BioQuakes

AP Biology class blog for discussing current research in Biology

Big Cat, Little Bird

A fishing cat in a bird's nest

Credits: Allama Shibli Sadik & Muntasir Akash / De Gruyter

 

Cats don’t hate water, contrary to popular belief. In fact, there is a species of wildcat evolved to hunt in water. 

Aptly named “fishing cats,” Prionailurus viverrinus is a species of South Asian cat that has evolved to fish. Unlike other felines, they have slightly webbed forepaws and double layered water-resistant fur. This gives them an edge over others as it means they won’t freeze when they fish, giving them an opportunity to pass this trait down and allows them to stay reliant on their fishing diet, unlike other cats who primarily rely on land prey. They are medium sized cats with yellowish fur, and black tabby stripes that gradiate into mottled spots.

They catch their prey by idling on the edge of a body of water, and scooping the fish out of the water. Very rarely do they wade in and put their head underwater to fish.

But their diet does not solely consist of fish. They are also known to eat small rodents, lizards, amphibians and birds in addition to fish.

The only problem is that with the monsoon season, it is nearly impossible to fish as the land prey is gone, and their usual waters are flooded or destroyed. These cats live in areas prone to flooding and the lack of infrastructure means that the prey cannot flee (also fish cannot sustain on land).

So what does the brilliant cat do?

It climbs trees and preys upon the bird colonies. It has been seen preying upon waterbirds (ie. herons, moorhens, cormorants) high within the tree canopy, snapshotted with camera traps.

This might just be its secret to success since the local population also relies on the fish and (since people have more power than these felines) will deter (and kill) these cats. These waterbirds are not just the cats’ benefit, but the benefit of the locals as well!

Unfortunately, due to brackish waters and the urbanization of wetlands, the clever species is slowly dying out. But that’s another article.

There isn’t a lot known about these guys, but there are ongoing research projects with them.

A “CRISPR” Way to Test for Melioidosis

Melioidosis is a deadly tropical disease that flies under the radar. Around 150-200 thousand people get it every year, and more than half of people diagnosed die. One of the largest problems of this disease is that it takes several days to diagnose, meaning it takes several days for patients to receive the correct treatments. However, a new test, using CRISPR, could change that.

A new test has been invented that uses CRISPR to detect a genetic target that is specific to Burkholderia pseudomallei, which is the bacteria that causes meliondosis. The new test can detect the gene with almost a 94% sensitivity. It was developed by researchers at the Mahidol-Oxford Tropical Medicine Research Unit, Chiang Mai University, Vidyasirimedhi Institute of Science and Technology in Thailand, and the Wellcome Sanger Institute in the UK. The results of this new CRISPR test mean that thousands of people could be saved annually from meliondosis, with an easy to use rapid test.

The disease is caused by Burkholderia pseudomallei, which is found in water and soil of sub tropical and tropical regions. It enters the body through cuts on the skin, ingestion, or inhalation. One of the reasons it’s difficult to diagnose is that the symptoms range from pneumonia to those of a chronic infection. This, paired with the fact its more common in rural areas, causes this disease to be under reported.

Currently, melioidosis is diagnosed in patients after bacterial samples are cultured, which takes three to four days. But, in Thailand, 40% of patients die after just a couple days while waiting for the tests to come back. Currently, there is no vaccine for this disease, but it can be treated with an antibiotic such as carbapenem. However, due to the range of the symptoms, many other and or wrong antibiotics are prescribed, which wastes time and money.

To develop a new test, researchers identified a genetic target specific to B. pseudomallei by analyzing over 3,000 B. pseudomalleigenomes. Their new test called CRISPR-BP34, ruptures bacterial cells and using a recombinase polymerase amplification reaction to amplify the bacterial target DNA for increased sensitivity. In addition to this, a CRISPR reaction is used to provide specifics. The researchers collected samples from about 100 people with the disease and 200 without, in order to test the legitimacy of the test. The new test got results in just four hours and enhanced the sensitivity from about 66% to almost 94%.

This relates to our study of the immune system in AP Biology. As we’ve learned in Biology, first macrophages and neutrophils are the first responders, and they attempt to engulf and destroy the disease. The helper T-cells try and coordinate the response while killer T-cells are attempting to destroy the disease. And cytokines signal molecules to come help defeat the disease. While these attempts by our body is unsuccessful more often than not, it still displays the immune system response learned in AP Biology.

This new test will help save thousands of lives by making diagnoses faster, which will allow the correct treatment to be given in hours, instead of days. This is truly a groundbreaking invention.

Where else do you think CRISPR can be used?

Had you ever heard of Melioidosis before?

Why do you think there is such a large range of symptoms for Melioidosis?Melioidosis world map distribution

The Effect of Ethylene Gas on Plant Growth

Researcher Brad Binder, Professor of Biochemistry & Cellular and Molecular Biology, University of Tennessee, and his team, through their study, accidentally discovered that treating seeds with ethylene gas (C2H4) can enhance the plant’s growth and stress tolerance. This discovery can be a potential breakthrough for improving crop yields and improving plant’s resilience to environmental stress. Where in most cases one gets traded for the other, this revealed that by exposing germinating seeds to ethylene in darkness it is possible to increase growth and stress tolerance.

Plants produce ethylene as a hormone to regulate growth and stress responses. The accidental discovery occurred during an experiment where seeds were exposed to ethylene gas during germination in darkness. The plants exposed had larger leaves, longer root systems, and sustained faster growth throughout their lifespan compared to non-ethylene-exposed plants. The researchers extended their investigation to various crop species, such as tomatoes, cucumbers, wheat, and arugula, and all of them increased growth and stress tolerance after their short-term ethylene treatment.

07070020boerderijloobergen

The observed effects indicated that brief exposure to ethylene during seed germination can lead to long-lasting growth and stress tolerance benefits. The researchers proposed that ethylene priming enhances photosynthesis, particularly carbon fixation, leading to increased CO₂ absorption and higher levels of carbohydrates like starch, sucrose, and glucose. These molecules contribute to both increased growth and improved stress resilience in plants.

In AP Biology we learned all about the Calvin Cycle! The Calvin Cycle is a series of biochemical reactions that occur in the stroma of chloroplasts during photosynthesis. The cycle starts when the enzyme RuBisCO captures carbon dioxide from the atmosphere, which is then attached to RuBP, forming a six-carbon compound. This compound splits into two molecules of 3-PGA, each containing three carbon atoms. Then ATP and NADPH are reduced, which generates light-dependent reactions that are used to convert 3-PGA into G3P, a three-carbon molecule. Some G3P then continues to cycle and is reused to regenerate RuBP, while the rest contributes to glucose production for cellular respiration. The Calvin Cycle is vital in converting carbon dioxide into glucose for plant growth and sustenance.

I chose this topic because I really loved the photosynthesis unit, and my favorite part about it was memorizing the Calvin cycle, and comparing it to the Citric Acid Cycle.

What specifically about the ethylene gas causes an increased efficiency in Carbon Fixation?

Gut bacteria effects the development of allergies!

Have you wondered why some people have allergies and some don’t? Well, researchers have found that the lack of certain gut bacteria can play a role in the development of allergies and autoimmune diseases.

Cornell Medicine researchers have uncovered an intriguing connection between gut bacteria and early immune system development. Their study, published in Science Immunology, reveals that certain bacteria in newborns produce serotonin, a neurotransmitter crucial for educating gut immune cells, particularly T-regulatory cells (Tregs). Tregs, or regulatory T cells, are a specialized subset of white blood cells that suppress immune responses to maintain immune tolerance and prevent autoimmune diseases. Tregs play a vital role in preventing allergic reactions to food and gut microbes during infancy. The findings shed light on the importance of beneficial gut bacteria in early immune system training and may offer insights into combating allergies and autoimmune diseases later in life.

This relates to AP bio through the importance of neurotransmitters in this research. In AP bio, we learned how neurons transport messages using a process involving neurotransmitters. In the process of transport for neurons, neurons communicate messages through a sequence of events involving electrical and chemical signals. When stimulated, a neuron generates an electrical impulse known as an action potential. This action potential travels along the neuron’s length, eventually reaching its terminal branches called axon terminals. Here, neurotransmitters are released into the synapse, the gap between neurons. These neurotransmitters bind to receptors on the neighboring neuron, causing changes in its electrical potential. If the combined effect of these changes reaches a certain threshold, it triggers the generation of a new action potential in the receiving neuron. This process repeats, allowing messages to be relayed from neuron to neuron throughout the nervous system.

Wow! It’s so fascinating how a person’s levels of certain bacteria can influence whether or not a person has allergies. I wonder how else can bacteria can influence a person’s health?

The Mystery of Huntington’s Disease: A Potential Breakthrough in Treatment

In the ongoing search to understand and combat neurodegenerative diseases, scientists have recently made a significant breakthrough in unraveling the complex mechanisms behind Huntington’s Disease. This progress not only sheds light on why this devastating condition progresses slowly but also offers a promising lead in developing effective treatments to halt its fatal course.

Huntington’s disease, a hereditary disorder, is caused by a genetic mutation involving the HTT gene. This mutation results in the repetition of a specific DNA sequence, ultimately leading to the destruction of brain cells and the onset of debilitating symptoms. Until recently, it was believed that the number of repeats in the HTT gene remained constant throughout an individual’s life. However, groundbreaking research presented at the annual meeting of the American Society of Human Genetics has revealed a discovery: in certain brain cells, these repeats can multiply over time, reaching hundreds of copies. This expansion of repeats within vulnerable brain cells is now understood to be a driving force behind the progression of Huntington’s disease.

Geneticist Bob Handsaker of the Broad Institute of MIT and Harvard, who spearheaded this research, emphasized the pivotal role of these repeat expansions in triggering the cascade of events that culminate in the death of brain cells. By examining individual brain cells from both affected and unaffected individuals, Handsaker and his team uncovered a pattern of repeat expansion within a specific type of brain cell known as striatal projection neurons. These expansions, reaching up to 1,000 repeats in some cases, were uniquely concentrated in cells susceptible to Huntington’s disease.

Additionally, the research revealed an important threshold where the activity of thousands of genes within these brain cells changes significantly. This point, reached at around 150 repeats of the disease-causing gene, leads to a quick decline in gene activity, resulting in cell death within months. The exact reasons behind this sudden change are still unknown, presenting a mystery for further study.

However, amidst these uncertainties, the research offers a glimmer of hope for potential interventions. By targeting the process responsible for repeat expansion, namely the malfunction of a DNA repair protein called MSH3, scientists envision a novel approach to slow the progression of Huntington’s disease. By preventing further expansion of repeats, it may be possible to halt the relentless deterioration of brain cells, thereby halting the disease in its tracks.

​​As learned, Genetic mutations are changes in the DNA sequence that can lead to alterations in the proteins produced by genes. In the case of Huntington’s disease, a mutation involving the HTT gene leads to the repetition of a specific DNA sequence, ultimately causing the disease’s devastating effects on brain cells. By targeting the malfunction of a DNA repair protein called MSH3, scientists aim to address the underlying cause of repeat expansion, offering a potential avenue for intervention. This demonstrates how knowledge of genetic mutations can inform strategies for treating genetic disorders.

This research marks a significant shift in our understanding of Huntington’s disease and opens new avenues for therapeutic intervention. It highlights the importance of exploring innovative strategies that go beyond conventional approaches focused solely on reducing levels of the disease-causing protein. As we delve deeper into the intricate mechanisms underlying neurodegenerative diseases, such as Huntington’s, we inch closer to the prospect of effective treatments that could transform the lives of millions worldwide.

In the words of Dr. Leora Fox, Assistant Director of Research and Patient Engagement for the Huntington’s Disease Society of America, this research represents a pivotal moment in Huntington’s research, offering renewed hope. As we continue to unravel the complexities of Huntington’s disease, this latest breakthrough stands as a sign of progress in the ongoing quest to cure this condition. Are you confident in this breakthrough? What are your thoughts?

 

New and Improved Cancer Treatments!

Did you know that new approaches to fighting cancer just use the patient’s own immune system?!                                                                                                                                      In recent years, researching and manipulating the immune system has quickly allowed for new tested and approved treatments that are becoming increasingly popular. This treatment is called Immunotherapy.

Although the immune system can fight cancer on its own, cancer cells can bypass the immune system and spread. Immunotherapy allows the immune system to have a stronger attack on the cancer cells in various ways. One type of immunotherapy treatment is Immune Checkpoint Inhibitors. Unlike other treatments, checkpoint inhibitors work with the immune system to target cancer cells rather than attack them directly. The immune system can distinguish between normal cells and foreign cells (cancer cells) while protecting the normal cells from being attacked. However, as previously stated, cancer cells can exploit the checkpoint proteins on immune cells (T cells) to evade the body’s immune response. In this process, there are two very important proteins involved: PD-1 and PD-L1. PD-1 is a checkpoint protein on the surface of T cells that functions as a regulator, helping to control and restrain the T cells (from attacking healthy cells in the body) when bound to PD-L1, a protein on both normal and cancer cells. So basically, the PD-1 checkpoints act
like a traffic light: green means go, and red means stop! Diagram showing cancer cells spreading into the blood stream CRUK 448

The most common immune checkpoint inhibitor is Pembrolizumab, more commonly recognized by KeytrudaPembrolizumab targets and blocks the PD-1 protein, which triggers the T-cells to find and kill cancer cells. This drug is received intravenously (IV) and is used for multiple cancers, sometimes independently, but it can also be combined with other types of treatment. Pembrolizumab is approved to treat breast cancer, lung cancer, melanoma, kidney cancer, liver cancer, and cervical cancer, among many other types.

 

In our AP Biology class, we discussed what causes cells to become cancerous, how those are then different from healthy cells, and how they metastasize. From learning how cancers develop, I wanted to do more research and found it very interesting how this complex matter is treated. Learning that there are various approaches to treating cancer leaves me wanting to research more. I find it so cool how this newer treatment, Keytruda, supports the body’s immune system because it proves how smart our bodies are, and since immune checkpoint inhibitors continue to be tested and approved, is very encouraging and hopeful as it is an example of science advancing.

What do you think about immune checkpoint inhibitors? Would you expect this kind of treatment to be more or less efficient than treatments you may be familiar with already?

CRISPR and Sickle Cell Disease

A blood smear of someone with sickle cell disease under a microscope

Scientists are starting to use genetic editing tools to edit out genetic diseases, starting with sickle cell disease.

Sickle cell disease is a non-dominant genetic disease that is the result of the red blood cells becoming well, sickle shaped. These cells then die early, and catch on things in veins, resulting in clots.

In addition, the cells aren’t able to properly deliver their cargo to cells- oxygen. The recipients then also promptly die early, resulting in a multitude of complications, many of which are potentially fatal.

CRISPR (short for “clustered regularly interspaced short palindromic repeats”) technology utilizes Cas9 proteins, guided with a sliver of RNA, and it will comb through the DNA and clip the matching strands off, in which it will either be forced to mutate, or function correctly (should it be a mutation that we are seeking to eliminate). 

In this case, CRISPR is being used to alter the genes that cause this disorder (that without morality, natural selection would have done its work in weeding it out) as a replacement for the support (i.e. blood transfusions) . 

Before the actual editing process, the patient’s stem cells are collected and the patient undergoes high dose chemotherapy to clear the existing bone marrow so that the edited cells can take prevalence

Casgevy, the name of one of the gene editing drugs, does exactly that. Blood is drawn, the blood is treated, then the now edited blood is reinserted into the patients bone marrow. It is currently approved for people 12 and over, but that is likely a base number and one’s doctor would properly evaluate for.

29 of 44 treated patients had achieved 12 consecutive months within the span of 24 months without SCD complications, and all 44 treated patients had successfully accepted the mutated stem. 

Common side effects included low platelet and white blood cell levels, mouth sores, headaches, itching, febrile neutropenia, vomiting, abdominal pain, and musculoskeletal pain.

How many other genetic diseases can CRISPR edit out?

Why are Blueberries Blue?

Have you ever wondered how certain fruits are such vibrant colors? Scientists globally have also pondered such characteristics. Some people think that objects obtain their colors by simply having the pigment inside. However, how our eyes perceive color is much more complicated than simply seeing the pigmentation.

Recently, research has been conducted on the color of blueberries. Blueberries are considered to be a “bloom” fruit, in that it has an epicuticular wax layer and dark pigmentation. This color does not come from smushing the fruit and watching the juice emerge, which led researchers to wonder where exactly it does come from. Researchers have discovered that blueberries are covered by a thin, waxy coating that is two microns thick. The researchers discovered this by removing the waxy layer and recrystallizing it to view the particles within the layer itself.

Within this layer, there are scattered particles in a random crystalline structure that reflect blue and UV light. Photons of light have certain pigments, and only a few of which are visible to humans. The photo below depicts which light is visible to humans. It is also notable that the pigment in blueberries reflects UV light, which is visible to birds.

FIO117: Figure 8.1

This directly relates to our AP Bio Photosynthesis Unit. In this unit we learned the reason why leaves are green. This is because leaves contain certain pigments (one being chlorophyll a) that absorb all wavelengths of light except for green, which is reflected.

Additionally, we learned in AP Bio that leaves are surrounded by a non-polar, waxy substance. This is the same on blueberries. It is interesting that learn that water will not easily penetrate through the skin of leaves as well as certain fruits due to the repulsion of non-polar and polar substances.

Do you know of any other epicuticular fruits? Can we investigate their pigmentation as well?

Uncovering One Mystery of Tardigrades

Tardigrades, are one of the more well known creatures of the microscopic world. Something that keeps them in the spotlight is their extreme survivability. However, when active tardigrades don’t have their toughness. They only have that survivability when they are dormant, or are in a state called suspended animation, read this blog to find out how they enter this state.

Tardigrades can be called water bears or moss piglets in addition to their official name. This is due to the fact that the location they are found in is typically in water in mossy or muddy areas. They are microscopic eight legged animals that when dormant are close to invincible. When needed, tardigrades can curl into a ball called a tun. One of the reasons they are able to do this is that water bears are invertebrates. When they are in a tun, tardigrades pull in their legs, release water, turn their insides to glass, and nearly stop their metabolism. Once in this state tardigrades can withstand radiation from x-rays and even trips into space.

Derrick Kolling, a chemist at Marshall University found that chemical changes called oxidation to the amino acid cysteine trigger the tun state, and they even found that when this process is reversed, it brings tardigrades out of their dormant state.

 

SEM image of Milnesium tardigradum in active state - journal.pone.0045682.g001-2

Scientists have wondered for a long time what causes tardigrades to go into the tun state, and this finding is an exciting discovery for the biology world. This discovery helps explain some unknown pieces of the biology of water bears as a tun, and there is even hope that this discovery can explain some biological aspects of other creatures in their respective tun state’s.

Kolling started this project almost out ofnowhere. After seeing tardigrades in the news frequently, he decided to find some and test them with an EPR Spectrometer, a device that studies atoms and molecules with unpaired electrons. This relates to our AP Biology class as we also found tardigrades for a lab, and we learned about their toughness, origins, and survivability.

After using the EPR Spectrometer to test a few different things, the researchers found that blocking cysteine oxidation prevented tardigrades from forming tuns triggered by exposure to high levels of salt or sugar. They found that blocking this oxidation also prevented water bears from surviving freezing. This suggests that cysteine oxidation is what triggers the tun state.

Prior to reading this, what did you think caused tardigrades to enter the tun state?

Do you think tardigrades really came from space?

Have you ever tried to find a tardigrade?

Post Includes edits and suggestions made by ChatGPT.

 

Can Alzheimer’s Disease be Transmitted?

https://www.flickr.com/photos/institut-douglas/2677257668

We have long associated Alzheimer’s disease as a condition that could come with aging, but have you ever thought that the disease could also be transmitted? 

 

In most cases, Alzheimer’s disease affects an older population group, as around 1 in every 9 people who are aged 65 or older in the US have Alzheimer’s. However, in January 2024, researchers have reported in the Nature journal that five people who received contaminated injections of a growth hormone in their early childhood years came to develop Alzherimer’s disease unusually early – between ages 38 and 55. This points to the potential that the contamination of the growth hormones to be a cause of the unusually early development of Alzheimer’s disease in the 5 people reported. 

 

These 5 people received hormone injections that are used to treat various growth disorders. The hormones are extracted from pituitary glands of cadavers (a practice no longer used), as the pituitary gland is the location in the body that produces growth hormones that signals the body for growth. However, sometimes these extractions are contaminated with infectious, misshapen proteins, which could cause serious problems in human cells such as preventing the cells from doing its regular jobs to forming clumps in cells. 

 

One of these infectious proteins that came along with the extracted growth hormones from pituitary glands of cadavers is the amyloid-beta protein, which research shows is a hallmark of Alzheimer’s disease as it accumulates in the brain. In class, we learned about the importance of growth hormone proteins in stimulating cell growth. When cells receive growth hormone signals, they are stimulated to keep dividing and growing, and conversely when they don’t, they will stop the cell reproduction cycle. However, for patients who were contaminated with the A-beta growth hormone protein, some harmful cells in their body would be instructed to keep on growing, dividing, and continuing their reproduction cycle, which could be a possible cause of Alzheimer’s disease. 

 

After learning about how it’s possible that Alzheimer’s disease could be developed through medical contaminations, what are some improvements you think should be made in medical settings that could prevent future situations similar to this?



Harnessing the Power of Photosynthesis for Sustainable Energy

Researchers at the University of Rochester have started on a project aimed at creating clean hydrogen fuel by mimicking the processes of photosynthesis.  Their project, as detailed in a publication in the Proceedings of the National Academy of Sciences (PNAS), delves into the realm of artificial photosynthesis, aiming to harness the power of nature to produce hydrogen fuel in an eco-friendly way. The project revolves around the use of Shewanella oneidensis, a bacteria, along with nanocrystal semiconductors. The bacteria serve as an efficient and cost free electron donor to the photocatalyst, a critical component in the artificial photosynthesis system. By using the unique processes of the microorganisms alongside nanomaterials, the team aims to pave the way for a clean energy solution to this ever so polluted world. The head researchers at Rochester aim to highlight hydrogen as an ideal fuel due to its environmental friendliness as well as a high energy per molecule source. However, it is extremely hard to extract in its pure form.

Leaf 1 web

Artificial photosynthesis represents a promising way for achieving this, witht he process of three key components: a light absorber, a catalyst for fuel production, and a source of electrons. The team’s system uses semiconductor nanocrystals for light absorption and catalysis, while utilizing Shewanella oneidensis as an electron donor. This remarkable bacteria possess the ability to transfer electrons generated from its metabolism to an external catalyst, facilitating the production of hydrogen gas from water when exposed to light. The project at the University of Rochester seeks to mimic the natural process of photosynthesis, a fundamental concept in AP BIO. Photosynthesis is the process by which plants use sunlight to synthesize foods from carbon dioxide and water. The most important process in photosynthesis that the researchers are trying to mimic is the process to break down H2O into H+ ions. By understanding the fundamentals of AP BIO and its study of Photosynthesis we can learn to appreciate nature and its amazing processes such as the one that the researchers are attempting to mimic. This study, if succeeded, would be revolutionary as it is a sustainable practice and would significantly help reduce the use of fossil fuels which would greatly help with global warming. I hope that this project succeeds and am extremely grateful for learning the fundamentals of Biology in AP Bio for me to be able to understand how photosynthesis works and how the researchers will attempt to mimic this process in order to better the world.

Can You Hear Photosynthesis Occurring Underwater ?

You may not realize it, but you have the ability to hear plants harnessing the sun’s energy to perform the reaction of photosynthesis. All you have to do is take a dive under water and listen carefully for the distinct “ping” noise made while down there. New studies have found that this “ping” is the sound that underwater plants, such as red algae, make when performing photosynthesis.

Montastraea annularis (boulder star coral) (San Salvador Island, Bahamas) 1

Algae and other underwater plants perform photosynthesis just like any other land plant. What this means is that they use the sun’s rays to chemically convert carbon dioxide and water into a sugar used for plant energy and oxygen as a waste product that flows throughout the planets atmosphere. In the underwater atmosphere, these oxygen molecules are tiny bubbles that race upwards in the water. Researchers have found that when these oxygen bubbles disconnect from the plants they make a sudden “ping” noise.

The noise was first recognized by researchers in Hawaii when the Hakai Magazine reported that healthy and protected coral reefs were making low frequency sounds, while damaged coral reefs were making higher pitched sounds.

One researcher from this magazine, Simon Freeman, said that “there seemed to be a correlation between the sound and the proportion of algae covering the sea floor.” To test this assumption, Freeman and his team transferred 22lbs of invasive red algae from the Hawaiian bay to a tank filled with sea water in attempt to hear the pinging sound without the noisy distractions of the ocean. As it turned out, this research team heard the same high frequency pings from this algae as they did from the distressed reefs.

Researchers claim that a large part of corals’ distress comes from all the algae that are smothering the corals, and this is why the distressed corals had a higher frequency noise: they had more algae covering its surface that perform photosynthesis and produce these oxygen bubbles. They believe with this finding that monitoring the sounds of the oxygen bubbles could be a fast and less invasive way of keeping track of the health of coral reefs.

This connects to what we have learned in AP Bio as in the process of photosynthesis, the chlorophyll of a plant absorbs light energy called photons, which excites the chlorophyll. The excited chlorophyll pass the photons from one chlorophyll to another until the energy reaches a special chlorophyll in the reaction complex center of Photosystem II known as the p680 chlorophyll. Once the photon reachers this special chlorophyll, p680 donates an electron to the primary electron acceptor in the thylakoid membrane to start the electron transport chain. In order to replace this donated electron, water molecules (one of the reactants of photosynthesis) are quickly split up resulting in an electron and replace the donated one, hydrogen, and oxygen as a waste product. This oxygen that is released at this point of the photosynthesis process is the oxygen that is released from all plants, including the underwater plants like the algae, when they perform photosynthesis. It is waste oxygen that is released from the algae underwater that forms the oxygen bubbles that detach from the plants and float upwards, and eventually make the “ping” noise underwater that you can hear when you dive in. Moreover, when we say you can “hear photosynthesis,” what you are really hearing is the oxygen bubbles created as a waste product of photosynthesis when they detach from the plants.

When going out to a beach and diving underwater, I would sometimes find myself hearing a faint little pinging or bubble popping noise. Could this noise I am hearing be the oxygen bubbles from the photosynthesis of underwater plants? What do you think?

Aliens!!! – Not the Ones You’re Thinking of, Though…

In the article I came across, it discusses an “alien invasion” of sorts; however, this isn’t just any alien. In fact, this alien can be under your feet right now: non-native earthworms. Earthworms (not the alien kind) are described as “[m]ostly invisible and largely unappreciated” – these friendly creatures are invaluable to not only farmers and gardeners but you! In fact, these creatures support a lot of the agriculture you have grown to love and enjoy. “What makes them so helpful?” I’m sure you’re asking. Well, mainly, earthworm movement leaves an unimaginable amount of tunnels that allow air, water, and important nutrients to penetrate deep into the soil. On top of that, their waste doubles as a rich fertilizer!

Lumbricidae

Earthworms are far from always being sunshine and rainbows, though. When the wrong type of earthworm reaches the wrong type of ecosystem, chaos can easily ensue. This is what’s happening now all across North America with alien earthworms. Research has shown that, specifically in the northern broadleaf forests of the U.S. and Canada, alien earthworms have caused severe stress on local trees such as sugar maples – Acer saccharum – by altering the microhabitat of their soils. Even more, it is affecting local farmers as well. This microscopic impact can cause a snowball effect, allowing invasive species of plants to spread in an expedited manner. Isn’t it interesting and ironic that an organism known for actually improving soil can lead to poorer-quality crops and lower yield rates?

The article also spoke about specific research – drawing on extensive records spanning from 1891 to 2021, researchers compiled a database encompassing native and alien earthworm species. This dataset was augmented by another documenting interceptions of alien earthworms at U.S. borders from 1945 to 1975. Combined with new machine learning techniques, the team reconstructed the probable pathways of origin and spread of alien earthworm species. Their analysis revealed the presence of alien earthworms in a staggering 97% of soils studied across North America, with a higher (and extremely concerning) presence observed in the northern regions compared to the southern and western areas. 

Alien earthworms constituted 23% of the continent’s total of 308 earthworm species and comprised 12 of the 13 most widely distributed species. The article gave a fascinating contrast as well: only 8% of fish species, 6% of mammal species, and 2% of insects and arachnids in the U.S. are of alien origin. Lead author of the study, Jérôme Mathieu, an associate professor of ecology at the Sorbonne, emphasized that these proportions are likely to increase even more due to human activities, posing a significant threat to native earthworm populations, and to the future of our agricultural sector.

In terms of linking this back to our AP Bio course, it is easy to mention how we just learned about food webs, food chains, and trophic levels. We learned how delicate these intricate ecosystems are, and learned that when invasive and non-native species are introduced into an ecosystem, it (the ecosystem) becomes prone to collapse. Further, we can continue to apply this to the genetics unit that we are learning right now; as earthworms change the fundamental pH and nutrients in the soil, new adaptations will likely need to arise to, well, adapt to new conditions.

Who knew that such a small creature could have such a huge (and dangerous) impact on the ecosystems around us? Let me know what you think about it.

 

A New Step for Fighting Allergies Has Been Taken

Scientists are one step closer to resolving your allergies. New studies have found that certain immune cells are responsible for causing allergic reactions to harmless things such as pollen, peanuts, and dander. Understanding where these allergens come from allows scientists to dive deeper into cures for them.

Depiction of a person suffering from Allergic Rhinitis

How Do Allergies Develop?

Allergies occur when the antibody IgE is released on innocuous proteinsIgE is produced by memory B cells. It is designed to ward off bacterial infections and neutralize toxins. However, sometimes it triggers an immune response to harmless substances. When a person is first exposed to an allergen, they release a large amount of IgE. The next time they are exposed to the allergen, they may have an allergic reaction. Specific memory B cells called MBC2s are responsible for remembering the proteins that spark the allergic reactions. As we learned in AP Biology, when the immune system is triggered, large amounts of responses occur in the body. The body will physically respond with symptoms such as hives, fever, or even anaphylactic shock. These symptoms are in parallel to symptoms of allergic reactions. These symptoms are in an attempt to rid the body of the invader. Inside of the body, the response begins with proteins on macrophages displaying the invader antigen and releases cytokines. T helper cells recognize the antigen and trigger an attack response. T killer cells kill infected cells while B plasma cells secrete antibodies to bind and neutralize the invader. The macrophages then eat and destroy it. Finally, T memory cells prevent reinfection while B memory cells patrol the plasma to prevent reinfection. This entire response occurs to people with allergies when there is a non-threatening pathogen in the system. 

Primary immune response 1

The Studies

Immunologist Joshua Koenig studied 90,000 people with allergies and their B-memory cells. He used RNA sequencing to find the specific memory-B cells, MBC2s, making the antibodies responsible for immune responses against parasitic worms and allergies. In people with peanut allergies, Koenig found an increased amount of MBC2s and an enhanced amount of IgE antibodies. 

 

In immunologist Maria Curotto de Lafaille’s study, she sampled children with and without allergies. She also found that children with allergies have more MBC2 cells than children without allergies. She found that cells switch from making protective IgE antibodies to allergy causing ones. Before the switch, cells made IgE, but not the protein. The RNA enables the antibody to switch the type of antibody it makes when it encounters an allergen. The signal switch depends on a protein called JAK. Stopping JAK production could prevent memory cells from switching to IgE production in contact with allergens. 

 

The Future

If scientists can find a way to manage the production of IgEs when in contact with harmless allergens, we could be looking at a potential cure for allergies! Would you participate in a treatment for allergies if it was applicable to you?

Tardigrades in Space?

Behold the tardigrade: the eight legged microscopic phenomenon sometimes known as the water bear. They have long been known for their fascinating resilience in extreme environments. And now, according to this article, scientists now believe that they have found the reason why they are so indestructible. It has to do with their ability to hibernate.

When under stress or in a dangerous environment, the tardigrades are able to curl up into a ball known as the “tun stage” and enter a dormant state. In these situations, their cells are able to detect when they are producing harmful substances called free radicals. These free radicals then come in contact with cysteines, an amino acid in our bodies. The cysteines oxidize the free radical, which oxidizes the signal that allows the tardigrades to enter their tun stage. The tardigrades can wake up from their tuns when the cysteine is no longer being oxidized, which can be seen when the conditions around them improve. According to this article these findings can provide plenty of insight about how tardigrades are able to withstand the conditions of space travel. If this process allows the tardigrades to survive in environments of extreme temperatures or stress, they would certainly be able to use the same strategies when they are sent to space.

Tardigrade

In addition to these findings about tardigrade space travel, other research has been done about how these tardigrades can help us make advancements in medicine. This article states that they can be used to preserve biological materials such as cells or tissues. We use the information gathered from their resilient hibernation abilities to make this connection to the medical field. This can be very helpful in the healthcare industry because these advancements will allow us to keep these life-saving materials alive for longer periods of time.

In AP Bio, we spent time learning about tardigrades and even got to do our own search for them in class. My lab group was able to find tardigrades in a moss sample from our school’s campus, and it was so interesting to see them in the microscope after much intense searching. Because of this, I was very interested to read about these new findings, and it is so fascinating to see how such a tiny organism can be so powerful. I look forward to seeing what other advancements can be made with tardigrades and I would love to hear your thoughts!

Stop Thinking Food Webs are so Simple!!

We have all learned about food chains and food webs: the producers perform photosynthesis to create their own food (autotrophs), the primary consumers eat the producers for energy (herbivores), the secondary consumers eat the primary consumers for energy (carnivores) and the tertiary consumers eat the secondary consumers for energy (carnivores). We also know that animals can often fit into multiple categories in a food web.

However, it is not quite as often that people explore the effects that just one population change of any part of a food web can have on the rest of the food web; that is to say that a producer decreasing in population would indirectly hurt a tertiary consumer’s population. That is the case because producers are how the food chain gets all its energy in the first place, so with less producers, less energy is in the food chain. Furthermore, as we learned in AP Bio class, each trophic level is merely 10% energy efficient in consuming the trophic level below; thus, each higher trophic level has less energy than the last. Not only is this lack of energy efficiency why there are only a few trophic levels in each food web, but that is why it is so vital for there to be enough (energy) producers in the food web. Additionally, with energy so scarce, any organism’s population size changing can have a dramatic effect on the other populations in its food web.

In the African savanna, Jake Goheen and his colleagues at the University of Wyoming and the Ol Pejeta Conservancy in Laikipia, Kenya, have taken investigating food web relationships to another level. They have spent about 15 years examining how acacia ants (genus Crematogaster) impact a food chain that they are not even a part of consumer wise. They have found that acacia ants protect whistling thorn trees from elephants, which would rip the trees apart: the ants, abundant in the savanna area, consistently protect the trees by swarming in the elephants’ nostrils and biting them from the inside out.

Whistling thorn acacia in Masai Mara

However, with the arrival of a new invasive species theorized to have arrived along with the shipping of human goods, called big-headed ants (Pheidole megacephala), acacia ants have been massively killed off in certain areas. Although the acacia ants are not part of the food chain consumption wise with the whistling thorn trees, the loss of the protection for the trees allows elephants to eat them. Then, much more grassland is opened up. According to Goheen and his colleagues, this open land, with approximately 2.67 times higher visibility than the land typically has (according to a separate study they did), hurts the diet of a higher trophic level predator, lions:

Goheen and his colleagues found that higher visibility in land with less whistling thorn trees helped one of the lions’ main prey sources, zebras, more than it helped them: their chance of taking down a zebra dropped from 62% to only 22% in areas with big-headed ants and thus minimal whistling thorn trees, according to Goheen’s study. Thus, lions pivoted to eating buffalos, which became 42% of their diet. Eating buffalos instead of zebras hurts lions because buffalos are more likely to injure them than zebras are, but buffalos and zebras are still both primary consumers, meaning they both have 10% of the energy of the producers that they eat; that is to say, although buffalos are more dangerous than zebras to lions, lions do not lose energy with their diet swap.

Regardless, more lion deaths from lions having to kill buffalos suggests that the invasive species of big-headed ants that killed off the acacia ants truly caused massive indirect changes in a food web that it and what it killed had nothing to do with consumer wise: to me, it seems apparent that there is much more to food webs than the basic, linear way people usually think about them.

What other ways do you think food webs are affected that we do not realize?

Tickle, Tickle! : Great Apes Demonstrate Playful Teasing

Marco the chimpanzee at the Center for Great Apes

Researchers from the University of California Los Angeles (UCLA), the Max Planck Institute of Animal Behavior (MPI-AB), Indiana University (IU), and the University of California San Diego (UCSD) have identified playful teasing behavior in four species of great apes. This behavior shares similarities with joking in humans, characterized by its provocative, persistent nature, and inclusion of play elements. The presence of playful teasing across all four great ape species suggests its evolutionary roots in the human lineage at least 13 million years ago.

Playful teasing, similar to joking, emerges in humans as early as eight months of age. Infants engage in repetitive provocations, such as offering and withdrawing objects as well as disrupting activities. In a study published in the Proceedings of the Royal Society B, researchers examined spontaneous social interactions among orangutans, chimpanzees, bonobos, and gorillas to identify teasing behaviors.

The study involved analyzing teasing actions, bodily movements, facial expressions, and responses from the targets of teasing. Teasers exhibited intentional provocative behaviors, often accompanied by playful characteristics. The researchers identified 18 distinct teasing behaviors, such as waving or swinging objects in the target’s field of vision, poking or hitting, and disrupting movements.

Although playful teasing shares similarities with play, it differs in several aspects. Teasing tends to be one-sided, initiated primarily by the teaser and rarely reciprocated. Additionally, apes almost never use play signals like the primate ‘playface’ or ‘hold’ gestures. Teasing occurs in relaxed contexts and involves repetition and elements of surprise, similar to teasing in human children.

To offer an explanation for this teasing behavior among animals, oxytocin (love hormone) may play a role in doing so as well as promoting positive social interactions. Oxytocin goes into effects by binding to specific oxytocin receptors in the brain such as G protein-coupled receptors (as learned in AP Biology). Oxytocin receptors then activates the primary signaling pathways, involving the phosphoinositide 3-kinase (PI3K) pathway. Activation of PI3K leads to the production of second messengers, which regulate various cellular processes that contributes to the warm and fuzzy feeling we get due to oxytocin.

The presence of playful teasing in great apes, resembling behaviors in human infants, suggests its existence in our common ancestor over 13 million years ago. This study sheds light on the importance of understanding the evolutionary origins of behavior and the need for conservation efforts to protect these endangered animals.

Personally, I can definitely attest to the evolutionary pass-down of these playful teasings as I still find myself engaging in the same behaviors, oftentimes scorned and unreciprocated.

What are your thoughts on these findings?

Immune Evasion Unveiled: The Thrilling Genetic Drama of Tumor Suppressors and Their Sneaky Dance with Cancer Cells

Cancer, an unwelcome antagonist in our lives, often emerges as the thief of precious moments with our loved ones and friends. Ever wondered how it manages to disrupt the narrative of our lives, stealing the scenes we hold dear? Or perhaps, reflecting on those stolen moments, have you found yourself questioning the resilience of the human spirit in the face of such a formidable foe? Cancer perfectly reflects the quote that Alfred from  “The Dark Knight” said to Bruce  ‘Some men just want to watch the world burn”. In this case Cancer just wants to watch the world burn because it gains nothing.

Cancer stem cells text resized it

A study conducted recently at Howard Hughes Medical Institute by Stephen Elledge highlights the strange role played by altered tumor suppressor genes. Compared to the common belief that implies mutations in these genes only encourage unrestricted cell growth. The study revealed that in excess of 100 defective cancer suppressor genes in mice may impair the immune system’s ability to identify and eliminate cancerous cells.  Do you know how the immune system is able to detects and eliminate cancerous cells? If not this is how. The immune system is able to identify and eliminate the cancerous cells by using  T cells. These T cells constantly patrol the body to identify cells that display abnormal or mutated proteins on their surfaces. These proteins, known as antigens, can be indicative of cancerous changes. Dendritic cells then engulf and process abnormal proteins from cancer cells. They then present these antigens on their surfaces. They then present the cancer antigens to T cells.This activates specific T cells (cytotoxic T cells) that are capable of recognizing and targeting cells with the presented antigens. Activated cytotoxic T cells travel to the site of the cancer cells and release substances, such as perforin and granzymes, that induce apoptosis (programmed cell death) in the cancer cells. Successful elimination of cancer cells leads to the development of memory T cells. These memory cells “remember” the cancer antigens, providing a faster and more efficient response if the same cancer cells reappear. This challenges the conventional understanding that mutations in tumor suppressor genes primarily trigger unrestricted cell division. Instead, it suggests that such mutations can also impact the immune system’s ability to identify and eliminate cancerous cells through the T cell-mediated recognition process. This broader perspective underscores the complex interplay between genetic mutations, immune responses, and cancer development.

Tumor Growth

This has several key concepts that we covered in our AP Biology class, particularly related to cell regulation, cancer, and the immune system.

The immune system’s role in identifying and eliminating cancer cells is a significant aspect of the AP Biology curriculum. The discussion of T cells, dendritic cells, and the process of presenting cancer antigens aligns with the immune system’s functions and responses to abnormal cells. This aligns with what we learned in AP Bio regarding the immune system’s crucial role in defending the body against abnormal or potentially harmful cells, including cancerous cells because we got to see how the T Cells, Dendritic Cells, and Memory T Cells really work. We also got to see how the immune system also works directly with blood sugar levels. With various activities in class with the skittles as glucose and how the pancreases would either send a message to produce insulin or  glucagon depending on which the body needed to maintain a balanced blood sugar level.

 

Breaking the Chains of Sickle Cell: A New Dawn with Gene Therapy

The U.S. Food and Drug Administration has made a significant advancement in the treatment of sickle cell disease (SCD) by approving two new cell-based gene therapies, Casgevy and Lyfgenia, for patients aged 12 and older. Sickle cell disease is a genetic blood disorder that affects about 100,000 people in the U.S., predominantly African Americans, and is characterized by a mutation in the hemoglobin protein. This mutation leads to red blood cells adopting a crescent shape, which can obstruct blood flow and oxygen delivery, causing severe pain, organ damage, and potentially life-threatening complications.

The mutation in the hemoglobin protein that characterizes sickle cell disease (SCD) alters the structure and function of hemoglobin, which is crucial for transporting oxygen in the blood.  Hemoglobin is made up of four protein subunits, and in SCD, a mutation occurs in the gene that codes for the beta-globin subunit. This mutation leads to the production of an abnormal form of beta-globin known as hemoglobin S (HbS). In normal RBC (red blood cells), hemoglobin (a protein) has a particular shape. We learned in AP biology that proteins need a specific shape to carry out their function. In people with sickle cell anemia, that protein is mutated doesn’t have the correct shape, and cannot carry out its function.  The reason it doesn’t have the right shape is that the mutated hemoglobin sequence is modified at a single amino acid.

Under certain conditions, such as low oxygen levels, dehydration, or acidosis, HbS molecules tend to stick together, forming long, rigid chains within the red blood cells. These chains distort the shape of the red blood cells from their normal, flexible disc shape to a rigid, crescent or “sickle” shape. Unlike normal red blood cells that can easily move through the bloodstream, these sickled cells are stiff and sticky. Its interesting how such a small change can have such a significant effect in our body!

The crescent-shaped cells can get trapped in small blood vessels, blocking the flow of blood. This blockage prevents the delivery of oxygen to nearby tissues, which can cause pain and damage to tissues and organs. Furthermore, the sickled cells are more prone to breaking apart, leading to hemolysis (the destruction of red blood cells), which can cause anemia (a shortage of red blood cells) and other complications. The recurring blockage of blood vessels and the chronic shortage of red blood cells and oxygen supply lead to the severe symptoms and complications associated with sickle cell disease, including acute pain crises, increased risk of infections, and organ damage.

Casgevy stands out as the first therapy of its kind to employ CRISPR/Cas9, a groundbreaking genome editing technology, to modify patients’ hematopoietic stem cells. This process aims to increase the production of fetal hemoglobin in patients, which helps prevent the sickling of red blood cells. On the other hand, Lyfgenia uses a lentiviral vector to genetically modify blood stem cells to produce a variant of hemoglobin that reduces the risk of cells sickling. Both therapies involve modifying the patient’s own blood stem cells and reintroducing them through a one-time infusion, following a high-dose chemotherapy process to prepare the bone marrow for the new cells.

Crispr

These therapies represent a major leap forward in treating sickle cell disease, addressing a significant unmet medical need for more effective and targeted treatments. The FDA’s approval of Casgevy and Lyfgenia is based on the promising results of clinical trials, which demonstrated a substantial reduction in the occurrence of vaso-occlusive crises, a common and painful complication of SCD, among treated patients.

The approval of these therapies also underscores the potential of gene therapy to transform the treatment landscape for rare and severe diseases. By directly addressing the genetic underpinnings of diseases like SCD, gene therapies offer a more precise and potentially long-lasting treatment option compared to conventional approaches. The FDA’s support for such innovative treatments reflects its commitment to advancing the public health by facilitating the development of new and effective therapies.

However, it’s important to note that these therapies come with risks and side effects, such as low blood cell counts, mouth sores, and the potential for hematologic malignancies, particularly with Lyfgenia, which carries a black box warning for this risk. Patients receiving these treatments will be monitored in long-term studies to assess their safety and effectiveness further. Despite these challenges, the approval of Casgevy and Lyfgenia marks a hopeful milestone for individuals with sickle cell disease, offering new avenues for treatment and the promise of improved quality of life. If you were diagnosed with Sickle cell disease, would you try this no-treatment when available? Do the positives outweigh the negatives? Let us know!

The Cyathea Rojasiana: The Little “Fern” that Could (…Survive on its Own)

Have you ever wondered how some plants survive severe environments? Well, the Cyathea rojasiana is a prime example of this, as it can transform dead leaves into roots that keep the plant alive. The article, “Back from the Dead: Tropical Tree Fern Repurposes Dead Leaves” explains this plant and its amazing abilities. Cyathea rojasiana, a unique tree fern from Panema, converts its dead leaves into little roots that seek out nutrient-rich soil.

Cyathea arborea 1

The plant was found by plant biologists, notably Professor James Dalling. According to Dalling, the plant’s process of self-nourishment happens after the leaves have fully died and blended with the soil. The fern then reorganizes its leaves, absorbing nutrients, particularly nitrogen, from the soil via its newly created roots. Furthermore, even though the tree fern’s dead leaves appear to be disintegrating, they’re actually helping the plant survive. Since Panama’s soil is deficient in nutrients, this process is essential to the tree’s survival. 

 

To continue, after reading the story, I was reminded of the photosynthesis unit I learned in AP Biology. Photosynthesis, in simple terms, is the process by which plants transform light energy into chemical energy in the form of glucose through photosystems (II and I) and the Calvin cycle. Despite their differences, the sentiments remain the same. While the Cyathea rojasiana’s adaptation does not replace photosynthesis, it complements it. The tree obtains nutrients from the soil via its roots, ensuring that it gets the building blocks required for development and survival.

Photosynthesis en

In conclusion, as someone who enjoys planting and loves nature, it was very interesting to learn about this unique tree because it reveals a unique survival skill I was unaware of. The tree has learned to absorb nutrients while growing in soil that lacks nutrients. This shows how well some plants can adjust to harsh conditions, giving ideas for new and creative gardening methods. Additionally, learning about the Cyathea rojasiana provides information that can be used to enhance gardening. So, is this something you want to try and implement into your gardening routine? Let me know in the comments!!

 

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