coral reef fish in this way and highlights the importance of understanding and managing the impacts of invasive species on ecosystems.

Students in our AP Biology class are likely to be familiar with these concepts of nutrient cycling and the importance of nutrients in supporting the growth and productivity of an ecosystem. The study highlights how the nutrient cycle on coral reefs is disrupted by the presence of invasive rats, leading to a drop-off in nutrients in the surrounding seas and a lower nutrient content of seaweed for herbivorous fish. This can have consequences for the growth and productivity of the coral reefs and the overall health of the ecosystem.

SARS-CoV-2 Is Making My Heart Ache??

New research from the University of Maryland School of Medicine’s (UMSOM) Center for Precision Disease Modeling identifies the specific protein in SARS-CoV-2, the virus responsible for COVID-19, that causes damage to heart tissue.

Protein Structure Gif

Some experiments they did were performed on fruit fly hearts. When Nsp6 is present in a fruit fly heart, the heart shows structural defects compared to a normal heart without the viral protein. However, when fruit fly hearts with the viral Nsp6 protein are treated with the drug 2DG, the hearts begin to resemble normal hearts more closely.

In their latest study, researchers found that the Nsp6 protein is the most toxic SARS-CoV-2 protein in the fruit fly heart. They also discovered that the Nsp6 protein hijacks the fruit fly’s heart cells, activating the glycolysis process and disrupting the mitochondria, which produce energy from sugar metabolism. When they blocked sugar metabolism in fruit fly and mouse heart cells using the drug 2DG, they found that it reduced the heart and mitochondria damage caused by the Nsp6 viral protein.

Dr. Han, the lead researcher, says this about the protein : “We know that some viruses hijack the infected animal’s cell machinery to change its metabolism to steal the cell’s energy source, so we suspect SARS-CoV-2 does something similar. The viruses can also use the byproducts of sugar metabolism as building blocks to make more viruses,”


Drosophila melanogaster under microscope

Thus, the University of Maryland School of Medicine’s research identified the specific protein in SARS-CoV-2 that causes damage to heart tissue and has found a potential treatment for it. The protein, called Nsp6, activates the glycolysis process in heart cells and disrupts the mitochondria, which are responsible for producing energy through glycolysis and oxidative phosphorylation. By blocking the processes  with the drug 2DG, the researchers were able to reduce the heart and mitochondria damage caused by Nsp6. This discovery aligns with the topic of glycolysis and ATP generation in AP Biology as it highlights the importance of proper metabolism in the functioning of cells and the potential consequences of disruptions to this process.


Anxiety vs Sleep, A Battle of the Sexes


A new discovery has been made which may help explain the higher prevalence of sleep disruption and anxiety in women, not only leading to better treatments for anxiety and sleep but also strengthening our understanding of how the brain varies between the two sexes.

What We Know vs What We Don’t

Insufficient sleep is already known to be a cause of anxiety. However, this might not be the case for everyone, or at least to the same extent. When considering sex, “women are proven to experience a greater anxiogenic impact in response to sleep loss than men”. Yet it is unknown which regions of the brain govern sleep-loss-induced anxiety and how these regions’ reactions differ between men and women. A team of scientists led by Andrea N. Goldstein-Piekarski is attempting to find answers by using structural brain morphology. This method will allow them to link anxiety caused by sleep deprivation to the volume and shape of “emotional” regions of the brain between the two sexes.


Statistical Analysis

Using an ANOVA approximation with the equation below, the scientists were able to decipher whether the amount of anxiety reported via the PSG test for each of the sleep conditions is related to sex and the grey matter volume of the individual’s brain.  

(sleep-deprived[morning-evening]  – sleep-rested[morning-evening]anxiety ~ sex × grey matter volume)

Women demonstrated a significant Time × Condition interaction, expressing a nearly fourfold increase in anxiety on the sleep deprivation night relative to the full night of sleep in morning-evening anxiety. There was no Time × Condition interaction for men in morning-evening anxiety, however, some individuals did experience an anxiogenic response, indicating that this specific consequence of sleep loss is not completely sex-based.  

Women demonstrated a significant negative association between anxiety and gray matter volume in the emotion generation and integration region of the insula/

Gray743 insular cortex

IFG and a marginally significant negative association in the lOFC, which means that gray matter volume did not influence the women’s anxiogenic responses. This incredibly opposes men who, on average, demonstrated significant positiveassociations in the insula/IFG and lOFC. Therefore, although men as a whole did not demonstrate a significant increase in anxiety due to sleep deprivation, the variance of anxiogenic response in men was indeed related to variation in gray matter volume of these regions. 



These findings show that women do indeed experience more significant anxiogenic responses to sleep deprivation than men. They also show that the morphology of emotion-relevant regions can explain the variance and vulnerability of men to anxiogenic reactions to sleep deprivation. 

What Now?

Such findings suggest that for women especially, targeted sleep restoration may offer a novel, non-pharmacological therapeutic pathway for ameliorating anxiety. This research can also improve public health awareness about the importance of sleep, especially for those who are at a greater risk of anxiety disorders. 

Connection to AP Bio

Research from Johns Hopkins has shown that the anxiety and stress response can often lead to mitochondrial damage. Since anxiety and stress can cause the physical symptoms of increased heart rate and breathing, the mitochondria are pushed to provide more energy through cellular respiration. This can be detrimental to an individual who is in a constant state of stress and anxiety as the mitochondria have very little repair mechanisms, which would then harm the body’s overall production of energy. In relation to the study, this information conveys that sleep deprivation not only affects mood and physical performance but also organelles and basic cellular functions.


  • Structural Brain Morphology – the study of the structural measures of the brain, e.g., volume and shape 
  • Vulnerability Biomarker – any substance, structure, or process that can be measured in the body or its products and influence or predict the incidence of outcome or disease (WHO)
  • Anxiogenic – producing anxiety 
  • ANOVA – an analysis of variance between more than two groups
  • Polysomnography (PSG) – a test conducted to diagnose sleep disorders

Improvements for Kidney Cancer Treatments

Cancer is a disease where some of the body’s cells grow uncontrollably and spread to other parts of the body. Approximately 39.5% of men and women will be diagnosed with cancer in their lifetime and an estimate of cancer survivors in 2030 will be around 22.2 million – this study was done in 2020. In 2021 statistics showed that roughly one in every two people will get cancer in their lifetimes the biggest reason being that people are living longer lives, with the main range of people getting cancer being those over 70 years old. Recently the HSE – which is the Health and Safety Executive (HSE) is Britain’s national regulator for workplace health and safety. It prevents work-related death, injury, and ill health – has “discovered genes that are specific to the most aggressive subtype of clear cell renal carcinoma”. Clear cell renal carcinoma or ccRCC is a type of kidney cancer. The kidneys cleanse the blood of toxins and change the waste into urine, the two kidneys together filter 200 liters of fluid every 24 hours – balancing the body’s fluids. ccRCC is a rare type of cancer where when one looks at the cells under the microscope the cells look clear. For adults, ccRCC is the most common type of kidney cancer and it is more common in adults than in children. ccRCC makes up between 2-6% of childhood and young adult kidney cancer cases. Patients who are diagnosed with ccRCC tend to have a worse prognosis than patients diagnosed with different subtypes of RCC “with 5-year disease-specific survival rates of 50-69%, compared with 67-87% for papillary RCC and 78-87% for chRCC“. This recent genetic discovery by Grigory Puzanov, a research fellow at the HSE Faculty of Computer Science International Laboratory of Bioinformatics, could change the clinical treatment course of ccRCC patients.

Histopathology of renal clear cell carcinoma

Puzanov analyzed data from 456 patients with the disease identifying cancer subtypes that have favorable or unfavorable prognoses. His study reveals the ccRCC subtypes that are more dangerous than others and what specific human genes appear responsible for the progression of the disease. The discovery of this is significant for the early detection of tumors and for designing a personal treatment for the patient – this is especially important because most patients are diagnosed after ccRCC has already advanced to later stages. The way that Puzanov analyzed the data from the 456 tumor samples was using the k-means method – where the algorithm randomly chooses a centroid for each cluster – to create subgroups with similar characteristics. Through this Puznov was able to select 2,000 genes with high “variable expression patterns in ccRCC“. Gene expression “is the appearance in a phenotype of a characteristic or effect attributed to a particular gene” which allows the gene to be read and copied producing RNA (which is then used to synthesize proteins). He ran this algorithm on each tumor 100 times based on the 2,000 subgroups he had found previously. There were multiple testing stages run during this research study, in the first stage, each subgroup’s characteristics were tested on how their genetic factors could influence the course of ccRCC. Then Puzanov identified the crucial genes in particular for high to low survival subgroups and created a system of interaction for “proteins whose synthesis is encoded by these genes”. From this, he determined which genes created the highest number of “network connections”. Some of the key genes they found were noticed to affect the anti-tumor therapies they were running on patients with ccRCC  –  like CP, FGA, and FGG genes – this can help doctors in the future choose better working treatments for patients with malignancies. In our biology class, we have gone over mRNA and what it does, and how it is vital for protein production. It carries information from the DNA in the cell’s nucleus to the cytoplasm. Since mRNA carries information scientists can use mRNA vaccines to treat diseases, it also allows researchers to create mRNA cancer vaccines that activate the immune system to attack cancer cells. The known research on mRNA and the new information found from Puzanov’s research is bringing cancer treatment further.







Why don’t we have a cure to HIV?

HIV, Human Immunodeficiency Virus, is a severe virus that destroys the body’s immune system, which can later lead to AIDS(acquired immunodeficiency syndrome) if the virus is not treated. Since its discovery in 1981, there have been no proper ways to completely cure this virus, which led many people to wonder the same question: what does HIV do to our body that’s incurable?


Initially, when the virus enters the body, it uses a particular cellular protein called cyclophilin to bind with our cell receptor; it then receives our cell’s information and changes its shape to fit into the compartment. Once that’s done, HIV does a process that we often hear in biology: Receptor-Mediated Endocytosis. To further explain this, the cell is triggered by a specific ligand that matches the cell’s shape. When it’s inside the cell, HIV uses its own DNA and genes to replicate itself. After, the virus Exocytosis gets out of our cells and moves on to infect other cells in our body.

People might question why HIV is incurable? Other viruses do the same thing when entering our bodies, but they can still be cured. To answer this question, we need to go back inside the cells to see what the virus is doing there. While HIV replicates itself and infects cells, it also integrates with the host’s DNA to create reservoirs. When inactivated, the virus inside the pools are remained “silent.” However, once the current virus inside the body is used, a stimulus is sent to those reservoirs to reactivate the remaining virus and start the infection.

Despite its fatality over the years, with modern-day’s medical technology, a person with HIV can live just as long as those who are HIV-negative if the virus is detected early. With that being said, it is crucial to receive early treatments once you have HIV.

Gardening May Help Reduce Cancer Risk and Boost Mental Health

Get more exercise. Eat right. Make new friends.

SF Japanese Garden

A new study reveals that community gardening helps lower stress and anxiety, and reduces cancer risks. Researchers have found that those who gardened had elevated fiber intake and increased physical activity.

A study conducted by Jill Litt, a professor in the Department of Environmental Studies at CU Boulder, funded by the American Cancer Society, was the first-ever, controlled trial of community gardening found that those who started gardening ate more fiber and got more physical activity — two known ways to reduce risk of cancer and chronic diseases. They also saw their levels of stress and anxiety significantly decrease.

During this study, in the spring, Litt recruited 291 non-gardening adults and assigned half of them to the community gardening group and the other half to a control group. The adults in the control group were asked to wait one year to start gardening.

By fall, the adults in the gardening group were eating on average 1.4 grams more fiber per day than the control group. The gardening group’s fiber intake increased around 7%.

Fiber exerts a profound effect on inflammatory and immune responses, influencing everything from how we metabolize food to how healthy our gut microbiome is to how susceptible we are to diabetes and certain cancers. It also helps regulate the body’s use of sugars, helping to keep hunger and blood sugar in check.

The gardening group also increased their physical activity levels by about 42 minutes per week. The CDC recommends at least 150 minutes of physical activity per week. Only a quarter of the U.S. population meet the exercise guidelines. With just two to three visits to the community garden weekly, participants met 28% of that requirement.

The participants in this study also saw that their stress and anxiety levels decrease. Those who came into the study most stressed and anxious saw the greatest reduction in mental health issues.

This article relates to AP biology because as we learned in the blood glucose regulation simulation, exercise and eating well helps regulate blood glucose levels. Fiber also plays an important role in regulating blood glucose levels. It is important to keep your blood sugar levels in range to help prevent or delay long-term health problems. Staying in your target range can also help improve your energy and mood. This is also an example of a negative feedback loop.



Try to eat just one potato chip – it probably won’t happen.

Potato Chips or any junk food for that matter can be very addicting after just the first bite. The high concentrations of carbohydrates, sugars, and fats commonly found in these processed foods contribute to one of America’s greatest health risks, adult obesity. Today, over 40% of America’s adult population is considered obese and in the last 20 years, the prevalence of severe obesity has almost doubled to 9.2%. A single bag of Lay’s Potato Chips contains 15g of carbohydrates and around 170mg of sodium which could take around 15 mins of very intense workout to burn off. We have learned in AP Bio that consuming many carbohydrates without burning them off through exercise results in carbs converting into fatty acids during cellular respiration. So, when looking into obesity, researchers from Osaka Metropolitan University wanted to understand why “High-calorie foods — high in fat, oil, and sugar” tend to be overeaten.

Walmart Wenatchee 2

The researchers investigated the specific gene behind overeating and linked it to one named “CREB-Regulated Transcription Coactivator 1 (CRTC1).” In the past, trials on mice have indicated that when the CRTC1 gene is removed, they become more obese indicating that it “suppresses obesity”. But, it is now known that CRTC1 is found in all neurons around the brain so, they wanted to dive deeper and find the specific mechanism or neuron within this gene that reduced obesity.
First, Associate Professor Shigenobu Matsumura, who lead the research, hypothesized that “CRTC1 expression in MC4R-expressing neurons suppressed obesity because mutations in the MC4R gene are known to cause obesity.” So, they conducted trials on mice, manipulating the MC4R-expressing neurons to test their theory. It turns out that when on a standard diet, the original mouse and the one with the manipulated MC4R gene remained the same weight. But, when put on a high-fat diet, or one more resembling junk food, the mouse that was deficient with the CRTC1 MC4R neuron became “significantly more obese than the control mice and developed diabetes.” Reflecting on this outcome, the researchers have concluded that the CRTC1 gene plays a role in controlling our portions. Looking forward, the researchers hope this will lead to a better understanding of what causes people to overeat.

Mouse Brain Cross-Section

In our current AP Biology unit, we have been learning about cell respiration and the way our body consumes both O2 and food to create ATP energy. Our body can break down glucose through glycolysis, convert it into two Pyruvate, and then Acetyl CoA, to then create NADH and FADH2 through the Citric Acid Cycle to produce about 28 ATP energy molecules through Oxidative Phosphorylation. Other nutrients we consume like fats and proteins are also converted to ATP energy when needed but, when no energy deficit is created through activity, these nutrients along with excess glycogen are bound to insulin to create fat around the body. Looking forward, it is important to understand how addictive these unhealthy foods can be on a neurological and biological level, warning us of the dangers of overconsumption.

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