BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: research (Page 1 of 4)

A New Way To Treat Genetic Epilepsy?!

Researchers at the Francis Crick Institute have discovered a promising treatment for CDKL5 Deficiency Disorder (CDD). CDD is a form of epilepsy that affects children.  Some symptoms included seizures, impaired cognitive development, and repetitive body movements. CDD is a devastating condition that can make a family’s life very difficult. Furthermore, it is a complicated disorder to manage. CDD was first identified in 2004 and as of now, the only treatment is medications to manage the symptoms. That is why this possible new method to treat the disorder is so interesting to me. A possible cure would change many lives. This video tells the story of a family with a child diagnosed with CDD.

CDD is an X-linked disorder. X-linked disorders refer to genetic conditions that are associated with mutations in genes on X chromosomes. This means that if a male is carrying this mutation, they will be affected because a man typically only has one X chromosome. A woman, on the other hand, typically has two X chromosomes so if she has a normal gene on the other X chromosome then she would likely be unaffected by the mutation, but has the risk of passing it on to her child. The ratio of boys affected by CDD to girls affected by CDD is roughly 8 to 1 according to PubMed Central.

Figure 13 01 05

CDKL5 stands for cyclin-dependent kinase-like 5 which is a gene located on the X chromosome. CDKL5 is involved in the “formation, growth, and movement of nerve cells” (MedlinePlus). We know from AP Biology that a kinase is an enzyme that catalyzes the transfer of phosphates groups. This enzyme transfers a phosphate group to different proteins that alter specifically brain function. We know that kinases are involved in signaling pathways which makes them essential for coordinating cellular responses. Specifically in AP Bio, we looked at tyrosine kinase receptors. In this case, the kinase removes a phosphate from ATP to add it to tyrosine to created a fully activated phosphorylated dimer which will control cell growth and cell division. CDKL5 codes for an enzyme that plays a role in brain function and is responsible for the synthesis of proteins that help the brain develop.

Researches had the idea to boost another enzyme’s activity to make up for the lack of CDKL5. They looked at mice who lacked the CDKL5 enzyme. Scientists measured the level of a molecule that is targeted by the CDKL5 enzyme called EB2. In the mice that did not produce CDKL5, researches still found that EB2 was being phosphorylated so there had to be a different enzyme similar to CDKL5 that was phosphorylating EB2 by transferring phosphates. EB2 was still getting phosphorylated because CDKL2 (cyclin dependent kinase like 2) was identified instead. Researches now aim to increase the level of CDKL2 in people who lack CDKL5 to see if this can stop symptoms of CDD from occurring. Increasing levels of CDKL2 could “uncover better treatments that could truly make a difference in the lives of the children with this devastating condition” (Margaux Silvestre).

My hope is that this research will not only help children with CDD, but also inspire research on other kinases and help find alternative kinases to cure more diseases.

 

Astronomy tools used to detect COVID-19 !?

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

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

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

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

From Bacteria to Biotech: The Surprising Similarities in Immune Systems

Bacteria have always been considered harmful and something to be avoided, but according to a recent study by the University of Colorado Boulder, bacteria might just hold the key to unlocking novel approaches to treating various human diseases. The research reveals that bacteria and human cells possess the same core machinery required to switch immune pathways on and off, meaning that studying bacterial processes could provide valuable insights into the human body’s workings. Moreover, researchers found that bacteria use ubiquitin transferases – a cluster of enzymes – to help cGAS (cyclic GMP-AMP synthase) defend the cell from viral attack. Understanding and reprogramming this machine could pave the way for treating various human diseases such as Parkinson’s and autoimmune disorders.

CRISPR, a gene-editing tool, won the Nobel Prize in 2020 for repurposing an obscure system bacteria used to fight off their own viruses. This system’s buzz reignited scientific interest in the role proteins and enzymes play in anti-phage immune response. Aaron Whiteley, senior author and assistant professor in the Department of Biochemistry, said that the potential of this discovery is much bigger than CRISPR. The team discovered two key components, Cap2 and Cap3 (CD-NTase-associated protein 2 and 3), which serve as on and off switches for the cGAS response. Understanding how this machine works and identifying specific components could allow scientists to program the off switch to edit out problem proteins and treat diseases in humans.

CAS 4qyz

This discovery opens new avenues of research as bacteria are easier to genetically manipulate and study than human cells. Whiteley said that the more scientists understand about ubiquitin transferases and how they evolved, the better equipped the scientific community is to target these proteins therapeutically. The study provides clear evidence that the machines in the human body that are important for just maintaining the cell started out in bacteria, doing some really exciting things. The ubiquitin transferases in bacteria are a missing link in our understanding of the evolutionary history of these proteins. Thus, this research shows the importance of studying evolutionary biology, and how it can provide valuable insights into human health.

The study highlights the similarities between bacteria and human cells in terms of their immune response, specifically, describing how cGAS (cyclic GMP-AMP synthase), a protein critical for mounting a downstream defense when the cell senses a viral invader, is present in both bacteria and humans. This similarity suggests that portions of the human immune system may have originated in bacteria, a concept explored in the evolutionary biology unit. In this past unit, we discussed the origins of life, and how all life originated from a simple bacteria cell. This bacteria cell, though many many many repeated cycles of evolution and natural selection allowed for variation within its species and the formation of new species through the processes of speciation.

 Cancer Detection Using CRISPR Gene Editing

Currently, many are accustomed to invasive cancer diagnostic methods such as endoscopies, colonoscopies, and mammograms. Driven by the desire to discover new methods, a group of researchers from the American Cancer Society developed an alternative method, which is a significant contribution to cancer detection.

Utilizing CRISPR gene editing as their approach, the group of ACS researchers developed an easy-to-use mechanism for detecting small amounts of cancer in plasma. CRISPR gene editing is a method that scientists and researchers have been using to modify an organism’s DNA. CRISPR gene editing is often done for numerous reasons, such as adding or removing genetic material, creating immune defense systems, and repairing DNA. Their detection method also allows healthcare professionals in diagnostics to decipher between malignant and benign cancer-related molecules that they may discover.

CRISPR Gene-Editing

The first step that the researchers made to develop this approach was to design a CRISPR system that creates a manufactured exosome out of two reporter molecule fragments, which they cut. An exosome is a small vesicle that carries material such as lipids, proteins, and nucleic acids after branching out from a host cell. Exosomes are typically involved in detecting cancerous cells because they provide a glimpse into the host cell they branched out from. Therefore, cancerous cells are shown in their exosomes through biomarkers, like micro RNAs (miRNA). In AP Biology class, microRNAs are described as materials that bind to complementary mRNAs to prevent the translation from occurring. MiRNAs are a recent discovery, identified in 1993. It is now concluded that most gene expression is influenced by them, so the researchers made efficient use of miRNA in their experiment. The two fragments of the reporter molecule came together and interacted with the CRISPR’s materials.

Micro RNA Sequence

The researchers concluded that if the targeted miRNA sequence was evident in the combination, the CRISPR system they made would become activated and cut apart the reporter molecule. The researchers specifically targeted miRNA-21, which is often involved in cancer development. The researchers were able to detect miRNA within a combination of similar sequences and later tested their method on a group of healthy exosomes and cancerous exosomes. Their CRISPR system successfully differentiated between the healthy and cancerous exosomes, which makes this system effective for cancer detection. The researchers are confident that their CRISPR gene editing approach to cancer detection will make diagnosis easier on patients and a more efficient process overall.

 

Read it and wheat…

Wheat, corn, and rice are the most important crops around the world. As someone who enjoys baking, wheat is the base of almost all the desserts and bread recipes I bake. However, as I have become more interested in baking various types of bread, I wondered how gluten is formed and how bread textures change based on how long I kneaded the dough. According to Jessica R Biesiekierski in her article “What is Gluten”, Gluten is “complex mixture of hundreds of related but distinct proteins, mainly gliadin and glutenin.” The gluten matrix is essential to the quality of bread dough. It has the ability to act as a “binding” agent and is also used in marinades and even capsules in medication.  The biology of gluten and its structure depend on the ration of glutenin and gliadins. Each component has different functions that can effect “viscoelasticity”. In her article Biesiekiersk, worked to find evidence that “exposure to gluten may be increasing with changes in cereal technology”. There are many diets and intolerances caused by gluten such as the gluten free diet, gluten disorders, coeliac disease wheat allergy and sensitivity. In conclusion of their study, they determined “Gluten is a complex protein network and plays a key role in determining the rheological dough properties and baking qualities.” However, they came across a challenged. They learned that protein structure can “vary dependent on several factors”. Ultimately, make “analysis and definitions difficult”. And overall they conclude that “further work is needed to completely understand non-coeliac gluten sensitive”.

Another study that researched viscoelasticity is by is Peter R. Shewry, Nigel G. Halford, Peter S. Belton, and Arthur S. Tatham studied “The structure properties of gluten: an elastic protein from wheat grain”. According to Science Direct, viscoelasticity refers to a material’s tendency to act like a fluid or a solid. An additional article that explores viscoelasticity.

Vehnäpelto 6

They manipulate the “amount and composition” of HMM subunits concerning the strength or change of gluten structure and properties. These scholars describe wheat as a plant with many properties, however, they emphasized “viscoelasticity”. In terms of this research, viscoelasticity is “the balance between the extensibility and elasticity determining the end use quality.” The scholars use the dough as an example stating that “ highly elastic (‘strong’) doughs are required for bread making but, more extensible doughs are required for making cakes and biscuits”. In the study, these scholars focused on the HMM protein subunits of gluten. At least 50 different types of gluten proteins can be produced during the kneading process; however, these researchers have chosen to focus on the HMM subunits of glutenin. HMM, subunits, X type, and Y type can be only found on one chromosome in wheat cells. These two subunits are 70 % accountable for the viscoelastic variations in bread. This presentation allowed the researcher to see how stable and unstable the subunits were which would play a role in their ability to interact with peptides. In addition, these peptides may relate to the role of gluten in stabilizing the structures and interactions of the subunits.

US Navy 050102-N-5837R-011 Culinary Specialist 3rd Class Joshua Savoy and Culinary Specialist 3rd Class Davy Nugent prepares bread in the bakery aboard the Nimitz-class aircraft carrier USS Abraham Lincoln (CVN 72) Both articles emphasized the importance of protein structure. AP Biology greatly emphasizes the importance of Organic compounds. Proteins have a few structures that are ultimately composed of sequences of amino acids to create polypeptide chains. From primary structure proteins can become more complex by forming alpha helixes and beta pleated sheets. From that point 3D structures can be made. Gluten has a very structure characterized by “high allelic polymorphism encoding its specific proteins, glutenin, and gliadin”. This leads to wheat producing “unique types and quantities of these compounds”, these types and quantities can vary based off “growing conditions and technological processes”.

Self-Assembling Hydrophobic Sandwiches

You read that correctly! Researchers at Rice University in Houston, Texas alongside Jeffrey Hartgerink have made a significant advance in injury treatment, illness education, and drug candidate by testing the self-assembling abilities of 3D printed nanofibrous multidomain peptide hydrogels, referred to as “hydrophobic sandwiches.” 

Hydrogel

The main goal of Hartgerink’s team was to create a structure that could house cells and help them grow tissue by 3D printing the peptide ink. The printing allows researchers to recreate the complexity of biological structures due to their soft and flexible tissue-like feel, making this a major scientifical discovery and advantage. Hartgerink and his team describe their printed peptides as “hydrophobic sandwiches” due to their design, flexibility, and behavior. The peptides were printed to have one hydrophobic side and one hydrophilic side, allowing them to flip on top of each other when placed in water and resemble sandwiches. Like we learned in AP Biology, the hydrophillic qualities of one side will attract water, and the hydrophobic qualities of the other will repel water. Hydrophobic molecules repel water because they are nonpolar molecules, so they are not attracted to water, which is polar. Once the “sandwiches” were stacked after flipping in the water, they formed the hydrogels which can be vital to tissue engineering and wastewater treatments. 

Hydrogel Structure

The multidomain peptides have already been utilized due to their self-assembling nature for regenerating nerves, treating cancer, healing wounds, and encouraging tissue development throughout the body. Rather than only focusing on this aspect of the peptides, Adam Farsheed, a lead author in Hartgerink’s study, wanted to specifically highlight the fact that these peptides are an ideal 3D-printing ink choice due to their self-assembling nature. When testing the “sandwiches,” Farsheed took a unique, brute-force approach to add more of the material, rather than chemically modifying it, to test its function and ability to reassemble itself after deformation. He proved that adding more peptide material lets the peptide reassemble and heal itself extremely well after being deformed. This discovery will make the hydrogels an ideal candidate for scientific and medical usage.  

Through continued testing, he was also able to confirm that the peptides behave differently depending on their charge. The peptide cells with a negative charge tended to ball up on the substrate of the experiment and the positively charged cells spread out and started to mature on their own. Farsheed has confidently stated that their findings will allow the group to “control cell behavior using both structural and chemical complexity.” Both Hartgerink and Farsheed have made incredible contributions to the world of science through their studies using 3D-printed peptide hydrogels. 

 

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. 

 

 

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