BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Disease (Page 1 of 2)

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

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

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

 

Coronavirus. SARS-CoV-2

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

 

The Revolutionary Way Of Detecting Diseases

How it works

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

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

How it connects to AP bio

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

Stromal lipofuscinosis of the seminal vesicle -- extremely low mag

What can this do for our future?

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

 

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

 

Racial Discrepancies in Kidney Disease: Why They Exist and How Researchers Are Addressing Them

Racial Discrepancies in Kidney Disease

“While Black people make up about 12% of the U.S. population, they comprise 35% of Americans with kidney failure.” (The New York Times) “They are 3 times as likely to have kidney failure compared to White Americans.” (Kidney.org)

What causes these statistics? According to the New York Times, it’s a mix of social, economic, and genetic factors. 

One gene variant, APOL1, is responsible for the genetic predisposition to kidney disease. Having two copies of this variant is prevalent in people of sub-Saharan descent, and it’s the main contributor to kidney disease. The variants make bodies resistant to efforts taken to moderate one’s blood pressure, a significant risk factor of kidney disease. 

Dr. Olabisi, a kidney specialist at Duke University, advises against attributing all racial disparities of kidney disease to genetics. To do so would be to ignore the drastic effects of social and economic inequalities that lead to these jarring statistics. 

Identifying the Gene Variant 

About a decade ago, Harvard researchers began looking for the cause of kidney disease. They found that the APOL1 gene, which normally destroys harmful protozoa, had variants that intensified the function of the gene, making it detrimental to the body. 

These variants evolved in people of Sub-Saharan descent because they originally protected against African sleeping sickness. There is another type of variant that averts malaria but can cause sickle cell disease. Similarly, the APOL1 variant protects against one disease, but possibly causes another. 

As we learned in class, sickle cell anemia is rooted in a difference of amino acids in the primary structure of the hemoglobin of red blood cells. In position 6 of the structure, there should be glutamic acid. However, there is valine, causing the protein to fold oddly in its tertiary structures. In its quaternary structure the cells don’t react with each other as they should. As a result, he cell creates a “sickle” shape, which cannot transfer oxygen through it as successfully as the round shape. 

Sickle Cell Disease (27249799083)

Researchers have delved into numerous hypotheses over the year. They considered using medications to block the gene’s variants from harming the body. To find out if APOL1 was required for the kidneys to function, they consulted an Indian farmer whose kidneys functioned properly even though he didn’t have the APOL1 gene. They created a drug, and while the the dose still has to be adjusted, it’s on its way to being successful. 

Semantics of Genetic Predispositions  

The topic of genetic predispositions raises concerns among academics about the rhetoric that we use to describe people who are affected by the APOL1 gene variants. 

Many people of different ethnicities and races have certain genetic predispositions to diseases. For example, Ashkenazi Jews have genetic predispositions to diseases such as Gaucher disease, which affects the spleen and liver, and African Americans people are more likely to have sickle cell disease.  

Professor of biological sciences at North Carolina Agricultural and Technical State University warns against harmful rhetoric when he says, “We don’t want to fall into the myth of the genetically sick African.” I agree with his statement

It is scientifically accurate that different ethnicities have genetic predispositions to certain diseases. However, acknowledging that can be a slippery slope, especially when you consider that the most commonly known genetic predispositions effects marginalized members of society. This rhetoric partially absolves societal leaders (scientists, public servants) of effecting change in implementing preventative measures, such as improving healthcare.  This rhetoric can easily slip into having Social Darwinist undertones that portray marginalized groups as genetically inferior. Do you think awareness of the language we use is important in academic spaces? Please answer in the comments if you have an opinion on this. 

Ongoing Research

On another note, two twin brothers’ experiences helped further researchers’ understanding of the variants. They were asked to be part of a study that tested an arthritic drug on Black Americans to see if it could cure kidney disease. They tested positive for the APOL1 variants, which came to explain one of their kidney failures. 

Researchers believe that the APOL1 variants are harmful when there are secondary factors involved, such as an antiviral response to lupus like interferon. 

Dr. Olabisi’s study is pending, but in the meantime, Vertex, a drug company, wants to conduct its own research. There’s only one problem: scientists haven’t agreed on how the variants cause kidney disease, so it is unclear what a new drug should obstruct. Vertex, though, has still had some success. 

They predicted that “the variants spurred APOL1 proteins to punch holes… in kidney cells” (The New York Times) 

After testing on animals that were given the APOL1 variants, they found a drug that worked by identifying that it eliminated 47.6% of protein in urine, which points to improved kidney function. This is a significant step the ongoing research of trying to determine how to treat kidney disease. 

In Dr. In Olabisi’s study, he plans to test 5,000 members of his community for kidney disease and the APOL1 variants, and then prescribe them with the drug used for arthritis. 

These scientists and doctors are optimistic about the future of their research, and therefore, the future of kidney disease treatment and prevention, especially as it pertains to those disproportionately affected.

Next Time You Think Losing An Hour Or Two Of Sleep Won’t Hurt… Think Again.

We’ve all been there. It’s a busy week, it’s getting late, and you’re tired, but you still have a lot to do for tomorrow.

A Cartoon Man Sleeping At Work

You convince yourself that if you sacrifice your sleep during the week and make it up on the weekend everything will be okay. Right? Well, unfortunately, according to the Mount Sinai School of Medicine, quite the opposite is true.

Research completed by Mount Sinai Hospital demonstrates that reducing the amount of sleep you get each night can lead to an increased risk of inflammatory disorders and heart disease. The researchers monitored 14 healthy adults that normally sleep 8 hours a night and had them sleep 6-7 hours for 6 weeks. They then drew and analyzed their blood, finding an increased number of immune cells, many of which did not function properly to protect against infections. An increased number of immune cells may seem beneficial, but in reality, if the number gets too high, immune cells can overreact and create inflammation. The DNA structure of the cells was also altered, which provides evidence for their decreased ability to defend against illnesses.

The researchers continued the study with testing on mice and found that even after having sleep recovery time, the mice still had changes in their immune system. The mice’s immune cells were rewired and reprogrammed to function under the stresses of having disrupted sleep, producing more white blood cells, which put the mice at a greater risk of having inflammation or a disease. These results serve as evidence to prove that sleep recovery cannot reverse the effects of lack of sleep.

Diagram of a white blood cell CRUK 028

The cells experience this change due to limited time to repair injured cells. As we sleep, our bodies turn their attention to our immune system, repair damaged cells, and release growth hormones. When we have disrupted or limited sleep, our bodies are not able to carry out these functions, causing greater susceptibility to health problems. It is important that our cells are able to complete their tasks, and it’s even more important that we can remove and replace cells that cannot. As we learned in AP Biology, the lysosome plays a major role in helping damaged cells perform apoptosis (programmed cell death). If our bodies are not given the time to carry out apoptosis and replace old damaged cells with new immune cells, our bodies are at greater risk for metabolic abnormalities and replication errors, connecting sleep deprivation to disease risk. So the next time you’re thinking of sacrificing sleep to do work, I hope you remember the health consequences and reconsider your decision 🙂

 

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. 

 

 

How To Map A Cell

In order to understand diseases on a cellular level, scientists must learn as much as they can about cells. One of the ways this is done, is through Nanomechanics. Through nanomechanics, scientists can measure many aspects of the cell. They can find the thickness, softness, viscoelasticity, and incompressibility, or how capable the cell is of being compressed. Living cells, specifically eukaryotic cells, are made of a plasma membrane with solids inside of it. The solids can range from proteins, to DNA, to organelles, to much more. As these solids move within a liquid type of mixture, they are considered viscoelastic. Through the use of Atomic Force Microscopy or AFM, a cell’s viscoelasticity can be mapped. Moreover, nanomechanics is able to find the rate at which a molecule spins by using Young’s modulus.

201710 SingleCell

Even further in the cell, scientists can now determine how the lipid bilayer of a cell change. Through AFM, the physical properties of the cell’s lipid bilayer have been seen to change due to the concentration of cholesterol. Low cholesterol regions had a more elastic lipid bilayer, while regions with less cholesterol were less elastic. Additionally, it was observed that during ionization, the elasticity of the lipid bilayer decreases as well.

Cell membrane detailed diagram blank

As scientists reveal more about the cell, they connect what they have learned to diseases. When a cell changes, or organelles it is composed of change, it can be a sign of disease. By looking into cells through ways such as optics-based non-invasive Brillouin microscopy, scientists can study the mechanical properties of cells and the smaller components that compose them. From using this type of technology, scientists have also learned that living eukaryotic cells are one of the softest materials on the planet. AFM uses the forces placed on the cell by the microscope to determine the properties of the cell.

Human eye detail, from- Human eye close up (cropped)

One specific use of nanomechanical mapping on cells is in microsurgeries conducted on the eye. Many ocular diseases are due to a change in the mechanical properties of the eye. Some diseases can be caused by macular holes or macular puckers. Through microsurgeries, the damage to the eye may be fixed. Scientists conducted measurements on cells on a nanometer scale in order to understand what microsurgeries are necessary to be performed. Moreover, nanomechanics allows scientists to understand how the proteins of the eyes work, and how mutations and other tissue can affect the eye. If specific mutations of causes of diseases can be found on a cellular or subcellular level, it would aid in the development of drugs that would be used against the diseases.

Dr Jessie Price: Her Impact on the World of Vaccines

Dr Jessie Price, a black female veterinary microbiologist who changed the veterinary field for the better.

Dr. Price’s Path to Success: Academic Life

Born January 1, 1930, Dr. Jessie Price lived in Montrose Pennsylvania with her mother Teresa. Teresa Price was a huge motivator for her daughter’s success and pushed her daughter to flourish academically. As an adolescent, Dr. Jessie Price attended surrounding public schools, all were predominantly white. During this time, it was typical for graduates to jump into a career to support their families, however Teresa Price valued academics greatly and supported her daughter’s notable academic talent. Dr. Price attended the College of Agriculture at Cornell University, where her tuition was covered by her resident status, as she spent a year in Ithaca taking more classes at a nearby high school after graduation. Her goal to attend medical school was not met due to financial costs, however, she found her passion in microbiology. In 1953 she earned her bachelors degree in microbiology, then returned to receive her masters degree in veterinary bacteriology, pathology, and parasitology in 1956. in 1959, the same year she received her masters degree, she earned her Ph.D after completing her dissertation, “Studies on Pasteurella anatipestifer Infection in white Pekin Ducklings” published by the Journal of Avian Diseases. Dr. Price’s research career officially began in 1959 as she worked at the Cornell University Duck Research Laboratory.

Her Research

While working as a research specialist at the Cornell University Duck Research Laboratory, Dr. Jessie Price “focused on the identification and controlling bacterial diseases in commercial white Pekin ducklings” (Quintard Taylor). All of her hard work and focus lead to her discovery of how to recreate the disease in these ducks and create a vaccine against it.

Pasteurella Anatipestifer and the Vaccine

At this time around “10%-30% of the duckling population was lost in the first 8 weeks of their lives due to disease” (poc2.co.uk), this meant an extreme loss of money in the poultry farming business. Dr. Jessie Price found Pasteurella anatipestifer in the ill ducks she researched which caused the life threatening respiratory issues in the animals. Other symptoms include tremors and discolored diarrhea. Pasteurella anatipestifer is a septicaemic disease, meaning a pre-existing bacterial infection enters the blood stream and is highly transmittable. Dr. Jessie Price began the process of research by obtaining fluid from the duck’s cranium. This fluid was then kept in a glass container and stored in order to be used as a study subject.  “Duck broth” is then stored and examined for experimental culture. This research led to the discovery of the Riemerella Anatipestifer vaccince, one of the many vaccines that derived from this research, which works to prevent R. anatipestifer infection at early stages in the ducks life (when they are most susceptible to infection).

Duck Color Colorful Water - Free photo on Pixabay

Ultimately Dr. Price’s research saved the poultry industry and the hundreds of thousands of dollars lost due to poultry death. She passed away in 2015 and Cornell University includes more information on the disease in the College of Veterinary Medicine.

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.

 

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.

Can you get a disease from being outside?

The Alzheimer’s diseases and several genetic defects have been identified to connect with early onset family genetics. In this study chemists, toxicologists, and biologists have researched the environmental effects connected with health issues. The researchers examined the point that the human race would have all gone extinct if our bodies didn’t have the ability to metabolize, absorb, or excrete trace substances. In 2005, there was a lot of talk about the “exposome” causing many diseases. This research topic is very  interesting because it explains that everything you are exposed to can cause cancer. The fact that our exposome is everything we contact in our lives is concerning. Average light, invisible car exhaust and ambient street noise are all linked to birth defects. And now Alzheimer’s has been statistically linked to the environment.

Although Alzheimer’s is generally linked with age, researchers also believe it is linked to living in cities and poorer neighborhoods. According to new research unveiled at a recent global gathering of Alzheimer’s experts in London, stressful life events, poverty and racial inequities contribute to dementia risk in late life. A Study at the University of Wisconsin looked at levels of socioeconomic disadvantages such as poverty, education, housing, and employment to determine whether there was a stronger link to developing Alzheimer’s than by chance alone. They found that people in poor neighborhoods had worse cognitive performances in all aspects, which is linked to the fact that they had disproportionately higher levels of the Alzheimers disease biomarker in their spinal fluid. This could be considered an example of the effects that their exposome pose on their health. For example, in poorer neighborhoods, they have less access to healthy foods, safe exercisee options and healthy environments. This unhealthy environment leads to increased risk of diabetes,  cancer, and early death.

Strong Genes Equal Strong Immune System

Although scientists have long agreed that antibodies are in integral part of building up the body’s immune system, there is new evidence that strongly suggests genetic factors play a large role in determining how well the immune system builds and uses these antibodies when fighting disease.

https://commons.wikimedia.org/wiki/File:Redhead_twins.jpg

In a recent study, “researchers from James Cook University’s Australian Institute of Tropical Health and Medicine (AITHM) and the University of Queensland’s (UQ) Diamantina Institute have analyzed blood samples from 1835 twins and thousands of their siblings.” The team looked at the body’s immune response to “six common human viruses, including the Human Herpes virus, Parvovirus, Epstein Barr virus and the Coxsackie virus.” The team determined that genes passed down by parents are the major factor in how powerfully an immune system responds to diseases. “These genes determine whether you mount an intense or weak immune response when confronted with a viral infection,” says Associate Professor Miles.

“Demonstrating that antibody response is heritable is the first step in the eventual identification of individual genes that affect antibody response.” The researchers’ next goal is to identify the superior genes in order to, “imitate ‘super defenders’,” and “design next generation vaccines.”

 

The Zombie Apocalypse is Coming! – Sort of…

Imagine a disease that, once it infects another organism, it completely takes control of their body and uses it for further infection and mutilation. This is exactly what is happening in the incredibly noisy (100 decibels to be exact) seasonal insects, named the periodical cicada (Magicicada sp.). However much you might like or absolutely hate these insects (like me), they unfortunately are suffering from a rampant parasitic fungus that is essentially taking control of these bugs and turning them into zombies. This zombie fungus is incredibly brutal to the cicadas, causing their almost-lifeless body to be driven around by this fungus, losing parts of their own body while gaining another cicadas head that becomes attached during forced copulation by the fungus to infect more cicadas. It is pretty much like “The Walking Dead” in the insect world, with cicadas being driven around by a parasite infecting others at a rapid speed with insect parts flying all over the place. 

This fungus, the Massospora cicadina, typically begins its infection on the insect when the cicada nymphs come to the surface after about 17 years of feeding off of plant roots underground. When the come up, about 3-5 percent of the cicadas are infected by spores, which are conidia or asexually reproducing cells, and multiply by the thousands within the bug while hoping to spread to more and more cicadas in the trees. This is known as the stage I infection. A stage II infection by this parasite consists of sexually produced spores whose goal is to end up in the soil and wait, withstanding all environments, until the next cicada arises. After the infection takes place of either type of spore, the cicada essentially falls apart as their abdomen enlarges with white-spores, losing their reproductive segments as well as several of their limbs. But the catch is that, of course, the cicada doesn’t realize and therefore it carries on with its barely lifeless self and performs the tasks of any normal cicada. Including more copulation.

Pictured here is a Cicada affected with this fungus, missing half of its abdomen.

Not only do the cicadas with stage I walk around constantly with their open wound and drag along spores while the cicadas with stage II fly around spreading spores from their abdomen, but this zombie parasite also tremendously manipulates the insects sexual behaviors. As stated in the original paper in Scientific Reports, “It is relatively common to find a healthy cicada with its genitalia plunged into the abdominal spore mass of an infected partner or to see healthy cicadas attached to fragments of abdomen or terminalia that have torn free from infected partners during attempted copulation.”. But that’s not all. These parasites also cause male cicadas to take up female mating behavior and flick their wings in response to other male cicadas. One thing leads to another, and now it has been concluded that this fungus is more present in male cicadas since these infected males are now more willing to mate with both female and male cicadas, spreading the infection to both. Although many scientists and researchers (including myself) thought that maybe this parasite simply caused a feminizing effect within the insects, this practice of male wing flicking only occurs in cicadas with a stage I infection. Therefore this disproves what was previously hypothesized, since if this feminizing effect was a case, it would occur in every infection, not just the first stage.

Either way, these spores have been researched to manipulate and control a cicada’s behavior, whether it be sexual or not. But, who knows what this parasite might mean for humans as we already know how brutal and sadistic it can be. Do you think that this topic should be more heavily researched for not only cicadas wellbeing but also ours?

But next time you see a cicada, be careful it doesn’t look to you to turn you into the next real life zombie!

To read more about this new parasite affecting cicadas in the original source, click here.

The Behavioral Causes of Obesity

Obesity is a big issue that is affecting the world today. Obesity is mostly caused by abnormal eating habits, which include overeating, but little is known about what causes overeating. To further understand the behaviors that lead to overeating and obesity, scientists from the Centre for Genomic Regulation and the Pompeu Fabra University in Barcelona, Spain conducted research on mice. There findings were published in Addiction Biology.

The scientists put the mice in an environment where they are only fed high calorie foods. Their diet consisted of chocolate bars and their normal food. As the mice started to gain more weight, they started to become addicted to chocolate and started binge-eating it. They would eat the chocolate over their normal food, even though they were more full from eating their own food. Their new binge eating habits also changed their eating schedule. They started eating during the day, rather than at night.

In conclusion, this research made scientists aware that some people can be trapped in a binge eating state which can lead to obesity. Obesity is not just a metabolic disease, but is caused by behavioral issues. This research is helpful because people can now take preventative measures and go to therapy to change these eating habits. This research is very interesting because it can help solve obesity issues. To learn more about obesity behaviors and treatment, click here and here. 

Striped Field Mouse

 

CRISPR/CAS9: Potential to destroy malaria?

CRISPR. Sounds more like a new brand of potato chip than something potentially revolutionary (Bold new flavor. Bold new crunch. CRISPR.). Nevertheless, this tool used for easy gene editing and slicing is tearing up the science world because it could be the key to combatting disorders and diseases.

Recent research indicates that CRISPR/Cas9 based genome editing tools could aid in the fight against malaria, one of the “big three” diseases that has long affected and continues to affect humans worldwide. How is CRISPR/Cas9 able to do this?

CRISPRs (Clustered Regularly Interspaced Short Palindromic Repeats) originally are how bacteria protect themselves from foreign viruses. CRISPRs contain DNA from viruses that have attacked the bacteria, and so when a similar virus attacks, the bacteria knows that this virus and his DNA are bad. Essentially, CRISPRs allow bacteria to build up immunity. When foreign DNA is detected, the Cas9 enzyme is guided by the CRISPR and is able to cut the desired DNA. Scientists have come up with a way to engineer and manipulate the CRISP/CAS9 system into other organisms (such as mosquitoes) so that we can successfully edit genome sequences and genes to produce desired results. We take advantage by specifying which genes the Cas9 should cut/replace, and then it does just that. Therefore, the CRISPR/Cas9 system allows us new genome editing potential like none before.

Made by Viktoria Anselm.

How does this apply to mosquitoes and malaria? Scientists experimented with genetically modified malaria-transmitting mosquitoes (Anopheles gambiae), altering the fibrinogen-related protein 1 (FREP1) gene on them. This gene essentially codes for a protein that makes mosquitoes a vector for malaria. The scientists used the CRISPR/Cas9 to inactivate this gene.

The results produced mosquitoes with significantly less transmission of malaria to both human and rodent cells. However, these mosquitoes have “reduced fitness”: a significantly lower blood-feeding propensity, egg hatching rate, a retarded larval development, and reduced longevity after a blood meal. Essentially this means that these mosquitoes have a low chance of affecting populations of mosquitoes in the wild without being “pushed” by scientists, where scientists are “forcing DNA to inherit particular sets of genes.” This is called a gene drive. With a strong push for a couple of years, there is potential for worldwide mosquito populations to be significantly changed in 10-15 years.

Photo taken by JJ Harrison

I chose to write about this new research and potential breakthrough because it really means something to me, as I have lived in and visited countries threatened by malaria. I had to take preventative pills every morning, and I would have to sleep in a restrictive mosquito net. All that made me wonder about and feel for a kid in the same country who didn’t have those things and how he or she would manage without those barriers to malaria. Having said that, I really do believe this is a worthwhile option we should explore, and I think it can make a difference for the world.

What do you think? Do you think it is realistic for theses mosquitoes to change the entire mosquito population and effectively help reduce malaria transmission? Will CRISPR/Cas9 work as we hoped? Or is it too good to be true?

CRISPR/Cas9 Provides Promising Treatment for Duchenne Muscular Dystrophy

There are nine kinds of muscular dystrophy and of these, Duchenne MD is the most common severe form of childhood MD. It affects about 1 in 5000 newborn males, only in very rare cases has it affected females. DMD is a genetic disorder that causes progressive muscle degeneration and weakness. Patients usually die by age 30 to 40.

DMD is caused by the absence of a protein, dystrophin, that helps keep muscle cells intact. In 1986 it was discovered that there was a gene on the X chromosome that, when mutated, lead to DMD. Later, researchers discovered that the protein associated with this gene was dystrophin. From this information, we can tell that this disorder is sex-linked, which explains why women are mainly carriers.

No one has found an absolute cure for this genetic disorder until now. Even in recent years, people have discovered treatments that will make patients’ lives more bearable, but never reverse the disorder. As a result of these advances, mostly in cardiac and respiratory care, patients are able to live past teen year and as long as in to their fifties, though this is rare. Although there are still drugs being tested like Vamorolone (a “dissociative steroid,” is an anti-inflammatory compound), more treatments on the molecular level are now being considered. However, thanks to recent discoveries and research with the new genetic technology, CRISPR/ Cas9, scientists may have found a treatment for DMD.

This new approach to gene correction by genome editing has shown promise in studies recently. This particular correction can be achieved in a couple ways: one is by skipping exon 51 of the DMD gene using eterplirsen (a morpholino-based oligonucleotide). Studies over four years show prolonged movement abilities, and a change in the rate of decline compared to controls. The newest approach to gene correction using CRISPR/Cas9, which the article I’m writing about focuses on, was performed in this study as next described: the CRISPR/Cas9 system targets the point mutation in exon 23 of the mdx mouse that creates a premature stop codon and serves as a representative model of DMD. Multiple studies in three separate laboratories have provided a path and laid the groundwork for clinical translation addressing many of the critical questions that have been raised regarding this system. The labs also discovered by further demonstrations, that this is a feasible treatment for humans. Functional recovery was demonstrated in the mice, including grip strength, and improved force generation- all of which are very important and hopeful discoveries. It is estimated from these studies that this new method will pass clinical trials and go on to benefit as many as 80% of DMD sufferers. Even greater success rates are expected if this is performed in young and newborn DMD patients.

Junk Food Encourages Disease

According to a recent discovery posted in Science News, a typical American diet, consisting of poorly nutritional foods, leaves one prone to getting sick by weakening their immune system. Interestingly enough, this issue is rooted in cells that are not your own. In your gut microbiome, there are countless varieties and numbers of bacteria, all working away at the food that passes through your gut. Now, these bacteria are actually quite manipulative, and besides from feeding off of the food that you eat, teach your immune system what to attack, like an instructor or tutor for your immune system, albeit a biased one. These bacteria have colonized your body. They’re not just going to let some pathogen get in the way of their free meal ticket.

(What it looks like in there)

What happens when you eat certain foods, like junk foods, is that your gut microbiome changes. Different bacteria thrive on the fatty or sugary foods while other bacteria that survive off of more complex starches and carbs fade away, changing the demographic of your gut microbiome. This limited variety also limits the amount of invaders your immune system knows as hostile, or understands how to deal with, and therefore, you are more susceptible to disease, or medical complications.

(Actual photo of a biofilm found in the gut)

This was proven by taking samples from fit and obese humans and inserting them in otherwise sterile mice. Their resulting microbiomes grew, and the mice with the obese implant suffered more medical problems than the mice with the fit implant. This is because there were not enough “trainer” bacteria in the first mice’s gut to help train it to fend off disease, and thus it got sick more easily. So don’t go blaming your immune system the next time you get sick. It may be your fault for avoiding real, nutritional food (not just salad), and not taking care of it.

The moral of the story is to eat your vegetables and serve the bacterial overlords that have taken host in your body.

They’re good for you.

Trust me.

 

The Buzzing Battle of the Bees

Bee

http://commons.wikimedia.org/wiki/File:Bees_on_sunflower.JPG

 

There is a species of bees called “commercial” bees. These bees are kept by beekeepers to pollinate crops such as tomatoes, sweet peppers, and oilseed. This population of managed bees is coming down with “fast evolving viruses”, according to the University of Exeter in Science Daily News.

Then there are “wild” bees, free to fly around, not employed by beekeepers. The viruses that the commercial bees have are starting to spread to the wild bee population. Currently, researchers are “calling for new measures” to protect the wild pollinators, and confine the commercial, diseased population. In the article, Dr. Lena Wilfert said this can be controlled by beekeepers keeping a vigil eye and monitoring the commercial bees they own. It is their “responsibility” to do so. Also, interesingly enough, the international transport of these commercial bees must have more checks and security. They must be screened better, in order to get a better sense of how many have a disease, so they know not to set any of the commercial bees free into the wild.

The major cause of the spread is the Varroa mite. This spreads viruses, such as the Deformed Wing Virus, and may increase the power of the viral spread. It significantly weakens bees, causing their RNA to deteriorate. The article says that it has been “identified as an emerging disease in pollinators,” and there is a connection between wild bumblebees who have it, and commercial honeybees.

The poor management of the commercial bee community is the cause of this horrible break out of diseases among innocent wild bees. In the future, researchers plan to investigate which species of commercial bees are the major cause of the breakout and spread. The wild bee population is extremely important for our environment, and beekeepers need to realize that, and make sure their bee farm does not spread disastrous diseases.

 

*Additional information is found through the last two hyperlinks.*

*Original article is the first hyperlink.*

White-Nose Syndrome Threatening Brown Bat Species

In 2006, hibernating bats in upstate New York were identified with white-nose syndrome , a disease that produces a white fungal growth around the wings, mouth and nose of bats. The disease is a huge problem for North American bats, with it killing at least 6 million brown bats and the disease now spreading from New York to Mississippi and Canada. The disease may even threaten the entire bat species and disrupt the ecosystem. Scientific researchers have been studying WNS for over a decade and only recently have they developed a reason for its lethal effect on the North American bat population.

Researchers from the US Geological Survey and the University of Wisconsin learned that the fungus Pseudogymnoascus destructans kills brown bats by “increasing the amount of energy they use during hibernation”. When bats are hibernating during the winter, they must carefully save up their energy to survive without eating until the winter ends. The fungus drains bats of their energy and forces them to wake early and either starve or freeze to death. The study done by USGS measured how much fat was burned and at what rate during hibernation between non-infected and infected bats. Dr. Michelle Verant, a USGS National Wildlife Health Center scientist, found that bats infected with WNS used twice as much energy as the healthy bats during hibernation and had “potentially life-threatening physiologic imbalances that could inhibit normal body functions”.

The immune system of bats is very tolerant of pathogens and diseases that can be lethal to humans, like ebola and even some cancer cells. Bats are immune to many viruses and rarely show signs of disease so the visible white growth on the bats poses a huge threat to the ecosystem. Dr. David Blehert worked with Dr. Verant at the USGS National Wildlife Health Center and the WNS is scary because “here we have an animal that can survive some of the scariest viruses we know, and it’s undone by a common soil fungus.”

Brown Long-eared Bat

Brown Long-eared Bat

 

Main Article:

http://www.science20.com/news_articles/winter_hibernation_energy_drain_how_whitenose_syndrome_kills_bats-151997

Other Articles of Interest:

http://www.eurekalert.org/pub_releases/2015-01/usgs-hdw010215.php

http://www.nytimes.com/2015/01/13/science/no-time-for-bats-to-rest-easy.html?ref=science&_r=0

http://www.biomedcentral.com/1472-6793/14/10

http://en.wikipedia.org/wiki/White_nose_syndrome

 

Depression Infection?

Melancholy_2

 

Major Depression Disorder (MDD), most commonly known as “Depression”, is typically thought of as a genetic or neurological disease. However, Dr. Tuhran Canli, Associate Professor of Psychology and Radiology at Stony Brook University, suggests that MDD be recategorized as a result of a parasitic, bacterial, or viral infection. Canli’s paper, Biology of Mood & Anxiety Disorders, argues how possible pathways from these infections could cause MDD.

The causes of MDD are still unclear, therefore the research is delving more into the causes over the treatments. Dr. Canli suggests that by redefining MDD as an infectious disease, it will push future researchers to focus their attention on parasites, bacteria, or viruses.

Canli’s three major arguments for this change of MDD’s etiology are as follows:

1. MDD patients have a loss of energy, typically found in an illness. Also, the “inflammatory biomarkers in MDD suggest an illness-related origin”.

2. Parasitic, bacterial, and viral infections alter emotional behavior in humans.

3. The body is an ecosystem, made for microorganisms and genetics. These infections alter that ecosystem.

The redefinition of the causes of MDD could have significant help in finding the cause and eventual better treatment of the disease. Has depression been an infection all along?

 

Original article: http://www.sciencedaily.com/releases/2014/11/141114124307.htm

Picture: http://commons.wikimedia.org/wiki/File:Melancholy_2.PNG

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