BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Disease

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

Artificial Sweeteners: Safe or Sweet Misery?

Picture of Splenda

Picture of Splenda

Have you ever drunk a zero-calorie soda or eaten a sugar free dessert as a “healthier” choice or perhaps to even “cut calories”? If you’re like me, you have probably begrudgingly done this numerous times, maybe even at the request of your mom, despite your desire for that sweet snack. Well, new research has been conducted that suggests that the artificial sweeteners used to substitute sugar actually increase blood sugar levels-the exact condition they aim to avoid.

A study conducted by biologists, Segal and Elinav, of the Weizmann Institute of Science in Israel, showed that after 11 weeks of drinking water with the sweetener Saccharin, commonly found in Sweet’N Low, mice had higher glucose levels in their bloodstream, a symptom of diabetes. Additionally, the scientists conducted another experiment with seven volunteers who were given the maximum approved daily dose of saccharin for a week. This time Segal and Elinav found that four out of the seven subjects developed an unbalanced glucose metabolism similar to that of the mice. From this experiment, the scientists hypothesized that artificial sweeteners negatively affect our bodies and may promote disease.

Although these results are preliminary and are largely reflective of mice’s digestive systems rather than humans, the study raises a valuable caution for consumers to reassess their actions. As the science community continues to explore this study, are you going to continue consuming foods with artificial sweeteners.

For more information about the dangers of artificial sweeteners, please check out: http://well.blogs.nytimes.com/2014/09/17/artificial-sweeteners-may-disrupt-bodys-blood-sugar-controls/?_php=true&_type=blogs&_r=0

Dying Brain cells signal new brain cells to grow in songbird

BIRD

 

Original article: http://www.sciencedaily.com/releases/2014/09/140923182051.htm

In a recent paper written by leading author Tracy Larson and co-authors Nivretta Thatra and Brian Lee, they discovered a brain pathway that replaces brain cells lost naturally. This study could further the progress of using replacement cells for the neurons lost during aging, Alzheimer’s Disease, and other natural causes.

These scientists used songbirds, specifically Gambel’s white-crowned sparrows, as a model and observed that the area of their brain that controls song increases during breeding season, and decreases during other times in the year. After breeding season the cells in the area of the bird’s brain that controls songs undergoes programmed cell death. What is noteworthy about these dying cells is that they are also releasing a signal that reaches certain stem cells in the brain that will eventually redevelop the singing part of the brain by the time the next breeding season arrives. This process of developing new neurons from stem cells called neurogenesis normally occurs in the form of “regenerative” neurogenesis post brain trauma in mammals; however, it also occurs in the hippocampus in small amounts.

These songbirds could provide insight on how the human brain can perform natural neurogenesis and help replace neurons lost because of aging and neurodegenerative diseases. These finding may pave the way to alternative treatment for repairing human brains using neurogenesis and replacement cells.

The Ebola Epidemic: When Will it End?

Ebola Virus

The Ebola epidemic in West Africa has captivated international audiences the last few weeks.  Ebola Virus Disease is an often fatal disease which is systemic meaning it attacks all organs and tissue in the body. It can be spread through any human to human contact, making this disease highly contagious. The countries of Liberia, Sierra Leone and Guinea have been heavily affected by this disease. On tuesday September 23th the Center for Disease Control (CDC) based in Atlanta Georgia released new projections on the Ebola epidemic in Africa based on computer modeling.  The CDC released a best-case scenario being that if proper measures are taken the disease could be eradicated by January 2nd and a worse-case scenario that if disease is left unmonitored and continues as is, there will be approximately 1.4 million cases by January 2nd.   Doctor Thomas R. Frieden, the director of the Ebola epidemic, has stated that since the data was received in August conditions have improved slightly due to increased aid to the affected regions. Another report was released by the World Health Organization (WHO) which stated more conservative figures but also acknowledged that there could possibly be more due to unreported cases. The WHO report brings about the idea that the epidemic may not end and the Ebola virus will perpetuate in West Africa. It is obvious to health officials, such as Dr. Jack Chow, that even in a medium case scenario the amount of hospital beds and aid are rapidly being surpassed by the number of cases. The CDC does acknowledge this impending lack of bed and isolation unit crisis. One solution to this problem is to educate citizens on home care and send home care packages to support this movement.  Although some are dubious, Frieden states that home care had been effective in the smallpox crisis in the 1960s in Africa.  In addition to homecare, Doctor D. A. Henderson explains that funds and food play a huge roll in the containment and elimination of disease because when you give victims money and food there is no need for them to beg or go out to the market for food where they might encounter other human contact. How should this epidemic be handled? Is homecare an effective solution? Where should money be allocated, homecare or hospital expansion?

 

Link to Article:

http://www.nytimes.com/2014/09/24/health/ebola-cases-could-reach-14-million-in-4-months-cdc-estimates.html?ref=health&_r=1

 

Save the Devils

When most people hear the name Tasmanian Devil, they think of the small and ferocious little animal from the Looney Tunes named Taz. Just like in the show, Tasmanian Devils (carniverous marsupials)  are tough, rugged and very aggressive animals. Unfortunately, over the past two decades, a rare case of contagious facial cancer, with a 100% mortality rate, has decimated the population. Scientists have estimated that this specific cancer has wiped out about 85% of the entire population, almost to the point of extinction. The cancer is typically spread when the Devils bite each other in the face during battle, killing it in a matter of months. Scientists are working tirelessly to find out how this cancer is slipping by the immune system and hope to find a cure.

Until recently, scientists believed that the cancer was able to develop, without

being detected by the immune system, because Tasmanian Devils lack genetic diversity. However, a study led by the University of Cambridge claims it is much more complex. On the surface of most cells are histocompatability complex (MCH) molecules, which determine whether other cells are good or bad. If the cell happens to be a threat, then the cell triggers an immune response. According to the research, these DFTD cancer cells lack theses complexes and can therefor avoid detection.

Researchers also found that the DFTD cells have just lost the expression of MCH molecules and that its genetic code is still in tact (it can be turned on). By introducing specific signaling molecules, scientists believe they can force the DFTD cells to express these molecules, leading to the detection of the cancer. Not only will this research help save the Devils, but it will also give scientists a head start on contagious cancers in other species when the time comes.

Trial for New ALS Treatment Failed

Photo by: Nemo

Biogen Idec, a drug developing company, has recently discontinued their work on a new drug that was, hopefully, going to help patients with Amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s disease. A recent article explained that a new drug, known as dexpramipexole, was not effective in the phase 3 trial of the study.

Amyotrophic lateral sclerosis (ALS) is a disease where nerve cells “waste away and die.” These cells are unable to send messages to muscles, therefore symptoms include paralysis and muscle weakness. The progression of the disease is slow and “once the patient loses the function of muscles in the chest area, it becomes hard to breathe.” There is no known cure for this disease but scientists are looking for ways to prolong the disease.

Biogen Idec believed that the drug, dexpramipexole, was hopefully going to “slow the progression of loss of muscle function and prolong the lives of people with the disease.” While the phase 3 trial was not successful, the phase 2 trial of patients receiving dexpramipexole showed some success. 50% of the patients, in the second trial, showed a slower decline of muscular function. This was a big accomplishment for Biogen Idec but the phase 3 was not as effective. Therefore, Biogen Idec’s study involving a new treatment for ALS ended.

Even though Biogen Idec’s study was not effective, other companies have successfully found a way to slow the progression of ALS. Thus far, only one drug has been approved to help patients with ALS. This drug is known as Rilutek/Riluzole and it is only modestly effective.

Doctors are in need of a new drug that will help patients with ALS. I think its great that companies like Biogen Idec are involved in finding a way to treat this rare disease. I hope that researchers will use the information from the failed trial to find another way to treat ALS.

Genome Project Helps Connect Ethnicity to Diseases

Though people from all over the globe share over 99% of the same DNA, there are subtle differences that make us all individuals

Scientists at the Washington University School of Medicine in St. Louis have started the “1,000 Genomes Project” in which they will decode the genomes of 1,000 people from all over the world in hopes of finding genetic roots of both rare and common diseases worldwide. On October 31st, the results of DNA variations on people from 14 different ethnic groups were published, but the scientists hope for the project to expand to involve 2,500 people from 26 different world populations. According to Doctor Elaine Mardis, co-director of the Genome Institution at Washington University, “[scientists] estimate that each person carries up to several hundred rare DNA variants that could potentially contribute to disease. Now, scientists can investigate how detrimental particular rare variants are in different ethnic groups.”

 

We are One

Everyone on earth share 99% of the same DNA. That means you, your best friend, your mortal enemy, your boyfriend/girlfriend, next door neighbor, and The President of the United States all share 99% of your DNA. However, there are rare variants that occur with a frequency of less than 1% in a population that are thought to contribute to both rare diseases and common conditions (i.e cancer, diabetes). The rare variants explain why some medications do not effect certain people or cause nasty side effects (i.e insomnia, vomiting, and even death).

 

The goal of the “1,000 Genomes Project” is to identify rare variants across different populations. In the pilot phase of the program, researchers found that most rare variants different from one population to another, and the current study supports this theory.

 

The Study

Researches tested genomes from populations from the Han Chinese in Beijing (and the Southern Han Chinese in China) to Utah Residents with ancestry from Europe to the Toscani people of Italy to the Colombians in Columbia. Participants submitted an anonymous DNA sample and agreed to have their genetic material on an online database. Researchers than sequenced the entire genome of each individual in the study five times. However, decoding the entire genome only detects common DNA changes. In order to find the rare variants, researchers sequences small portions of the genomes about 80 times to look for single letter changes in the DNA called Single Nucleotide Polymorphisms, or SNPs.

 

The Results and Importance

The Study concluded that rare variants vary from one population to another. Researchers found a total of 38 million SNPs, including 99% of the rare variants in the participants’ DNA. In addition, researchers found 1.4 million small sections of insertions or deletions and 14,000 large sections of DNA deletion. The “1,000 Genomes Project” is incredibly important in medical science. It now allows researchers to study diseases, such as cancer, in specific ethnic groups. I personally think this project in incredibly important. As an Ashkenazi Jew from Eastern Europe, my family has a medical history of certain cancers and diseases. With the results of the “1,000 Genome Project,” researches could potentially find out why, and maybe even find a cure for some of these diseases.

Wait, you don’t hear that ringing, too?

Defined as “the perception of sound in one or both ears or in the head when no external sound is present” by the American Tinnitus Foundation, tinnitus affects 50 million people in the US and forty percent of veterans.  It can be caused by everything physical trauma or long-term exposure to loud noises (i.e. combat veterans or teenagers with iPods) to hormonal imbalance or aspirin use. Currently, there are many treatments available, although the success rate of these treatments varies. The main reason for this is that the best way of treating tinnitus would involve delivering medication to the inner ear, the site of the problem. Currently, doctors have no way of putting medication in the inner ear, but this could change  in a few years thanks to the the beginning of a new project by the US Department of Defense, who has commissioned Draper Laboratory to work out a

concept for a small delivery device inserted near the membrane-covered window—no more than three millimeters in diameter—separating the middle ear from inner ear. Once at the membrane the device … would release a drug into the cochlea… The plan is to embed wireless communications into the capsule so that a patient or doctor can control the dosage. After the capsule finishes delivering its supply of drugs, it would dissolve. 

 

Courtesy of: http://www.lesliewong.us/blog/2009/01/23/sony-mdr-v6-and-sennheiser-cx300-headphones/
These may be setting up my generation for a tinnitus epidemic many years from now.

 

The project is only in its beginning stages, so it will be years before patients can actually reap any benefits from this technology. However, I take comfort in knowing that should I develop tinnitus, I could possibly have access to better treatment than is available today. This is especially relevant to my generation; everywhere you look, there are teenagers blasting their iPods, unknowingly (or not caring) causing permanent damage. Despite the warnings received from adult, many teens will not listen, and will continue to cause damage with loud noise. Should this treatment be developed, the tinnitus that will be inevitable developed by a large portion of my generation will treated, and possibly cured.

This project also holds a personal significance for me.  As someone who wants to eventually enter the armed forces, I am relieved to know that such a common issue among veterans is coming a step closer to being eradicated. Despite the technology used today to prevent noise damage,  I know of Iraq and Afghanistan war veterans who are experiencing tinnitus, and even hearing loss. I’m glad that research is being conducted on a condition that, while it may not sound terribly crippling, can actually have a huge effect on one’s quality of life.

So, readers, do any of you have or know someone with tinnitus  If so, how did you or the person you know develop it? And, if you have it, would you consider one day utilizing this kind of treatment?

Post, discuss, talk with your friends. Discussion breeds awareness, which is key to arriving at a cure. 

 

 

http://www.scientificamerican.com/article.cfm?id=tinnitus-treatment

New Deadly Virus Discoved in Africa

Recently an article was released summarizing the discovery of a new disease in Africa. In 2009 a fifteen year old boy in a small village in the Democratic Republic of the Congo fell ill. The initial symptoms were malaise and a bloody nose, but quickly the boy developed an acute hemorrhagic fever. Within two days of the showing symptoms the boy died. Approximately eleven days later a thirteen year old girl who went to the same school as Patient One developed similar symptoms, and died three days later. At the local health center which both Patients One and Two visited, a thirty-two year old male nurse began to experience identical symptoms. He was moved to the hospital in Boma, Democratic Republic of the Congo, where the doctors drew blood and began to test for known viruses; they found nothing. However, very recently a research team used deep sequencing to determine the pathogen,which they dubbed “Bas-Congo Virus”, and posted their results in the Public Library of Science Journal. It was discovered that the virus belonged to the Rhabdoviridae family, best known for the Rabies virus. Interestingly enough, though, the Bas-Congo virus only shares 34% of the amino acids found in other Rhabdoviruses, meaning that it is very different. The discovery of this virus may end up being of great importance due to the possibility that the virus may return. In any case, we will have one less pathogen on this planet to identity lest there be another, more deadly, outbreak.

Vitamin D is linked to depression, so start sunbathing!

Haven’t been in the sun too much this winter season and feeling depressed? Well, it may be due to the fact that low levels of vitamin D are now linked to depression. According to a recent article, low vitamin D levels are already linked to cardiovascular diseases and various neurological problems. However, a new study links the connection between low vitamin D levels and depression. At the UT Southwestern Medical Center, researchers examined 12,600 subjects from 2006 to 2012. Results showed that subjects with higher vitamin D levels, who had a previous history of depression, had a larger decreased risk of depression at the time. Participants with low levels of vitamin D were shown to have signs of depression. Although the study the relationship of vitamin D and depression, the study did not show if increasing vitamin D in your diet actually reduced those depressive-like symptoms. Also, scientists have not confirmed whether or not low vitamin D causes depression like symptoms or if depression is causing low vitamin D levels. One could say low vitamin D levels are linked to depression however, adding vitamin D to your diet would not necessarily cure depression-like symptoms.

Many concepts around the idea of vitamin D being linked to depression are still unknown, but I think it is still a very important topic to discuss and important further research the subject.  The psychiatrists the UT Southwestern Medical Center have reported that major depressive disorder affects one in ten adults in the United States. One-tenth of our adult population has depression. When you put it into perspective, that is one person in a room of ten people. If that is the case,  then for me this is a field where the link between vitamin D and depression needs to be further researched. For now, it won’t hurt some sunshine to get your daily dosage of vitamin D.

 

Human Health in the Hands of a Naked Mole Rat?

Our genome is similar to that?!

         What do you think of when you see a naked mole rat? Do you think it is hideous because it has no fur? Do you think you would want to pet it? Whatever you think about this animal, you would never expect that it could improve human health. Who knew they could be the key to increase the human life span? Yep, that’s right! Naked mole rats, as ugly as they may be, are now considered extremely helpful and important in designing treatments for fatal diseases.

            A recent study discovered that the newly deciphered genome of the naked mole rat could help researchers learn more about evolution and even help design better treatments for diseases like cancer and stroke. Scientists believe that this genome will help decipher the naked mole rat’s unique traits, behaviors and social characteristics.

            Scientists who deciphered the naked mole rat’s genome used shotgun sequencing to read it. The naked mole rat was raised in a lab and once it was an adult, the scientists studied its genome. They read long sequences of the nucleobases that make up the rat’s DNA and then lined them up to find where they overlapped. Once they read the complete genome, the researchers compared it to the genomes of humans and mice.

            The researchers found multiple mutations in the naked mole rat’s genes that correlate to its characteristics. They found that the rat had turned off several genes related to vision because they live in the dark. They also saw a mutation in the gene that functions in hairlessness, which explains why these rats are bald. Naked mole rats live in low-oxygen burrows and stroke and heart attack deprive parts of the body from oxygen. By comparing the genome of the naked mole rat to the human genome and discovering how they survive in this type of low-oxygen environment, scientists can design more effective treatments to improve diseases that deprive the body of oxygen. The researchers sequenced the whole genome and will make it available free online, so groups that study genes involved in cancer and longevity can compare those genes to the mole rat’s genome. You can even look it up online and determine for yourself which genes you think are similar to ours!

            This new information about the naked mole rat’s genome can be extremely helpful for treatments that could increase the human life span and improve human health. Who knows, maybe the deciphering of the genome could even lead to find the fountain of youth! What do you think? Do you think the rat’s genome is similar enough to ours that scientists can design more effective medication for diseases? How far do you think these researchers are able to go? If you are unsure, just be sure of one thing, the next time you see a naked mole rat, be sure you look at it with a different perspective because in twenty years that very rat’s genome may lead to the cure for cancer!

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