BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: research (Page 1 of 4)

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.

A NEWclear Life

In a recent study at the University of Georgia, images of many different species of animals have been taken in Fukushima, Japan, where there was a nuclear disaster nine years ago. The people in the area had been evacuated to a safer place so that they wouldn’t suffer from the toxic radiation that causes cancer. However, animals like the wild boar, black bear, macaque, and raccoon dog (my pick for March Mammal Madness 2017) have been photographed in the area. Intrigued by how this could be possible, a team went to take data by taking tens of thousands of images of the different species.

Cameras were set in three different zones: high radiation, intermediate radiation, and low radiation. Humans are still inhabiting the low radiation area because it is safe enough where there is minimal contamination. Despite the nuclear contamination, most of the species inhabited the high radiation zone and the least inhabited the low radiation zone. 26,000 images of wild boars were taken in the uninhabited zone, 13,000 images in the restricted zone, and 7,000 in the inhabited zone. This was due to the fact that the animals were trying to stay away from human interaction and development. The team also evaluated the time of day when the animals were active, the elevation, and the type of terrain. Animals like the raccoon continued to be nocturnal in the uninhabited zone, while the wild boar was even more active during the day than before since it did not have to worry about being hunted. The Japanese serow differed from the rest of the animals as it actually spent more time in the human-inhabited zone because of the higher boar population in the uninhabited zone.

Although many would assume that animals would stray away from areas of high radiation like humans, the contrary occurred in Fukushima. The results showed that factors like human interaction, elevation, and habitat type played a larger role than the radiation levels for population size. How do you think these animals are able to survive in these conditions?

How Do Fish Get Their Shape?

Researchers in The National University of Singapore discovered how fish create their chevron pattern. 

The chevron shape itself and the shape’s function in locomotion have been used to infer the evolutionary relationships among chordates. However, the development of the chevron has not been fully researched until now. 

The research team mainly focused on the myotome, a group of muscles forming the spinal nerve root in fish. These muscles make up most of the fish body and help them become more efficient with side-to-side swimming motion. The myotome creates the “V”  pattern, or chevron pattern, in fish, which helps them increase their swimming efficiency. 

One factor that determines the shape of fish is the friction and stress of their muscles. When the myotome first develops in fish, it forms a cuboidal shape before it deforms into a V shape. Dr. Sham Tlili and Professor Timothy Saunders, head researchers of the project, used zebrafish embryos to examine the deformation process of the myotome from a cuboidal to V shape. Developing myotomes in embryos are connected to embryonic tissues, such as the notochord, and each connection has a varying level of friction. The researchers discovered that the sides of the myotome experience more friction than its central side. 

Picture of chevron pattern on fish

The team also revealed that cells of growing myotome become longer as muscle fibers are formed. This elongation incites a force, which is what creates the “V” pattern on fish. 

Professor Peter Wainwright, a biological professor in UC Davis, also determined that patterns of fish could be split into two groups: midwater fish and deep water fish. “As you get down into the water column, when you have more substrate and more complexity in the habitat, you definitely find more variation and elongation,” said Susman, one of Wainwright’s students. 

Professor Saunders, when asked about the results of the experiment, states that  “This work reveals how a carefully balanced interplay between cell morphology and mechanical interactions can drive the emergence of complex shapes during development. We are excited to see if the principles we have revealed are also acting in the shaping of other organs.”

 

What’s Happening with Human Gut Microbiome Research?

Researchers are on the brink of reveling strong links between the human gut biome and the health of the individual. The potential of this research seems limitless. The human gut biome is responsible for all sorts of conditions, ranging from inflammatory bowel disease to diabetes, multiple sclerosis, autism, cancer, and AIDS. Furthering our understanding of this biome could lead to cures for these conditions.

Soon, the first microbiome therapies will be available on the market for purchase. Rebiotix, the first acquisition of a microbiome company, is currently working on developing a therapy for C. difficile infections. In an interview, Lee Jones, founder and CEO of Rebiotix, said

It has become evident through research that the microbiota that humans carry have a significant impact on human health, [The C. difficile therapy] has the potential to be the first human gut microbiome product approved anywhere in the world.”

The C. difficile therapy would mark the first human gut biome therapy on the market, a major advance in medicine. This year is supposed to be an inflection point for human gut biome research. It is expected that research will finally show results proving that the therapies have effects on humans. If this comes true, the future for microbiome medicine is bright.

 

Secure Passcodes : Not Just For Your Computer… But For Your Gut

What is the Human Gut Microbiome?

Human gut microbiomes are made up of all the bacteria present in your gut. The Bacteria in your gut outnumbers the cells by a ratio of 10 to 1. While the presence of that much bacteria sounds like a bad thing, it can be confirmed that “the gut microbiome is very important for human health—that much we certainly know”.  The nearly 100 billion Bacteria cells per gram are actually what helps the body digest food and remove the bacteria that is bad for your gut.

 

(Left) Bacteria on vs not on the intestines       (Right) Gut Microbiome Graphic

A Unique Passcode

As said above, the human gut microbiome is essential to digesting food but more importantly keeping our body healthy. The thought of controlling a person’s gut bacteria in order to keep them healthy and fight illness is fascinating to scientists. The key to using the microbiome to fight sickness is in the “passcode” that is essential to unlocking its potential. Each microbe, according to recent research, requires a unique passcode. The research done by scientists according to phys.org says that once there is a way to determine the “passcode” it will unlock a whole new world of probiotic treatment in the future.

Why Else is the Microbiome important

According to other research done within the past few years, it has been found that sleep can also be linked to the human gut and stomach. The quality of sleep a person gets can be linked to their “biological rhythms, immune function, and nutrient metabolism” however it is still unknown to what extent the microbiome is affecting human sleep.

Conclusion

While researchers still have many questions about the human gut microbiome and how it contributes to health, wellness, and overall human biology, once they have come to some more concrete conclusions the impacts of controlling the bacteria in the human gut would exponentially improve the health of many people. It may sound weird that your bacteria have a “passcode” with which to be controlled, but hey, conclusive findings of the microbiome could even help you get a better night’s sleep! And who doesn’t want that?

Can Microbes Create Healthier Food?

A specific human gut microbe is making processed foods healthier. 

Researchers at Washington University School of Medicine in St. Louis wanted to find the chemicals in processed foods that correlate to diabetes and heart disease. In their study, the scientists used a bacteria called Collinsella intestinal (bacteria that contains an enzyme to break down Fructoselysine), which breaks down fructoselysine into small, harmless parts. According to Ashley R. Wolf, a researcher in the lab, “Fructoselysine is common in processed food, including ultra-pasteurized milk, pasta, chocolate and cereals.” This chemical has been linked to the cause of many diseases of aging.

When Wolf and her team tested the effects of feeding fructoselysine to mice that had Collinsella intestinalis, they not only discovered an increase in the amount of microbes in the stomach, but also found that the mice’s gut microbes had a stronger ability to break down fructoselysine.

“The new tools and knowledge gained from this initial study could be used to develop healthier, more nutritious foods as well as design potential strategies to identify and harness certain types of gut bacteria shown to process potentially harmful chemicals into innocuous ones,” says Jeffrey I. Gordon, a researcher of the lab.

Picture of human gut microbes

(“Courtesy of Pacific Northwest National Laboratory”)

Another study by Harvard University and the University of San Francisco, discovered that raw food was healthier than cooked food. They found that “cooked food allows the host to soak up more calories in the small intestine, leaving less for hungry microbes further down the gut; on the other hand, many raw foods contain potent antimicrobial compounds that appear to directly damage certain microbes.”

Although more research still has to be done to determine the effectiveness of the microbe, these discoveries help lead people into a healthier lifestyle. 

Can your diet’s effect on gut bacteria play a role in reducing Alzheimer’s risk?

Could following a certain type of diet affect the gut microbiome in ways that decrease the risk of Alzheimer’s disease? According to researchers at Wake Forest School of Medicine, that is a possibility.

In a small study, researchers were able to identify several distinct gut microbiome signatures in study participants with mild cognitive impairment (MCI), but not in the other participants with normal cognition. Researchers found that these bacterial signatures correlated with higher levels of markers of Alzheimer’s disease in the cerebrospinal fluid of the participants with MCI. Additionally, through cross-group dietary intervention, the study also revealed that a modified Mediterranean-ketogenic diet resulted in changes in the gut microbiome and its metabolites that correlated with reduced levels of Alzheimer’s markers in the members of both study groups.

“The relationship of the gut microbiome and diet to neurodegenerative diseases has recently received considerable attention, and this study suggests that Alzheimer’s disease is associated with specific changes in gut bacteria and that a type of ketogenic Mediterranean diet can affect the microbiome in ways that could impact the development of dementia,” said Hariom Yadav, Ph.D., assistant professor of molecular medicine at Wake Forest School of Medicine.

The randomized, double-blind, single-site study involved 17 older adults, 11 diagnosed with MCI and six with normal cognition. These participants were randomly assigned to follow either the low-carbohydrate modified Mediterranean-ketogenic diet or a low-fat, higher carbohydrate diet for six weeks then, after a six week “washout” period, to switch to the other diet. Gut microbiome, fecal short chain fatty acids, and markers of Alzheimer’s in the cerebrospinal fluid were measured before and after each dieting period.

The limitations of the study included the subject’s group size, which also accountns for the lack of diversity in terms of gender, ethnicity, and age.

“Our findings provide important information that future interventional and clinical studies can be based on,” Yadav said. “Determining the specific role these gut microbiome signatures have in the progression of Alzheimer’s disease could lead to novel nutritional and therapeutic approaches that would be effective against the disease.”

Each human contains trillions of organisms that influence our metabolism, immune function, weight, and even cognitive health. It is so fascinating to examine the role of gut microbiomes in the progression of Alzheimer’s disease. I believe diets can be very controversial, and I find it interesting to see researchers in this study show how the Mediterranean-ketogenic diet may be effective against Alzheimer’s. However, I am so intrigued to see where these findings may take us with approaches that may be effective against Alzheimer’s, whether they be nutritional or therapeutic approaches.

Human Disruption: Main Cause of Climate Change

 

Live Science, in a recent article about climate change, claims that according to a report released by the Intergovernmental Panel on Climate Change, there are many significant impacts that have occurred on our precious planet. Marine life overheating as it grasps for oxygen in warming oceans, rising seas swallowing islands and coastal areas, storms growing and causing flooding, coral reefs dying, rare species going extinct, are just some of the events that have occurred due to climate change. These are now used as a wake up call, implying that there’s far worse to come if we do not control human-driven climate disruption. 

The Special Report on the Ocean and Cryosphere in a Changing Climate presents its latest evidence that climate change is already underway and we are “on thin ice and running out of time to act,” said Bruce Stein, chief scientist for the National Wildlife Federation (NWF).

One of the main causes of this climate change are fossil fuels. If the use of these fossil fuels isn’t reduced and if global warming continues, it could have a huge negative impact on both wildlife and humans. Researchers recently found more than 200 dead reindeer in Norway; they starved to death due to climate change, which disrupted their access to the plants they eat. After the precipitation froze, creating “tundra ice caps,” a thick layer of ice that prevented the reindeer from reaching vegetation in their usual winter grazing pastures. This forced them to dig pits in shoreline snow to find seaweed and kelp, which are less nutritious than the reindeer’s usual fare.

In addition, there are several other effects that human activity has had on the environment. According to the IPCC report, 50% of the coastal wetlands have been lost over the last 100 years due to the results of human pressures and extreme climate events. They predict that by 2100, seas could rise by more than three feet, which could result in the displacement of millions of people. They also predict that by 2050, marine heat waves will be 50 times more frequent and the uppermost ocean zones could lose more than 3% of their oxygen, eliminating populations of marine animals and harming fisheries. Glaciers could be reduced by as much as 36%, affecting about 4 million people who live in the Arctic and around 670 million people who inhabit mountainous regions. The widespread loss of ice and snow could lead to water shortages, affect food security, and cause intense droughts and wildfires. Evidence has also suggested that warming oceans have caused an increase in tropical hurricanes according to the report. 

The Earth’s fate lies in our hands.  Debra Roberts, co-chair of the IPCC, says that we can control global warming if we create advances to all aspects of our societies, such as energy, land and ecosystems, urban and infrastructure, and industry. Roberts also suggests we must as early and decisively to avoid permanent changes and risks, all in an effort to improve our lives and achieve sustainability around the world. It will require “unprecedented” political actions to eliminate all the impacts that human-made carbon has created on our oceans. The youth are our strongest supporters to prevent the most severe consequences to our planet. 

 

Does Exposure to Toxins In the Environment Affect One’s Offspring’s Immune System?

A study has recently surfaced stating that maternal exposure to industrial pollution may harm the immune system of one’s offspring and that this impairment is then passed from generation to generation, resulting in weak body defenses against viruses.

Paige Lawrence, Ph.D., with the University of Rochester Medical Center’s Department of Environmental Medicine, led the study and conducted research in mice, which have similar immune system functions as humans. Previously, studies have shown that exposure to toxins in the environment can have effects on the respiratory, reproductive, and nervous system function among generations; however, Lawrence’s research is the first study to declare that the immune system is also impacted.

“The old adage ‘you are what you eat’ is a touchstone for many aspects of human health,” said Lawrence. “But in terms of the body’s ability to fights off infections, this study suggests that, to a certain extent, you may also be what your great-grandmother ate.”

“When you are infected or receive a flu vaccine, the immune system ramps up production of specific kinds of white blood cells in response,” said Lawrence. “The larger the response, the larger the army of white blood cells, enhancing the ability of the body to successfully fight off an infection. Having a smaller size army — which we see across multiple generations of mice in this study — means that you’re at risk for not fighting the infection as effectively.”

In the study, researchers exposed pregnant mice to environmentally relevant levels of a chemical called dioxin, which is a common by-product of industrial production and wast incineration, and is also found in some consumer products. These chemicals eventually are consumed by humans as a result of them getting into the food system, mainly found in animal-based food products.

The scientists found the production and function of the mice’s white blood cells was impaired after being infected with the influenza A virus. Researchers observed the immune response in the offspring of the mice whose mothers were exposed to dioxin. Additionally, the immune response was also found in the following generations, as fas as the great-grandchildren (or great- grandmice). It was also found that this immune response was greater in female mice.  This discovery now allows researchers to have more information and evidence to be able to more accurately create a claim about this theory.

As a result of the study, researchers were able to state that the exposure to dioxin alters the transcription of genetic instructions. According to the researchers, the environmental exposure to pollutants does not trigger a genetic mutation. Instead, ones cellular machinery is changed and the immune response is passed down generation to generation. This discovery explains information that was originally unexplainable. It is obviously difficult to just avoid how much toxins you are exposed to in the environment, but it is definitely interesting to see the extent of the immune responses in subsequent generations. We can only hope that this new information, and further discoveries, help people adjust what they release into this world that results in these harmful toxins humans are exposed to, and their offsprings.

 

 

 

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