BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: research (Page 1 of 4)

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 Cancer.gov, “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. 

Newly Discovered Neurons and Their Role in Maintaining Normal Body Temperature

The internal body temperature in humans and mammals is maintained at 37℃/96℉, unless disrupted by a force like an illness or heat exhaustion. Regulating the body to stay in the normal range is crucial for survival and for enzyme function.  Our internal body temperature is constantly being regulated by our hypothalamus, located at the base of our brain. The hypothalamus uses sensors from a mediator known as prostaglandin E which is brought about when an infection is present in the body. After PGE2 is present, it signals for the body to raise its temperature and combat the infection. If temperature levels are abnormal, the enzymes in our body have trouble functioning because they need specific temperature conditions to carry out reactions. Therefore, maintaining homeostasis throughout the body by regulating internal temperature is key to human survival.

Prostaglandin E

A team of researchers at Nagoya University in Japan were inspired by this process and decided to focus on the unknown neurons that make up the receptors of PGE2 and how this regulation process functions. The group of professors and colleagues successfully discovered key neurons that work to regulate the body temperature of mammals. This finding can be highly useful for creating future technology that can artificially fix body temperature related conditions such as hypothermia, heat stroke, and obesity.  

Neuron

Neuron

By using rats as a subject for their research, they exposed the rats to cold (4°C), room (24°C) and hot (36°C) temperatures to observe the effect of temperature changes on EP3 neuron response. After conducting the experiment, the researchers were able to conclude that exposure to the hot temperature led to an activation of EP3 neurons and the cold temperatures did not. Once they made this conclusion, they dug deeper into the neurons and analyzed the nerve fibers of the neurons to discover where the signal transmission occurs after sensing an infection. The researchers were able to conclude that the neuron fibers are spread out in different areas of the brain, mainly the dosomedial hypothalmus, which works to activate the sympathetic nervous system. Not only did they discover these fibers, but they also discovered the substance that EP3 neurons utilize to send signals to DMH. By observing the structure and chemical makeup, they found that this substance is a neurotransmitter known as gamma-aminobutyric acid (GABA), which inhibits neuron excitation. 

Finally, their findings support the idea that EP3 neurons are a major component of regulating internal body temperature and that they send out the GABA substance to signal to DMH neurons for a proper response. Their research proves that intiating a neural response decreases body temperature and inhibiting neurons leads to an increase in body temperature. Furthermore, their strong research in this area can support future development of advanced technology that will be capable of artificially adjusting internal body temperature. The anticipated technology could help prevent hypothermia, treat obesity to keep body temperature slightly higher and initiate fat burning, and be a key method of survival in hot environments. 

 

Ballerinas Got the Brains!

A 2013 research article conducted by scientists at the Imperial College of London has dived into the ballet world and researched the brains of ballerinas. Their research led to the discovery that dancers can suppress signals of dizziness using the balance organs of the inner ear. The vestibular system, found in the inner ear, consists mainly of smaller circular canals. Each canal recognizes different motions: Up and Down, Side to side, and tilting. These canals are filled with hair and liquid which move with your body to send signals to the brain using the acoustic nerve. With this information, your brain can process balance, dizziness, and vertigo. These researchers became curious about how ballet dancers can perform multiple balanced pirouettes without feelings of dizziness. And as a dancer, I would say this is because of the technique of spotting which involves rapidly moving the head to keep one’s eyes on a fixed spot.

However, this study has proved that wrong. So, with the help of 29 ballet dancers and 20 rowers, the researchers put it to the test. Their method of testing involved putting the volunteers in a dark room and spinning them on a rotating chair. They then timed how long it took for the dizziness to stop. In addition, the researchers measure eye reflexes triggered by the vestibular organs and later completed MRI scans of the patient’s brain structure. The data they collected showed that the eye reflexes and perception of spinning lasted a shorter time with the dancers than with the rowers.

From this point, doctors wondered how they could transfer this ability to their patients. After taking an in-depth look at the dancer’s brains it was concluded that the cerebral cortex and cerebellum were the most affected. The cerebral cortex is found in the largest part of the brain and is responsible for speech, judgment, thinking and reasoning, problem-solving, emotions, learning, and the senses. While the cerebellumMajor parts of the brain, a fist-sized portion found in the back of the brain, uses neurons to coordinate voluntary muscle movements and to maintain posture, balance ,and equilibrium. In the AP Biology curriculum, learning the nervous system helps in one’s understanding of transport and membranes. The nervous system sends signals across the plasma membrane of a cell to the brain. With this signal, the cerebellum and cerebral cortex can process information and signal parts of the body to move. From looking at the MRI scans, scientists discovered that the dancer’s cerebellum was smaller. Scientists believed dancers would be better off not using their vestibular system and solely relying on “highly coordinated pre-programmed movements”. Scientists believe it is not necessary for dancers to feel dizziness so, their brains adapted to suppress that feeling. As a result, the signal that goes to the cerebral cortex is reduced. So, if scientists and doctors monitor the cerebral cortex they could begin to understand how to treat patients affected by chronic dizziness.

 

 

NMT5: A New Enemy To SARS-CoV-2?

In the past few months, scientists in the United States have developed a potential new antiviral to SARS-CoV-2.   The drug, called NMT5, is effective against several variants of SARS-CoV-2, the virus that sent the planet into lockdown only a few years ago.

As stated in the journal Nature Chemical Biology, NMT5 coats SARS-CoV-2 particles as they travel through the body.  Thus, when the virus attempts to attach to the ACE2 receptor proteins of the cell, NMT5 attaches first.  The drug changes the shape of the cell’s receptor upon attachment, which makes it harder for SARS-CoV-2 to infect the cell, and on a larger scale, the organism’s body.

In order to ensure that the drug isn’t toxic, researchers tested NMT5 on healthy cells.  According to the National Institute Of Health, it was “found that NMT5 was non-toxic and only changed receptors that were being targeted by the virus. These effects lasted for only about 12 hours, meaning the receptors functioned normally before and after treatment”.  In fact, in an experiment that used hamsters as models for the human immune system, NMT5 reduced SARS-CoV-2’s ability to bond to ACE2 receptors by 95%!

A significant reason NMT5 is so effective is that it not only limits one particle of SARS-CoV-2, but the effectiveness of the virus as a whole, when present. When a SARS-CoV-2 particle with NMT5 attaches to an ACE2 receptor, it adds a nitro group to the receptor, which limits the ability of the particle to attach to the receptor for 12 hours by changing the receptor’s shape.  Thus, no COVID-19 particle can attach to the ACE2 receptor – even ones that haven’t been surrounded by NMT5.  Stuart Lipton, a professor at The Scripps Research Institute, states that “what’s so neat about [NMT5] is that we’re actually turning [SARS-CoV-2} against itself”, as particles surrounded by NMT5 serve to limit the ability of other SARS-CoV-2 particles.  The drug has excited scientists studying SARS-CoV-2 around the world, as they have “realized [NMT5] could turn the virus into a delivery vehicle for its own demise” (PTI, The Tribune India).

Cell reception and signaling are incredibly important to both viruses and the human immune system.  A virus works by infiltrating a cell through cell receptors that line the outside of the desired cell’s phospholipid bilayer.  Viruses attach to these receptors and infect the cell as a result.  SARS-CoV-2’s process is depicted below, as it attaches to the ACE2 receptors described earlier.  The immune system works by recognizing the virus at hand and signaling B-Lymphocytes and T-Lymphocytes to destroy the virus and infected cells.  B-Plasma cells surround the virus, as shown below, which neutralize it and allow it to be engulfed and destroyed by macrophages.  Cytotoxic T-cells kill cells already infected by the virus.  Both B and T Lymphocytes are activated as a result of T-Helper cells, as T-Helper recognize the virus when a piece of it is displayed at the end of a macrophage, and signal the Lymphcytes by releasing cytokines (another example of cell reception and signaling).  This process is all shown in the image below, with the specific virus depicted being SARS-CoV-2.

Fphar-11-00937-g001

However, NMT5 prevents the initial infection from happening when SARS-CoV-2 enters the human body by bonding with SARs-CoV-2 particles before they attach to cells, which allows for the immune system to quickly destroy the virus.  By blocking SARS-CoV-2’s access to receptors, the drug stops the particle before it can infect a cell and do any damage. Since cell receptors are specifically shaped, and any change in form results in a loss of normal function, the ensuing change in shape of a receptor limits any SARS-CoV-2 particle from attaching to said receptor, further limiting the virus’s damage by blocking cell reception from occurring. Thus, the immune system kills the virus without major symptoms.

All in all, the development of NMT5 is exciting for scientists all around the globe.  If it is as effective as studies show, it could play a major role in limiting the effects of SARS-CoV-2.  Hopefully, all goes well, and you should be hearing a lot more about the drug sometime soon.

If you have any updates or questions on NMT5, I invite you to share them in the comments below.  Thank you for reading my blog post, and stay curious!

Clearing Up COVID-19 Brain Fog

Many people who have recovered from COVID-19 still suffer long-term effects from the terrible virus. From fatigue to loss of smell, to depression and anxiety, there are a wide variety of long-term conditions caused by COVID-19. One condition especially frustrating for patients is known as “COVID-19 brain fog.

Noun confusion 2900892.svgAccording to Harvard Health, COVID-19 Brain Fog is the term used by patients to describe their feeling that their thinking is “sluggish, fuzzy, and not sharp.” Doctors can run tests on patients who feel like they are suffering from this condition; however, oftentimes the tests come back normal. Scientists have several theories regarding the cause of brain fog. For one, COVID-19 can have lingering effects not related to the brain. As I mentioned earlier, patients can suffer from various conditions, which can distract them, impairing their ability to think clearly.

Health Matters interviewed neurologists Dr. Mitchel Elkind and Dr. Alexander Merkler to learn more about COVID-19 Brain Fog. The doctors noted that patients can sustain brain damage from a stroke during their  COBrain Exercising.pngVID-19 infection, and this would be an obvious cause for cognitive differences; however, Dr. Elkind mentioned that “some people seem to have this brain fog out of proportion to their illness.” In theory, patients who had mild coronavirus symptoms should not have long-lasting cognitive effects, but the medical community is finding that they do. One possible explanation is immune system activation.

Like any virus, when the immune system releases molecules to help itself fight off SARS-CoV-2 without background.pngSARS-CoV-2, some of the molecules can affect the nervous system. Sometimes the body can overreact and start attacking normal cells, which is when we start seeing effects such as COVID-19 Brain Fog. The immune system recognizes the viral proteins, but sometimes it mistakes similar-looking proteins in the brain and ends up attacking those. Fortunately, scientists are researching possible treatments for this devastating condition. 

At Augusta University, researchers are developing a drug to treat COVID-19 Brain Fog. It has not been tested yet, but the drug is a polyphenol molecule. One polyphenol molecule, EGCG, inhibits SARS-CoV-2 from binding to host-cell receptor ACE2, thus preventing the virus from entering the host cell. Dr. Stephen Hsu, Professor of Oral Biology and Oral Health and Diagnostic Sciences at Augusta believes that in combination with EGCG technology, EC16, will “yield benefits for Long-COVID relief and protection.”

AP Bio Sidenote 🙂

This connects to AP Bio through the possible treatment of brain fog. EGCG acting as an inhibitor connects to receptor-mediated endocytosis because it blocks the ligand, in this case SARS-CoV-2, from binding to ACE2 and so the cell does not accept the SARS-CoV-2.

I chose this topic because I am interested in the long-term effects COVID-19 has on individuals as well as society.

Ever wonder if you were exposed to COVID-19? This new device may be able to help.

Riding a public train. Traveling on an airplane. Or just shopping in a public mall. These are all ways someone may contract COVID-19 without realizing that a stranger around them is infected. Traveling via public transport can expose you to unwanted germs, especially when travel times exceed 15 minutes resulting in longer exposure to a possible carrier of the virus. According to the CDC, being exposed to someone with COVID-19 for more than 15 mins results in a “Higher Risk” scenario of contracting the virus. According to Johns Hopkins Coronavirus Resource Center, there have been over 600 million cases of COVID-19 across the globe. What if you could detect COVID-19 particles around you and then change your seat accordingly to reduce exposure?

Well, scientists out of Tohoku University have created a battery-less device which can detect COVID-19 particles in the air, causing a signal response on the device telling you of the virus’s presence. The device generates power via “alternative magnetization caused by vibration” which can detect “bending vibration energy” and transmit the detection wirelessly. The scientists first objective was to modify a “0.2mm thick Fe-Co/Ni plate with a rectifier/storage circuit”. This unit can detect substances that adhere to the clad plate through the change in vibration and resonance frequency. The ability to use this device without power as well as the ability to adjust triggers for its response are the key reasons it was chosen. 

The next task for the scientists was to adjust the transmission device to detect type “229E (HCoV-229E)”, one of seven strains of human coronavirus. Coating the clad surface of the plate using targeted proteins, in this case a CD13 protein caused the resonance frequency or vibrations of the device to decrease when exposed to this certain COVID-19 strain. Through repeated tests, they were able to verify that these coated plates could transmit the detection of the type “229E (HCoV-229E)”virus without needing an external power source, “something not capable with current biosensors“.

Proteins stimulating responses in our cells when fighting a virus like COVID-19 occur during the Cell Signaling process that we are studying in AP Biology. Through the process of an Immune Response to a virus, after the virus is broken down inside a macrophage, a MHC2 protein will bring part of that virus to the outside of the macrophage to signal a helper cell. The Helper T Cell then has a protein of its own called a CD4 protein which will pair with the MHC2 protein to identify the shape of the virus. In this part of the Immune response to a virus, we see a protein transferring information to a helper t cell, similarly we see a protein on the surface of these coated clads identify a strain of COVID-19 and then send a signal.

As the scientists continue their research on batteryless biomedical devices, they hope to further “develop our device and see if it applies to other viruses, such as MERS, SARS and COVID-19“.

Is Covid-19 Becoming Immune to Us?

The Coronavirus has been a focal point for each individual in the past three years. Regardless of your age, gender, ethnicity, or even location, COVID-19 has been the one commonality for everyone. Because of COVID-19’s immense reach and detriment, scientists have worked tirelessly to source treatments and provide them to the people. Although the initial treatments worked in the beginning, as the virus grew and adapted, scientists, doctors, and Coronavirus professionals were forced to follow suit. To this day professionals are still trying to keep up with the ever-changing nature of the virus.

New research shows that initial Coronavirus treatments are slowly becoming more and more ineffective as the virus continues to mutate. The initial treatments for COVID-19 mainly consisted of monoclonal antibodies. Simply put, these are antibodies targeted to a specific illness, Coronavirus in this case. Because the antibody is targeted to one specific disease, as the disease mutates the antibody can no longer be applied to the newly altered disease. For example, recently the US Food and Drug Administration issued information regarding one Coronavirus antibody, Evusheld. They essentially stated that there is an increased risk of COVID-19 as certain variants cannot be neutralized or treated by Evusheld, the current monoclonal antibody. These new changes are critical for those with weakened immune systems who are reliant on strong antibodies to protect them.

To continue, scientists are exploring new ways and attempting to find new treatments for mutated viruses. They do this by seeking out vulnerable parts of the virus and creating an antibody for it. A former Harvard Medical School Professor, William Halestine, hopes that these new treatments will soon be in clinical trials for research.

One example of these clinical trials is currently being administered in Brazil and South Africa by Immune Biosolutions, a biotechnology company. Here they have created a new mix of antibodies and administered them to patients with both mild and high-severity cases of COVID-19. Two of the antibodies in the mix aim at a region of a spike protein where the virus would attach to the human cell. They want these antibodies to block this region and prevent the virus from attaching.

This process can connect to multiple concepts and ideas learned in our AP Biology Class. First, we learned about ligands and receptors, where each ligand is shaped specifically to its own receptor. In this scenario, the virus and antibody are both specific ligands for the spike protein and can only attach to specific spike proteins. This can be compared to our understanding of ligands docking with shape-specific receptors. Second, our understanding of antibodies can be paralleled with the company’s antibody mix. We learned that cells have a certain adaptive immunity to respond to new viruses. This can connect to the company creating new antibodies to adapt to the new virus. Furthermore, we learned that cells can have humoral or antibody-mediated responses, Immune Biosolutions antibody mix is exactly this, a humoral response.

I personally believe that there will be a point where the efforts of scientists and professionals surpass that of the virus. Where we can take control of the virus rather than working for it.  Hopefully, we as humans will eventually stop having to create newer and newer antibodies as the virus slows its mutations.

SARS-CoV-2 without background

 

Can Reactive Oxygen Species Maintain Stem Cell Function and Prevent Inflammation?

Have you ever wondered what “gut health” really means? What keeps your gut microbiome functioning properly, maintaining homeostasis, and preventing inflammation? Originating from oxygen, reactive oxygen species (ROS) that are highly reactive function as central indicators of cellular flaws and issues in the body, such as inflammation. Nai-Yun Hsu of Mount Sinai has stated that “Reactive oxygen species released by stem cells are critical in maintaining a heathy gut via maintaining proper balance of intestine barrier cell types.”

File:Inflammatory Bowel Disease MTK.jpg 

A team of researchers from the Ichan School of Medicine at Mount Sinai have gone in depth about the importance of these oxygen species for stem cell function, avoiding inflammation, and repairing wounds in a recent study. Using mice as models, the researchers were also able to conclude that microfold cells, called “m cells” regulate an organism’s gut immune response, and emerged from a loss of ROS in mice and humans. 

 

The experiment was conducted in vino and in vitro conditions with the mice cells, and ex vivo conditions with human intestinal biopsies post-colonoscopy. Both the human intestinal biopsies and mouse cells were utilized to determine the amount of ROS in the body to support a finding. In addition to determining the amount of the oxygen species, the biopsies and mice were used to analyze the “gene expression profile” of barrier cells in intestines of mice and humans that are diagnosed with a “subtype of IBD known as ulcerative colitis.”  

 

A decrease in these oxygen species can lead to TNF’s emergence in the body, which is a substance that attempts to maintain homeostasis in the body and avoid inflammatory diseases, like IBD and ulcerative colitis. They have concluded that losing species like NOX1, a protein that creates these species, is directly linked with inflammatory diseases like Inflammatory Bowel Disease (IBD). Judy H. Cho, MD, has stated that the study is a breakthrough “in defining the key role of oxygen species in maintaining a healthy epithelial barrier for IBD.” These reactive oxygen species are relevant to AP Bio considering the information we have learned about general biological systems and cells, which function to maintain homeostasis in the body. The mitochondria, which is an organelle of the cell covered in AP Bio, receives signals from gut bacteria that reveals inflammation. While the mitochondria is typically known as the site of cell respiration and performing reactions, new evidence has shown a relationship between the gut microbiota and mitochondria to trigger immune responses and activate barrier cell function. These processes relate to changes to the mitochondria that occur from gut-related issues in IBD patients, meaning that there is a connection to ROS. 

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Gut Microbiota

As a conclusion to proving the direct link between the highly reactive oxygen species and treating inflammation, these researchers encourage and plan to conduct further study on this topic, but for using “oxygen species-stem cell modulation therapy” to potentially treat IBD patients. 

 

 

Optimus Prime, Megatron, Proteins? The New Transformer Vaccine Candidate!

Amid the global outbreak of COVID-19, with no end in sight after nearly two years, the future wellbeing of humans is in danger. Coughs, fevers, and shortness of breath have lent way to millions of deaths across the globe. As thousands of researchers relentlessly work to find solutions to this virus, multiple vaccine candidates have emerged. Specifically, in the United States, millions of Americans have received doses of the Pfizer-BioNTech, Moderna, and Johnson & Johnson’s Janssen vaccines. However, scientists at Scripps Research recently recognized a new, self-assembling COVID-19 vaccine as a potentially more efficient and effective way to fight this worldwide battle.

 

Primarily, it is critical to understand how vaccines function as they help protect the immune system. The COVID-19 vaccines currently in effect are mRNA-based; in other words, the messenger RNA signals one’s body to produce a harmless viral protein that resembles the structure of a spike protein. The body, with the help of T-Helper cells, recognizes this structure as a foreign invader as B cells bind to and identify the antigen. The T-Helper cells will then signal these B cells to form B-Plasma cells and B-Memory cells. When getting the vaccine, the B-Memory cells are especially important as they prevent reinfection. This is a process known as adaptive immunity. Here, in the event of future infection with the spike-protein COVID-19, the memory cells would help carry out the same response more quickly and efficiently. Essentially, this process acts as the body’s training in case of any future infections.

 

While the Scripps Research COVID-19 vaccine would evoke a similar immune response to that described above, it differs from other candidates in how it assembles in the human body; this new vaccine would be comprised of proteins that are able to self-assemble. On their own, these nanoparticle proteins would transform into a sphere protein structure surrounded by smaller proteins, mimicking the coronavirus’s shape. Here, the self-assembled spike proteins are more sturdy and stable than in an mRNA-produced structure. Thus, it more accurately prepares the body for future infection with COVID-19. In fact, multiple tests found that mice who were given the experimental vaccine were able to fight off not only SARS-CoV-2 but also SARS-CoV1 along with the alpha, beta and gamma variants.

 

Nonetheless, influencing the public to get a newer vaccine instead of the well-trusted vaccines already in production requires proof of the candidate’s benefits. Primarily, as mentioned, early results find that this new candidate would perform well with many different strains of COVID-19. Additionally, researchers assert that this vaccine would be relatively simple to produce on a mass scale. Lastly, scientists found that this vaccine may well be more protective and long-lasting than current vaccine candidates. Although the process of vaccine approval is lengthy and often difficult, I am hopeful for the future of the Scripps Research vaccine if it is put into production. Moreover, I believe that such experimentation with self-assembling nanoparticle proteins transcends the current pandemic. The benefits of this field present a wide array of opportunities, and I look forward to seeing what its future may hold.

 

What do you think? Are these transformer-like self-assembling particles a gateway to the future of medicine or an unnecessary distraction from effective treatments already in circulation?

How are new COVID variants identified?

COVID variants are of high concern for scientists studying the disease. Some variants can be more infectious or cause more severe illness. Additionally, some variants can evade vaccines by having different surface proteins than the variant the vaccine was created for. This causes the antibodies produced from the vaccine to be less effective against other variants. In AP Biology class we discussed how the Delta Variant, first identified in December 2020, has a different spike protein structure than the original virus from which the vaccine was created from. This allows the variant to be more infectious, and make the vaccine less effective against it. But, what are COVID variants? And how are they discovered? Hand with surgical latex gloves holding Coronavirus and A Variant of Concern text

COVID variants are “versions” of the virus with a different genetic code than the original one discovered. However, not every mutation leads to a new variant. This is because the genetic code of the virus codes for proteins. Some mutations will not change the structure of the protein and thus not change the virus. So, COVID variants can be defined as versions of the virus with a significantly different genetic code than the original virus.

To detect new COVID variants, scientists sequence the genetic code of virus which appears in positive COVID tests. Scientists look at the similarity of the genetic sequences they find. Then, if many of the sequences they get look very similar to each other, but different to any other known virus, a variant has been discovered.

To sequence the RNA of the virus, scientists use what is called Next Generation Sequencing (NGS). To understand how NGS works, it is best to start with what is called Sanger Sequencing. Sanger Sequencing utilizes a modified PCR reaction called chain-termination PCR to generate DNA or RNA fragments of varying length. The ending nucleotide of each sequence is called a ddNTP, which contains a florescent die corresponding to the type of nucleotide. The addition of a ddNTP also terminates the copying of the particular sequence. The goal of this PCR reaction is to generate a fragment of every length from the start to the end of the sequence. The sequences can then be sorted by length using a specialized form of gel electrophoresis. The sequence is then read by using a laser to check the color of the fluorescent die at the end of each sequence. Based on the color and size, the nucleotide at that position of the genomic sequence can be found.

Sanger Sequencing Example

The difference with NGS is that many sequences can be done in parallel, allowing for very high throughput. In other words, with NGS many COVID tests can be sequenced in once.

Vitamin D Points to Potential Life-saving Therapeutics for Severe Cases of SARS-CoV-2

A promising new joint study by Purdue University and the National Institutes of Health (NIH) suggests that active metabolites of vitamin D are linked to reducing lung inflammation after SARS-COV2 infection. And no, before you break out your vitamin D pills, the vitamins inside your capsules are quite different from the active metabolites studied. Because of this, these researchers are warning those infected with COVID-19 against taking excessive supplements of vitamin D in hopes of reducing lung inflammation.

The researchers identified an autocrine loop involving vitamin D which allows T-helper (Type 1) cells to activate and respond to the active metabolites of Vitamin D which represses the signaling protein, Interferon Gamma. Distinguishing features of Interferon Gamma is the central role it plays in promoting inflammation

Interferon Gamma

Structure of interferon gamma. The two chains are colored in red (chain A) and green (chain B).

Although interferon gamma sounds wildly unrecognizable at first, we have actually learned about these proteins more broadly in our AP Biology class. Interferon Gamma is actually a type of cytokine! Regarding this cytokine’s structure, the proteins that compose interferon gamma are dimerized (sounds familiar? This is because we have also previously learned about dimerization through the tyrosine kinase receptor pathway in class!). 

Along with the suppression of Interferon Gamma, Interleukin 10, a cytokine with potent anti-inflammatory properties, is amplified. This is significant because this cytokine prevents damage to the host and maintains normal tissue homeostasis by reducing inflammation.

IL10 Crystal Structure.rsh

Structure of interleukin 10 as published in the Protein Data Bank.

In the near future, these pathways could be exploited therapeutically to accelerate the shutdown program of hyper-inflammatory lung cells in patients with severe SARS-CoV-2 infections. But for now, before vitamin D is adopted to treat COVID-19, clinical trials are still needed. However, research findings like these are critical to creating effective treatment not just for those infected with SARS-CoV-2, but also other respiratory diseases as well.

What do you think about this new discovery? Do you think this could lead to scientific progress regarding the treatment of inflammation?

New Covid-19 Pill! Will it work?

Pill 2

In a study conducted by Tina Saey, she looked at Merck’s Covid- 19 pill Molnupiravir and how it is affecting hospitalization rates of Covid-19. Molnupiravir, “an antiviral drug that can be taken at home” is the first medicine that can be taken orally that is approved to help fight off Covid-19. The drug is typically administered to patients who have mild to moderate Covid within five days of their symptoms appearing. Molnupiravir has been tested several times and is now waiting on the FDA for formal approval. This new pill could be a game-changer, but will it really be as great as it seems?

Ms. Saey states that “finding an early treatment hasn’t been easy”, so when Molnupiravir came around experts praised its development. Initially, the pill showed great signs of preventing hospitalizations and death from Covid-19. The results were so promising, a 48% decrease in hospitalizations, that the trial ended early so that the pill might become available to the public faster. However, when all the data was collected and analyzed the reduction in hospitalization rate dropped to 30%. The unexplained decrease happened when participants in the placebo group were no longer experiencing severe symptoms. Due to the decrease in reported effectiveness, the FDA’s antimicrobial drugs advisory committee came to a split 13-10 decision on whether the drug should be available for emergency use. 

The main concern for authorizing Molnupiravir is that the pill could create even more dangerous versions of the Covid- 19 coronavirus. The drug works by making mutations in the RNA. This is when a change occurs that affects nucleic acids, the building blocks of RNA. A handful of these mutations could land in the spike protein. Spike proteins interact with the cell receptors located on the host cell; in terms of Covid-19 it helps the coronavirus break into cells. The spike protein could also burst into other proteins making the virus more transmittable. James Hildreth, an immunologist stated that, “the potential for this drug to drive some very challenging variants into the public is of major, major concern.” Although this is a possibility it seems unlikely because, after five days of usage, infectious viruses in participants taking Molnupiravir were no longer detectable. 

SARS-CoV-2 without background

Spike Protein

Overall, there is much promise but also notable concerns to the new drug Molnupiravir. I believe that this new medicine, even with its downsides, could save hundreds of thousands of lives. As Ms. Saey states, “a 30 percent reduction in hospitalizations and deaths is worth giving the drug temporary authorization.”

The Common Misconception Around Antibiotics & New Findings

Gfp-medicine-container-and-medicine-tabletAntibiotics as a treatment are never fun – not only are you most likely dealing with a bacterial infection, but you need to take them on a strict cycle and can be quite aggressive on your stomach. I once had to go on antibiotics for treating a sinus infection, and it didn’t quite make me feel better after taking it. So after, I went on the same antibiotic, Cefuroxime, and took a higher dose, but I was not consistent in taking it and started feeling ill. This reaction was due to the antibiotics impact on the protective bacteria in my stomach’s microbiome. I soon learned more about the effects the antibiotics had on my stomach’s microbiome, and realized the common misconception around antibiotics – that they only benefit one’s health – and how some of the symbiotic relationships with bacteria in there are essential to digestion and immune protection. 

Biological overview

Antibiotics have been around since 1928 and help save millions of lives each year. Once antibiotics were introduced to treat infections that were to previously kill patients, the average human life expectancy jumped by eight years. Antibiotics are used to treat against a wide variety of bacterial infections, and are considered a wonder of modern medicine. However, they can harm the helpful bacteria that live in our gut.

The word antibiotic means “against life”, and they work just like that – antibiotics keep bacterial cells from copying themselves and reproducing. They are designed to target bacterial infections within (or on) the body. They do this through inhibiting the various essential processes we learned in Unit 1 about a bacterial cell: RNA/DNA synthesis, cell wall synthesis, and protein synthesis. Some antibiotics are highly specialized to be effective against certain bacteria, while others, known as broad-spectrum antibiotics, can attack a wide range of bacteria, including ones that are beneficial to us. Conversely, narrow spectrum antibiotics only impact specific microbes.

Antibiotic resistance mechanisms

The Human stomach is home to a diverse and intricate community of different microbial species- these include many viruses, bacteria, and even fungi. They are collectively referred to as the gut microbiome, and they affect our body from birth and throughout life by controlling the digestion of food, immune system, central nervous system, and other bodily processes. There are trillions of bacterial cells made of up about 1,000 different species of bacteria, each playing a different role in our bodies. It would be very difficult to live without this microbiome – they break down fiber to help produce short-chain fatty acids, which are good for gut health – they also help in controlling how our bodies respond to infection. Many antibiotics are known to inhibit the growth of a wide range of pathogenic bacteria. So, when the gut microbiome is interfered with using similar antibiotics, there is a high chance that the healthy and supportive microbes in our stomachs are targeted as well. Common side effects of collateral damage caused by antibiotics can be gastrointestinal problems or long-term health problems (such as metabolic, allergic, or immunological diseases). There is a lot of new research on the gut microbiome, some even suggesting that it impacts brain health by influencing the central nervous system. It is essential that we know more about how we can optimize its overall well-being.

New Research

Tackling the Collateral Damage to Our Health From Antibiotics

Researchers from the Maier lab EMBL Heidelberg at the University of Tübingen have substantially improved our understanding of antibiotics’ effects on gut microbiomes. They have analyzed the effects of 144 antibiotics on our most common gut microbes. The researchers determined how a given antibiotic would affect 27 different bacterial strains; they performed studies on more than 800 antibiotics.

The studies revealed that tetracyclines and macrolides – two commonly used antibiotic families – led to bacterial cell death, rather than just inhibiting reproduction. These antibiotic classes were considered to have bactericidal effects – meaning that it kills bacteria rather than just inhibiting their reproduction. The assumption that most antibiotics had only bacteriostatic effects was proven not to be true; about half of the gut microbes were killed upon being treated with several antibiotics, whereas the rest were just inhibited in their reproduction. 

These results expanded existing datasets on antibiotic spectra in gut bacterial species by 75%. When certain bacteria in the gut are dead, and others are not, there can exist an reduction of microflora diversity in the microbiota composition; this concept is referred to as dysbiosis. This can result in diarrhea, or even long term consequences such as food allergies or asthma. Luckily, the Researchers at EMBL Heidelberg have suggested a new approach to mitigating the adverse effects of antibiotics on the gut microbiome. They found that it would be possible to add a particular non-antibiotic drug to mask the negative effects the antibiotics had. The Researchers used a combination of antibiotic and non-antibiotic drug on a mouse and found that it mitigated the loss of particular gut microflora in the mouse gut. When in combination with several non-antibiotic drugs, the gut microbes could be saved. Additionally, they found that the combination used to rescue the microbes did not compromise the efficacy of the antibiotic.

It has been known for a while that antibiotics were impactful on gut microbiome, but its true extent had not been studied much until recently.  More time is needed to identify the optimal dosing and combinations, but the research coming from the Maier lab is very substantial as it fills in “major gaps in our understanding of which type of antibiotic affects which types of bacteria, and in what way,” said Nassos Typas, Senior Scientist at EMBL Heidelberg.

Your Inner Chimpanzee

 

Chimpanzees

What is the closest living relative we have (evolutionary speaking)? That’s right, chimpanzees!! Our evolutionary paths separated us about five to six million years ago leading to the chimpanzee of today, and us humans of the 21st century, but we still have much in common. Like humans, Chimpanzees use body language to communicate. They often kiss, hug, pat each other on the back, hold hands and shake their fists. They even laugh when they get tickled. At the same time, a lot has also changed. Not only do we stand on two legs and are relatively hairless, but we also have brains that function differently. 

 

Recent research from Lund University has found the answer to what in our DNA makes our brains different. Created by Shinya Yamanaka, the study used a revolutionary stem cell technique. Yamanaka discovered that if reprogrammed specialized cells can be developed into all types of body tissue. It was even recognized by the 2012 Nobel Prize in Physiology or Medicine. 

 

The researchers used stem cells grown in a lab. Their partners in Germany, the US, and Japan reprogrammed the skin cells. Then Johan Jakobsson, professor of neuroscience at Lund University, and his partners examined the stem cells that they had developed into brain cells. Using the stem cells, the researchers specifically grew brain cells from humans and chimpanzees and compared the two cell types. The researchers then found that humans and chimpanzees use a part of their DNA in different ways. This appears to play a significant role in the development of our brains.

 

What the researchers learned was different in part of our DNA they and I found so unexpected. Unlike previous research in the part of the DNA where the protein-producing genes are — about roughly two percent of our entire DNA, the difference that was found indicated that the differences between chimpanzees and humans appear to lie outside the protein-coding genes. The research found that it is actually located a so-called structural variant of DNA in what has been labeled as “junk DNA,” a long repetitive DNA string that has long been deemed to have no function. This was thought to have no function. 

 

This data suggests that the basis for the human brain’s evolution is a lot more complex than previously throughout genetic mechanisms, as it was supposed that the answer was in that 2 percent of the genetic DNA. These results indicate that the overlooked 98 percent is what has been significant for the brain’s development is instead perhaps hidden in, which appears to be important. 

 

Researchers hope to answer that question one day. But there is a long way to go before they reach that point. The question that now remains is instead of carrying out further research on the two percent of coded DNA should they delve deeper into all 100 percent. Even though exploring the missed ninety-eight percent is a considerably more complicated task for research. 

 

One question that also definitely still remains is why did the researchers want to investigate the difference between humans and chimpanzees in the first place?  

 

Well, Johan Jakobsson believes that in the future the new findings will prove his belief that the brain is the key to understanding what it is that makes humans human. How did it come about that humans can use their brains in such a way that they can build societies, educate their children and develop advanced technology? It is fascinating!” (Lund University). He hopes that this research will contribute to answers about things like genetically-based questions about psychiatric disorders, such as schizophrenia. As for me, I wonder if this continued research will tell us anything about how Chimpanzees will evolve. 

 

 

Can Fruit Flies Really Help Cancer Research?

Fruit fly (7424411436)In a study conducted at the University of California, Berkeley, researchers identified similarities between fruit flies and humans with cancer and believe this research could lead to prolonging the lives of cancer patients. Cancer, a disease where cells “grow uncontrollably and spread”, was diagnosed in 18.1 million new cases and claimed the lives of 9.5 million new patients worldwide as recently as 2018. The Berkeley researchers took a new approach to tackle cancer by “launching an attack against the destructive chemicals cancer is throwing off.” They believe this new method could increase patients’ survival rate and overall health.

David Bilder, a UC Berkeley professor, stated that the goal of the research was “to help the host deal with the effects of the tumor, rather than killing the tumor itself”; this represents a different approach to cancer treatment since most current treatments focus on killing the tumor and the unhealthy cells. Conventional treatments create serious side effects in patients as the treatments impact healthy cells too. Bilder’s research attempts to interfere with the blood-brain barrier, a feature of the central nervous system which is key in regulating microorganism entry and exit from the bloodstream and interstitial brain fluid. It is believed that inflammation caused by tumors leaves the blood-brain barrier open, but interfering with that process might slow tumor growth allowing for improved patient quality of life and life expectancy. This process could eliminate the need for toxic drugs that harm healthy cells while targeting cancer cells.

During the research a few years ago, Bilder’s team also learned some interesting new information about the impact of insulin on cancer. They concluded that tumors in fruit flies release a substance that blocks the effects of insulin. Insulin, a type of protein that coordinates organism activities while maintaining normal blood glucose levels, is a crucial component of our body system. It allows cells to absorb glucose which can serve as energy or convert to fat if necessary. Without insulin, cells are unable to use glucose as fuel and bodies would start breaking down their fat and muscle resulting in weight loss. This can pose an issue because it could lead to cachexia (an effect of cancer where patients are unable to maintain weight) which sadly kills ⅕ of cancer patients. Although more research is needed to investigate the relationship between insulin and cancer in humans, sugar may play a role in the growth of cancer.

 

CSIRO ScienceImage 355 Representation of Insulin Structure

Insulin Structure

I believe that this new approach to cancer treatment is a fascinating angle to effectively treat cancer patients. As someone who has experienced cancer in two close family members, I know firsthand how draining the treatments are because they target healthy cells as well as cancerous ones; this treatment simply diminishes these side effects. As Bilder states, “We think this is a real blind spot that hasn’t allowed scientists to address questions about how the tumor is actually killing outside of its local growth.” It could offer a “complementary way of thinking about therapy.” It is great to see new ways of thinking address a disease that impacts so many people.

Bias in Science: History, Representation, and Medicine

Science is not objective. Scientists may value fact, but they are still people too, influenced by identity and implicit and explicit biases in their research. Racism has pervaded every aspect of society since the country’s founding, and scientific institutions are no exception. From historical racist research practices to a modern reluctance to support Black Lives Matter or actively diversify the field, scientists have participated in and promoted racism for centuries. Scientists cannot claim objectivity now as an excuse to not be antiracist.

Throughout American history, unethical, racist research has contributed to scientific “progress”, but that is not regularly acknowledged. Although the past cannot be undone, fields should at least recognize the horrific means by which some research was done. For example, gynecology was borne of unethical experiments done on enslaved women and children. The “Tuskegee Experiment” withheld treatment of syphilis from hundreds of Black men just to see how the disease progressed. Henrietta Lacks, a Black woman with cervical cancer in 1951, had some cells taken from her tumor without being informed of this. The cells from her tumor, now known as HeLa cells, have been used since the 1950s for biomedical research. Since cancer is characterized by an improperly regulated cell cycle, with either too much cell growth or too little cell death, cancer cells can grow and divide excessively. This particular line of cells has been able to grow and divide endlessly, due to the presence of an active version of telomerase during cell division. This enzyme prevents the typical shortening of telomeres in cell division that leads to cell aging and death, making the cells “immortal” and the cell line usable to this day. Though they have been used in various research advances, her name was only connected to them in the 1970s. Her family, still with limited access to healthcare themselves, received no financial benefits and had no say in how the cells were used. Henrietta Lacks’ case is a more recent example of unethical research practices affecting Black people.

The questions scientists choose to study, whom they choose to include, and how they apply their results all bias research. Scientists of marginalized identities are much more likely to explore topics relevant to minority groups. So then, the lack of diversity among scientists also contributes to biased research priorities. In 2016, only 9% and 13.5% of science bachelors degrees were given to African Americans and Latinos respectively, and only 5% and 3.8% of doctoral degrees in science and engineering went to women and men from underrepresented minorities. Almost 70% of scientists and engineers employed full time are white. When issues like COVID-19 and climate change disproportionately affect marginalized groups, the lack of diverse representation can prevent representative research or solutions. Scientific institutions need to work on hiring and retention of Black, Latinx, and Indigenous scientists, in part by creating less hostile work environments and increasing DEI efforts.

The lack of diversity in clinical trials also decreases the inclusivity of science and medicine. Even though about 40% of Americans are nonwhite or Hispanic, the clinical trials for new drugs tend to have much whiter samples, with some having 80 to 90% white participants. Since these drugs will be used to treat all people, diverse samples are needed to determine the efficacy and side effects that can vary across ethnicity and sex. The 1993 National Institutes of Health Revitalization Act that required greater inclusion of women and minorities in NIH research samples did improve the proportion of female subjects, but not so much for minority groups. Even for diseases that disproportionately affect marginalized groups, those groups are grievously underrepresented in the clinical trials. 

One such disease is COVID-19. Even though the rates of infection, severity, and death are greater for Black, Latinx, and Indigenous Americans, these groups are underrepresented in clinical trials. Trials for drugs to treat COVID-19 did not accurately reflect the most affected populations at the research sites. Some studies also did not report the race and ethnicity of participants as required by the FDA. Remdesivir has shown to somewhat decrease recovery time, but since disease severity and outcomes are worse for minority groups, the benefits of improvement may not necessarily extend to them. This is why proportional representation of affected populations is so important in clinical trials for drugs.

One cause for lack of diversity in clinical trials is that minority groups can be unwilling or unable to take part, for reasons including fear of discrimination, lack of time or resources, inaccessibility of recruitment centers, language barriers, and fear of exploitation based in historical precedent. However, these barriers should be on the researchers to address, not on the marginalized groups. A possible solution could be to have the FDA enforce that drugs should be tested on samples that demographically reflect the populations that will be using them.

In the end, research institutions and scientists need to examine their biases in order to determine who they are serving, and then who they mean to serve. Efforts to increase diversity cannot be passive, but instead should involve active recruitment and work to eliminate the barriers in place. In an academic institution, that might mean a more inclusive work environment and better outreach and mentorship programs. For clinical trials, this could be reducing the financial burden of participation and building better relationships with minority communities that may have been hurt in the past. Science is meant to help people, so we need to be better moving forward, as well as acknowledge the damage scientists have done in the past.

Suleman Hussain’s Journey into Biomedical Research

Antigens are foreign substances which induce an immune response in the body, especially the production of antibodies. The antibodies then latch on to the foreign substance in an attempt to mark them to be destroyed. This ability to bind to specific molecules makes antigens ideal probes in cell research, where they are used to latch onto, and thus help isolate and identify, molecules of interest in and on cells. Suleman Hussain, a researcher in the lab of Daniel Higginson and Simon Powell at MSK, discovered a novel and efficient way of preparation, fixation, and embedding of tissue for electron microscopy.

His research proved that Antibodies raised against aldehyde-fixed antigens improve sensitivity for post-embedding electron microscopy. To prove their hypothesis, he and his team immunized rabbits with antigen pre-fixed with glutaraldehyde (GA, which is commonly used in electron microscopical investigations). The results were consistent with their hypothesis, thus marking the discovery that will improve future biomedical research in terms of efficiency.

Despite all of his accomplishments, Suleman Hussain has experienced numerous hardships due to his sexuality. Being a member of the LGBTQ community, Hussain had trouble finding himself. He lived in India where homosexuality was criminalized so he kept his true self under covers, hidden from the rest of the world. Hussain grew up Muslim so to this day, his family still doesn’t know that he’s gay or that he’s married. “But I have grown more comfortable and more confident in myself. At this point, if they somehow find out then I’m ready for it.”

The reason why visibility of LGBTQ people in science is so important is because we serve as examples to gay teens, who go through a lot. For them to be inspired to do what they are really capable of, that’s what motivates me to be visible. It’s become much easier now overall than what it was before, but still there are a lot of homeless LGBTQ teens and higher rates of suicide too. So in that sense it’s very important for them to have examples.

-Suleman Hussain

Did ants originate from zombies? This fungus will give you the answers.

There is a certain fungus that turns ants into zombies, but afterward, they explode. When ants are just walking by minding their own business they step on fungal spores. It attaches to the ant’s body and the fungal cell goes inside of the ant. The fungus feeds from within and increasingly multiples cells and it is called, Ophiocordyceps,   mainly living in the tropics. The danger about this fungus is that the ant is unaware of this whole process, it goes about its daily life, searching for food and bringing back to its nest. However, the fungus takes up half of an ant’s body mass. It undergoes a parasitic relationship where the fungus benefits, while the ant is harmed.

Once the fungus is done feeding, the ant will feel a needle-like sensation. What is happening here is that the fungus is pushing on the ant’s muscle cells. And the cell signals also get sent to the ant’s brain, then the ant will climb upwards above its nest. Ophiocordyceps does something very weird where it allows the ants to move upwards to a leaf above ground and then the ant bites down, where it locks its jaw. Then it sends out “sticky threads that glue the corpse to the leaf.” The ant’s head then bursts open, called a “fruiting body”, where it looks like horns projecting from the ant’s heads and the horns disperse more of these fungal spores onto its nest below it leaving behind a trail of spores. 

Hornlike antlers that come out of the ant’s head

There is still so much that is unknown about Ophiocordyceps because scientists don’t even know what kind of chemical gets into the ant’s brain causing it to climb. There are ants that age back to 48 million years old gripped onto leaves.  Scientists thought there was one species that zombified ants but it turns out there are at least 28 different fungal species that attack other insects as well. Dr. Araújo drew out a family tree to see what was infected by Ophiocordyceps. It became known that all Ophiocordyceps species come from a common ancestor, first infecting beetles larvae, not hemipteran.

The beetles that are affected by the larvae live in eroding logs.

“They’re mostly solitary creatures, with a very different life history,” compared to ants, she said.

It can now be inferred that possibly millions of years ago when this was happening to beetles, ants picked up the fungus if they were living in the same logs. Thus a constant cycle and more spreading of fungal spores. Even though natural selection favored keeping the ant’s host healthy and away from parasites, Ophiocordyceps had to find a way to make the ant leave the nest, not far enough from its environment, but just in the right place to send out the spore to infect whatever other ants were living around it. 

Because this behavior is so unordinary it is not possible that only one gene is responsible for all of this. They keep finding new species. Dr. Hughes and Dr. Araújo are still researching to find that there are hundreds of other species of Ophiocordyceps that are yet to be discovered.

Is Air Pollution Exposure In Childhood Linked To Schizophrenia?

Research has shown that pollution affects physical health, but does air pollution also affect our psychological health? A study, which combines genetic data from iPSYCH with air pollution data from the Department of Environmental Science, reveals that children who are exposed to a high level of air pollution while growing up have an increased risk of developing schizophrenia.

“The study shows that the higher the level of air pollution, the higher the risk of schizophrenia. For each 10 ?g/m3 (concentration of air pollution per cubic metre) increase in the daily average, the risk of schizophrenia increases by approximately twenty per cent. Children who are exposed to an average daily level above 25 ?g/m3 have an approx. sixty per cent greater risk of developing schizophrenia compared to those who are exposed to less than 10 ?g/m3,” explains Senior Researcher Henriette Thisted Horsdal, who is behind the study.

To put this research into perspective, the lifetime risk of developing schizophrenia is approximately two percent, which is equal to two out of a hundred people developing schizophrenia in one’s life. For people exposed to the lowest level of air pollution, the lifetime risk is just under two percent. The lifetime risk for people exposed to the highest level of air pollution is approximately three percent.

“The risk of developing schizophrenia is also higher if you have a higher genetic liability for the disease. Our data shows that these associations are independent of each other. The association between air pollution and schizophrenia cannot be explained by a higher genetic liability in people who grow up in areas with high levels of air pollution,” says Henriette Thisted Horsdal about the study, which is the first of its kind to combine air pollution and genetics in relation to the risk of developing schizophrenia.

The study included 23,355 people in total. Out of those people, 3,531 developed schizophrenia. Through the results of this research one can see that there is an increased risk of schizophrenia when the level of air pollution during childhood increases; however, the researches cannot comment on the cause. Instead, the researched emphasize that further studies are needed before they can identify the cause of this association.

Schizophrenia is thought to mainly be a result of genetics, brain chemistry, substance use, and exposure to viruses or malnutrition before birth. So, I think it is very interesting that exposure to air pollution during childhood may be a cause as well. Additionally, I hope that these findings and further studies become very useful to schizophrenia research and prevention, as schizophrenia is a very serious mental illness and there is no cure.

 

How are ocean conditions harming its animals?

A recent article written by Rachel Nuwer discusses the dangers of ocean acidification and how the ocean environment could compromise the fishes’ ability to swim and feed. The existence of one of the world’s most threatening predators is being threatened by ocean warming and acidification. Sharks might lose their place at the top of the marine food chain due to the changing ocean environment. As carbon dioxide levels rise in the ocean, it increases the acidity of the water. As this factor starts to rise, the teeth and scales of sharks may begin to damage, which compromises their ability to swim, hunt, and feed. According to research published in Scientific Reports, acid-base adjustments have proved to be the first piece of evidence of “dentical corrosion” caused by ocean acidification conditions. After investigating the impact of hypercapnia on a specific shark species and analyzing the acid-based regulation, the team concluded that the denticle corrosion could increase denticle turnover and compromise the skin and protection of the shark species.

A close up on the denticles and scales of a wild shark

The harsh conditions placed on the sharks could cause several consequences and ultimately could affect the whole ocean community. Biologist Lutz Auerswalk states that sharks could be displaced as apex predators, which could disrupt the whole food chain. In addition, great white sharks are already endangered, and these conditions could wipe them out completely, he states. Ocean research Sarika Singh and Auerswald, while studying over beers, stumbled upon a unique idea. After realizing that the high acidity of beet and many other carbonated beverages causes human teeth to erode, they wondered what effect more acidic ocean water might have on shark teeth.

Most studies on ocean acidification examine species that specifically build shells or other calcium-based structures, including corals and shellfish. Because sharks are large and challenging to work with, only a few studies have been conducted about how acidification might impact these animals. Only one paper has examined the effect of pH on sharks’ skin denticles or scales. The study used small-spotted catsharks and exposed them to different environments and filmed their swimming patterns. After analyzing a pectoral fin skin sample, they did not find a specific impact. However, the results were possible constrained by the low carbon dioxide concentration the researches used, compared with the high levels of acidity already present in many oceans.

To begin exploring this question for themselves, Auerswald and Singh conducted an experiment and focused on puff adder shy sharks, a small species that is easy to handle. They decided to investigate the acidification effects on the bigger scales. They divided the sharks into control and experimental groups and observed the results. After a few months, the electron-microscope analysis revealed that the concentrations of calcium and phosphate in the sharks’ denticles were significantly reduced. They noticed damaged scales on many of the sharks as well. Though the corroded scales might not impact their ability to hunt, for larger species such as the great white shark, scales play an essential role in hydrodynamics. Because denticles are responsible for an increase in swimming speed, damaged denticles could slow sharks down and make it more difficult for them to catch prey. Because many animals have been wiped out, we must strive to protect all the species that are deeply impacted by this condition.

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