Will dogs save us from allergies?

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Picture from: Rennett Stowe

Dog is man’s best friend. Man is dog’s…predictor for allergies?

A recent study showed dogs with owners that suffer from allergies are more likely to suffer from allergies themselves. Researchers also found that dogs that live in urban environments are more likely to have allergies than dogs in rural environments. The same correlation between urban environments and allergies is found in humans. Humans in rural environments come in contact with more species of microbes than their urban counterparts. It is thought that contact with many microbes early in life may protect humans from developing allergies. The same phenomenon is thought to occur in dogs. It appears man and man’s best friend have more in common than originally thought.

Allergies in humans and dogs have been on the rise in the western world. There have been many studies to look at the causes of these allergies in humans, but few have looked into the causes in dogs. Researchers at the University of Helsinki in Finland wanted to change this. We already know that humans who live in urban environments are more likely to have allergies than human who live in rural environments. Hakanen and colleagues wanted to know if the same is true in dogs.

Researchers sent surveys to almost 6000 dog-owners in Finland. The survey asked questions about the dog’s breed, the dog’s current environment (urban v. rural), the dog’s environment at birth, the dog’s allergies, and the owner’s allergies. When analyzing the data, they removed dog breeds known to be genetically prone to allergies, so they could focus on environmental factors. After compiling the data, Hakanen et. al. concluded that dogs who live in urban environments are more likely to have allergies than their rural counterparts. It is important to note, the data are influenced by how much time the dog spends outside and how much contact the dog has with farm animals. Strangely, living in larger human families can also protect dogs from developing allergies. This suggests that we might protect our dogs from allergies; similar to the way they protect us from developing allergies.

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Allergy symptoms in dogs can include itchiness, sneezing, hives, constant licking, itchy ears, and itchy, runny eyes. Picture from: Dani

Researchers cannot be certain the cause for differences in allergies between urban dogs and rural dogs and dogs in smaller vs. larger families, but they do have some theories. In humans, the microbiota, or the microbes that live in our bodies and do not cause illness, are an important factor in allergy development. It is thought that humans who grow up in rural areas come in contact with and are colonized with environmental microbes that protect people from allergies. The microbiota is also thought to be important for development of allergies in dogs. Dogs living in rural environments may come into contact with more environmental microbes that protect them from allergies. Furthermore, dogs in larger families likely come into contact with more species of microbes because each family member harbors a unique microbiota.

Though many of the study’s findings are similar between dogs and humans, one difference between human and dog allergies seems to be the impact of birthplace. A dog’s birthplace is not a predictor for allergies in dogs like it is in humans. Researchers think a dog’s birthplace may be less important because dogs are usually removed from their birth environment fairly early (7-8 weeks), when compared to humans (18yrs).

Hakanen and colleagues were able to identify multiple environmental factors important for predicting if a dog will develop allergies. However, the most striking finding of the study was actually in the dog owners. Dogs with owners that have allergies are more likely to have allergies. Though this is not a new finding, it suggests that the factors important to developing allergies in humans and dogs may be the same. The idea that the same factors could influence allergy development in both dogs and humans is particularly intriguing considering dogs suffer mostly skin and food allergies and few respiratory symptoms. Respiratory symptoms from pollen allergies are among the most common in humans. Furthermore, the immune responses that cause allergic symptoms in dogs and humans are different. This suggests the factors influencing allergy development may be important for all mammals despite differences in their immune systems.

There is still more research to be done to determine the factors that lead to allergies in dogs and humans. However, the studies of Hakanen et. al. and others suggest that if we can determine the factors important for developing allergies in dogs, for which it is easier to gather environmental and health information, we may be able to apply these findings to humans. So in addition to being the best listeners, best cuddlers, and our best friends, dogs may just be our best chance to cure our allergies.

Peer edited by Christina Parker

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Getting to the Heart of the Matter: “Fish are friends, not food”

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Repeat after me: “Fish are friends, not food”

When most people think about “Finding Nemo,” they likely think about Nemo, the adventurous young clownfish who got caught up in a fishy situation (no pun intended) and ended up in a dentist’s fish tank. Or, they might remember Marlin, the overprotective father. However, what about Dory? Though some might characterize Dory as loopy, she was the real hero who saved Marlin and Nemo’s lives and reunited father and son. Who would have thought that the loopy blue tang fish would be the unsung hero?

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Zebrafish (Danio rerio), possibly the key to treat/cure heart disease

Just like Nemo, humans have their own fish hero too: the zebrafish. The zebrafish is a tropical freshwater fish that is currently used in many research labs as a powerful model organism for studying various diseases such as heart disease, cancer, diabetes, and gastrointestinal disease. You might be thinking that there is no way a 3-5 cm fish, with fins and no lungs, can model human disease; humans are extremely different from zebrafish. However, zebrafish are much more similar to people than one might initially think. In fact, according to a paper published in Nature, 84% of genes known to be associated with human disease have a zebrafish counterpart. You might also be wondering why not use mice? After all, they’re at least mammals. Good question!

Zebrafish models actually have many advantages over mouse or rat models:

  1. Zebrafish reproduce more frequently (every week) than mice and rats.
  2. Zebrafish can easily be genetically manipulated to study a disease; it takes less time to generate a zebrafish mutant line than a mouse mutant line.

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    Picture above shows zebrafish blood vessels labelled in red and lymphatic vessels labelled in green

  3. In zebrafish, important pathways can be easily blocked and examined by simply adding the drug to the water. This allows for more cost effective and faster identification of new drugs and new uses for current drugs.
  4. The zebrafish is see-through; fluorescence markers can be used to “highlight” various cells in tissues and organs. Imagine being able to see individual cells migrate from one location to the next and form an entire heart that begins to beat 24 hours later- in real time. THAT’S AMAZING!

Other advantages of the zebrafish are disease specific. For example, zebrafish are an advantageous model for studying congenital heart disease because they can survive severe cardiac defects that are typically lethal in mice. Therefore, the zebrafish model allows scientists to follow a disease longer than they would be able to in a mouse model. Zebrafish models of heart failure have been found to exhibit similar defects to those found in patients with heart disease. In addition, zebrafish heart models have provided genetic evidence that certain signaling pathways protect humans against heart problems.

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Zebrafish organs or tissues can be easily visualized because they are see-through

One of the major reasons why people succumb to heart attacks is because heart cells get damaged and die; heart cells have little to no capability to regenerate (make more of themselves). The zebrafish heart, on the other hand, has the capability to regenerate and replace injured heart tissue after damage. Therefore, scientists are using the zebrafish to figure out what factors or pathways are involved in that process, so they may be able to help the human heart heal itself after being damaged during a heart attack. Heart disease is the leading cause of death in the U.S. and worldwide; so, many lives can be saved with the help of a little striped fish, like Dory.

With that in mind, it’s probably safe to say that fish are friends (and not just food).

 

Peer edited by Breanna Turman.

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Fun Facts About Cephalopods

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Octopus are intelligent cephalopods capable of using tools, opening containers, and even play  Photo by: Elias Levy / Flickr

Class Cephalopoda is home to some of the most intelligent and mysterious critters in the sea. Including species of octopus, squid, cuttlefish and nautilus, cephalopods are a type of mollusk that have have lost their hard outer shells. Cephalopods get their name from the Greek word “kephalópoda” meaning “head-feet”, because their arms encircle their heads. Both squid and cuttlefish are known as ten-armed cephalopods because they have eight short arms and two long tentacles (as opposed to eight-armed cephalopods like octopuses).

You surely recognize the sly octopus and the charismatic cuttlefish, but how much do you really know about this class of invertebrates?

Check out these three fun facts:

Squid and cuttlefish may look similar, but don’t be fooled.

For a quick way to tell the two apart, watch them move underwater. Squid are fast-moving predators, where cuttlefish are slower and move by undulating long fins on the sides of their bodies. If that doesn’t work, check out their eyes: squid have round pupils, where cuttlefish pupils are W-shaped. And perhaps the easiest indicator of all? Squid have sleek, torpedo-shaped bodies, compared to the broader, stout body of the cuttlefish.

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Large cuttlefish (from Komodo National Park), while they look similar to Squids, they actually have unique characteristics

Class Cephalopoda is home to one of the most venomous creatures on earth.

The blue-ringed octopus’ venom is 1,000 times more powerful than cyanide, and this golf-ball sized powerhouse packs enough venom to kill 26 humans within minutes. It produces a potent neurotoxin called tetrodotoxin, a potentially deadly substance also found in pufferfish. The venom is produced by symbiotic bacteria in the animal’s salivary glands and is more toxic than that of any land mammals.

So, what happens if you’re bitten by a blue-ringed octopus? First, the venom blocks nerve signals throughout the body, causing muscle numbness. Ultimately, it will cause muscle paralysis—including the muscles needed for humans to breathe, leading to respiratory arrest. If you ever encounter this blue and yellow beauty, back away in a hurry—its bite is usually painless, so you might not know you’ve been bitten until it’s too late.

Octopuses are smarter than you think.

When we think of animal intelligence, it’s vertebrates like dolphins and chimps that get most of the credit. But make no mistake—the octopus holds its own in a battle of wits. Cephalopods have large, condensed brains that have sections entirely dedicated to learning, a trait that is unique among invertebrates. Octopuses’ brilliant problem-solving abilities have been documented time and time again; for example, the infamous Inky the Octopus who slipped through a gap in its tank in a New Zealand aquarium and slid down a 164-foot-long drainpipe into Hawke’s Bay. There’s also evidence octopuses have personalities, and react differently based on how shy, active or emotional they are.

There you have it! Now, go out and impress your friends with your knowledge of these quirky and intriguing invertebrates!

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Stop Insulting Anglerfish Sex

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A deep sea anglerfish called a goosefish and is a member of the Lophiidae family – Sladenia remiger.  Image Credit: NOAA Okeanos Explorer Program, INDEX-SATAL 2010

You may have seen the anglerfish sex video floating around the Internet recently, with titles like “The worst sex in the world is anglerfish sex, and now there’s finally video.” While the video is worth a watch, I think most behavioral ecologist would beg to differ with the main assertion: there’s a lot of bad sex in the animal kingdom.

Why is anglerfish sex supposedly so terrible? A male anglerfish bites a females when he finds her, and then hangs onto her for the rest of his life, essentially turning into a living sac of sperm. But hey, at least he’s alive. In contrast, some species of male widow spiders somersault into the mouths of females as they mate, impaling themselves on their mates’ fangs. It sounds like an evolutionary enigma–why would an organism ever willingly sacrifice itself?–but turns out that that self-sacrifice can increase a male’s chances of fathering the female’s offspring.

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The female bed bug (the larger of the two) is traumatically inseminated by the male (bottom) through her abdomen.

Traumatic insemination” is another great example of not-so-great sex. In this case, bed bug females are the ones getting royally screwed, because traumatic insemination is a nice way of saying males stabbing females through the abdomen with their penises. The sperm then travels through the female’s hemolymph (the insect equivalent of blood), until reaching the ovaries and fertilizing the eggs. Males mate with all available females, because the last male to mate with any given female has the best chance of fathering her offspring. However, females who are subjected to these multiple matings pay a high cost: they have shortened lives and reduced reproductive output, because they have to allocate energy to healing the wounds and dealing with any resulting infections.

People often assume that two organisms mating with one another have the same “goals.” After all, both males and females are presumably invested in having as many healthy offspring as possible. But this is only true up to a certain point. Female widow spiders don’t need males to remain alive after mating, and in fact gain an advantage from eating the male (a ready source of nutrients that will help her with her next clutch!). In contrast, male widow spiders obviously benefit from not being eaten, and instead living to mate another day. Similarly, mating multiple times via traumatic insemination is costly to female bed bugs, who only need enough sperm to fertilize their eggs, while male bedbugs benefit from mating as many times as possible.

These are examples of what biologists call sexual conflict. While the source of conflict is obvious in the widow spiders’ and bed bugs’ cases, sexual conflict occurs anytime male and female genetic interests don’t align. In fact, the only time there is absolutely no potential for conflict is when males and females have exactly the same lifetime reproduction, so that each is equally invested in all of their shared offspring, with no opportunities for having offspring with other partners. In contrast, conflict can arise whenever one sex has the opportunity to improve their chances of having more, or better, offspring. This can happen in many different ways, such as: eating your partner, mating multiple times with the same partner, or even mating with multiple partners.

As a result, sexual conflict isn’t likely in anglerfish, at least those species which only have one mate for their entire lives. Although there are genera of anglerfish where females can have up to 8 males hanging off of her! So there’s potential for sexual conflict there, since the males will presumably compete to father her offspring and could do so in ways that are harmful to the female. However, anglerfish are incredibly hard to study because they generally occur in the deep sea. Frankly, male anglerfish have way more going for them than you might’ve ever thought–keep that in mind next time someone’s making fun of them.

 

Peer edited by Karen Setty.

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Honey Bees: Conservation Icon or Environmental Problem?

Bzzzzztt! Oh, sorry. That was just the sound of another honey bee dying. Seriously though, honey bee populations are crashing all over the world – we’ve lost nearly 60% of honey bee colonies since the 1970s. But there’s good news! Honey bees might be on the verge of making a comeback. Numerous conservation agencies and local businesses are making hard attempts to increase the number of honey bee colonies in all sorts of places – Barack Obama even launched a special task force in 2014! So, with all these good bee-vibes, why did one prominent bee researcher write a perspective article in Science poo-pooing the spread of honey bees as conservation icon? Let’s break it down.

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Apis mellifera, the European honey bee and maybe your best friend?

Get to the point. What’s the problem?

Sure, right away. As mentioned above, honey bees are vanishing at an alarming rate. Much of this phenomenon is associated with something called Colony Collapse Disorder (CCD). One day, all the bees are happy and making honey, then the next the workers have suddenly vanished and abandoned their queen and hive. In a frustrating turn of events, nobody knows quite what is causing CCD. Many experts believe CCD is attributed to a variety of factors: increased use of pesticides, a virus-harboring parasite, poor nutrition, climate change, and even cell phones (OK, you caught me: that last one isn’t widely supported). At this point, about 40-50% of established hives don’t survive to the next year – a significant change from decades past. If this worrisome trend continues, honey bee populations could plummet with a cascade of consequences.

Do honey bees really matter, though? I hardly eat honey.

Great rhetorical question (and also, what’s wrong with you?)! Honey bees are indispensable to our nation’s agriculture. While several staples of American agriculture such as wheat and corn are wind-pollinated, many others need help from other organisms to spread their pollen from one flower to the next. In fact, honey bees are essential for the pollination and production of a huge variety of crops such as apples, cantaloupes, almonds, and avocados. Honey bee-pollinated foods contribute more than 15 billion dollars to the US agricultural economy and their continued decline could increase consumer costs of these foods to ten times their current price.  

Honey bee products also make up their own economy. Honey produced by American beekeepers is a 300-million-dollar industry, while hive by-products such as beeswax, have niche markets as well (who here hasn’t heard of Burt’s Bees?).

https://www.pexels.com/photo/bee-on-flower-811691/

Honeybees play an essential role in the reproductive cycle for many flowers and plants that produce our food

The benefits of managed hives aren’t limited to large scale commercial farmers or beekeepers. Many people report that keeping bees improves the health and vibrancy of their own gardens. Consuming locally-produced honey might (emphasis on might) also help with allergies, attuning your body to the pollens it’ll be lambasted with in spring and fall. Local hives also present a fantastic opportunity to teach lessons about biology to students of any age – did you know honey bees are actually the only domesticated superorganism? (Don’t know what a superorganism, is? Look here. See, learning opportunity!)

Ok, so what’s up with this anti-honeybee article? Is the guy just a jerk?

Dr. Jonas Geldmann is actually a renowned conservation researcher at the University of Cambridge, and probably a great guy! His recent perspectives article in Science highlights a growing concern among environmental conservationists. While honey bees are fascinating and powerful machines of agriculture, high densities of managed hives also present an environmental quandary. A growing body of research suggests that domesticated honey bees, with up to 60,000 bees in a hive, may be harmful to their wild, native neighbors. Honey bee hives require huge amounts of nectar and pollen to stay healthy and produce honey, potentially placing them in direct competition with native pollinations for food. Additionally, honey bee hives can become incubators for parasites and pathogens that can be directly transmitted to other bee and insect species, impacting their health and fertility. While the jury’s still out, the accumulating evidence suggests that introducing honey bee hives can measurably reduce local populations of native bee species, which can have negative impacts on the local environment.

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Piedmont azalea (Rhododendron canescens) is native to North Carolina

Native pollinators, which include thousands of distinct bee species as well as butterflies, moths, bats, flies, ants, and birds, are also capable of performing a significant portion of the pollination needs of both agricultural and non-agricultural plants. In many cases, native plant species have uniquely adapted to be efficiently pollinated by their native pollinators. A beautiful example of this is the flowering azaleas, which bloom in the early spring. Unlike many flowering plants, azalea pollen is hidden deep inside their flowers – where only native bees know to look.­­­­­ North Carolina is home to several native species of deciduous azaleas, none of which can be pollinated by domesticated honey bees. Similarly, crop plants such as squash, alfalfa, and blueberries all have native bee species that are significantly more efficient at fulfilling their pollination needs than their domesticated relatives.

Unfortunately, many native pollinators are experiencing serious population declines similar to the honey bee. For evidence, we only have to look back at the agriculture industry. In the past, native pollinators were the sole source of pollination for many of the food crops that are now completely reliant on managed honey bee hives. While the honey bee has done a fantastic job of keeping these foods from vanishing off our shelves, it won’t be able to maintain the diversity of our nations flora alone. It is imperative that we keep our native pollinators in mind when discussing conservation efforts and adopt policies that promote the health and wellbeing of both native and domesticated bee species.

What can you do?

Fear not, for all is far from lost! Helping out is simple! Native and domesticated species of bee both struggle with some of the same issues: a lack of resources (nectar and pollen) and exposure to pesticides. When buying plants for your own garden, look for native species that produce plenty of nectar and pollen (also known as bee-food!) and ensure that they are pesticide free. If you’re feeling overwhelmed, contact your local beekeepers association or honey bee researcher – they will often have resources available such as this one from the North Carolina Cooperative Extension. While tending your garden, try to avoid using pesticides and only use natural, bee-friendly ones if you must – many local garden supply stores will carry such products. There are also ways to help if you aren’t an avid gardener! In an ideal world, we’d all buy locally-sourced, pesticide-free produce (which you can do! Talk to growers at your local farmers market about their practices), but that process can be a bit daunting. While imperfect, USDA certified organic foods are grown using naturally-sourced pesticides (like raw copper or sulphur), which likely aren’t as toxic to local pollinators. By sticking to these practices, anyone can promote the health of native pollinators and honey bees, alike.

Peer edited by Erica Wood.

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The Terminator of the Genome

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The real Terminator

“Listen. Understand. The Terminator is out there. It can’t be reasoned with, it can’t be bargained with… it doesn’t feel pity or remorse or fear…and it will absolutely not stop. Ever. Until you are dead.” In the movie “The Terminator”, the Terminator’s one job was to kill a woman whose son will later hurt his cyborg people. You may wonder what the Terminator has to do with molecular biology but it’s actually quite relevant. We have a ‘terminator’ in our body called p53; its job is to kill rogue cells and prevent cancer from spreading through our bodies at all costs.

p53 works as a gatekeeper in the cells of our body. Just like how gates prevent criminals from getting out when they’re not supposed to, our cells have gates and security to prevent rogue cells, like cancerous cells, from squeezing past checkpoints that make sure cells are normal and healthy. Cells grow, mature and reach a point where they need to divide to make new cells. Each of these steps have checkpoints that make sure the cells are normal and healthy so that the new cells aren’t abnormal or cancerous. Without this security, cancer cells would be running rampant in our bodies. Many cancers are caused by a loss of security in the cell, allowing cancer cells to grow and divide without being stopped at these checkpoints. p53 is one of these gatekeepers. Its function is crucial for cell regulation, cell death and checking cells to make sure they’re not abnormal and cancerous.

When a cell grows and divides, it stops at certain checkpoints in that process to make sure nothing is abnormal and that it is a healthy cell. p53 acts at these checkpoints in the cell to inspect and ensure that the cell isn’t mutated or messed up in any way. If the cell passes inspection, then it moves along and keeps growing and then exits the cycle of growing and dividing. If p53 catches a rogue cell trying to sneak past a checkpoint with mutated DNA or too many chromosomes, it calls in a whole arsenal of molecules called caspases that kill the cell through a process called apoptosis or prevent the cell from making new cells.

Gatekeeper molecules are very important to the cell because they prevent mutated cells from growing and making more mutated cells, eventually leading to cancer or neurodegenetive disease. p53 is activated by cell stress, like external heat or toxins. Stress signals that there is something wrong with the cell division process and that there needs to be more stringent inspection of cells to determine the cause of cell stress and to get rid of it. The problem becomes when gatekeeper molecules themselves are mutated like how border guards can be corrupted or bribed. When p53 in a cell is corrupted, nothing else is checking the cell’s genome to see if it is mutated. These cells get a free pass to divide, thrive and build up in places they shouldn’t be, which is what causes cancer.

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p53 (blue) interacting with DNA (orange)

p53 is mutated in over 50% of cancers like ovarian cancer, breast cancer and colorectal cancer. When working properly, p53 is a tumor suppressor but when it is mutated, is becomes an oncoprotein, a protein that promotes cancer. Two copies of p53 or two gatekeepers are needed in each cell in order for p53 to inspect and shut down rogue cells properly. However, in cancer, one of these copies of p53 is mutated and the other copy is unable to keep up with all the inspections that need to be done. In aggressive cancers, the remaining copy of p53 can become mutated into an oncoprotein and help rogue cells grow, divide and spread to other parts of the body.  

There are various ways that the body tries to prevent mutant p53 from enabling cancer to grow. One of these is through the protein Mdm2 which targets p53 for degradation. When the cell is happy and under low stress, p53 does not need to cause cell death. However, if p53 is mutated it will try to kill the cell. At this point, Mdm2 destroys p53 because it can see that p53 isn’t working properly. Mdm2 is responsive to p53. If p53 levels go up, Mdm2 levels go up as well so that the cell is working properly and is regulated. However, in cancer, Mdm2 can be shut down by other mechanisms so that it can’t shut down p53.

At UNC, Yanping Zhang’s lab studies the Mdm2-p53 pathway. In particular, they study what happens when Mdm2 is mutated and can’t degrade abnormal p53. Thus far, they have found that under conditions of low stress, Mdm2 can be mutated and not have any adverse effects on the cell. However, mice that do not have any Mdm2 were not viable because, left unregulated, p53 constantly killed the cells no matter if they were abnormal or not.

p53 is an amazing protein that works hard to terminate all the abnormal cells in our body. Hopefully, through more study, we can find ways to prevent the mis-regulation of p53 and thus help treat cancers due to p53 mutations.

Peer edited by Samual Honeycutt and Mimi Huang.

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Epigenetics: The Software of the DNA Hardware

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Scientists identified the genes of the human genome to understand how the genes influences the function and physical characteristics of human beings.

The Human Genome Project (HGP) was an amazing endeavor to map the full human genome, and so intense an effort that it required an international collaborative research team. One of the ultimate goals of this project was to shed light on human diseases and find the underlying genes causing these health issues. However, the HGP ended up creating more questions than answering them. One thing we found out is that most diseases are complex diseases, meaning that more than one gene causes the disease. Obesity is one such example of a complex disease. This is in contrast to cystic fibrosis which is a disease caused by a mutation in a single gene. To further complicate diseases, there are gene and environment interactions to consider. A gene-environment interaction is a situation in which environmental factors affect individuals differently, depending on their genotype or genetic information. The possible number of gene-environment interactions involved in complex diseases is daunting, but the HGP has given us the information necessary to start better understanding these interaction.

Although the HGP did not end up giving us the answers we were looking for, it pointed us in the direction we needed to take. We needed to consider the role of environmental factors on human health and disease. For not only are complex diseases not fully explained by genetics alone, but another aspect of these diseases remains unexplained by genetics: the health disparities seen within diseases like obesity, diabetes, cancer, etc. The HGP showed us that not all diseases are caused by single mutations and that genetic diversity does not explain the differences in health outcomes. The environment plays a big part.

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Epigenome  is the software that controls gene expression to make the different cells that make up the human body.

Gene-environment interactions begin to answer why genetics alone cannot explain  varying health outcomes by considering that the environment may have varying effects on our genetic data. However, there is another dimension to our genetic background that could better answer why genes often can’t be mapped directly to a disease. Imagine that our genome is our computer hardware, with all the information necessary to create the cells we are composed of. However, something needs to configure the genome to differentially express genes so as to make skin and heart cells from the same DNA. Skin and heart cells have the same information (DNA) in their nucleus but only express what’s necessary to function as a skin or heart cell. In other words, software is needed for the hardware. For us, that software is the epigenome. The epigenome consists of a collection of chemical compounds, or marks, that tell the genome what to do; how to make skin and heart cells from the same information. The epigenome, unlike the genome, is flexible. It can change at key points in development and even during the course of one’s lifetime. This flexibility makes the epigenome susceptible to environmental factors and could explain: (1) Why our genome alone cannot explain the incidences of diseases such as obesity, (2) the health disparities within these complex diseases, and (3) the transgenerational inheritance of complex diseases like metabolic syndrome, defined as a cluster of conditions such as high blood pressure and high blood sugar that increase your risk for heart disease and diabetes.

Now of course, the more we find out the more questions are left unanswered. As stated before, the epigenome can change due to lifestyle and environmental factors which can prompt chemical responses. However, the mechanisms by which things like diet and smoking induce these chemical responses is unclear. But researchers have started to fill in the gap. For example, certain types of fats, like polyunsaturated fatty acids (corn oil is high in these), can generate highly reactive molecules and oxidative stress, which can cause epigenetic alterations. Tobacco smoke contains a mixture of chemicals that have been independently investigated with mixed results on the epigenetic effects. Psychological stress, more specifically child abuse, has been seen to cause increased methylation (a sort of mark on the genome) of a receptor for hormones responsible for metabolism (glucocorticoid receptor) in suicide victims. This has also been seen in mouse models where higher maternal care of pups decreased methylation of the glucocorticoid receptor. Increased methylation usually decreases the expression of the glucocorticoid receptor, and decreased methylation would increase the glucocorticoid receptor’s expression.

The HGP was an amazing endeavor of science and has given us amazing insight into the structure, organization, and function of the complete set of human genes. It has also helped point us in a new direction to better understand chronic diseases and seek to find the solutions to address the burden of disease.

Peer edited by Mejs Hasan and Emma Hinkle.

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Heart to Heart

https://pixabay.com/en/heart-curve-bless-you-healthy-665186/

Hearts and heart health are front and center throughout the month of February.

The month of February is a big month for hearts. Between Valentine’s Day and American Heart Month, you cannot escape heart-shaped decorations and reminders to exercise daily. And while many of us are fortunate that our heart health can be maintained through diet and exercise, there are some cases where that is not enough. Individuals with certain congenital heart defects, weakened heart muscles, or other types of heart disease may need a totally new heart. In the United States, about 2,300 heart transplants occur each year with over 70% of those patients surviving for five years afterwards. This high survival rate is in stark contrast to the early days of heart transplants in the late 1960s and 1970s, and it is largely due to advances not in heart physiology, but the immune system.

Our immune systems are exceptionally good at identifying foreign invaders and attacking them. In the cases of bacterial or viral infections, the immune system’s voracious assault on foreigners keeps us healthy. However, in the case of a heart transplant, where foreign tissue is introduced to the body to save the patient’s life, such voracity is detrimental to survival. A distressing catch-22 emerged as early heart transplants were performed – doctors gave patients powerful immunosuppressants to prevent rejection of the heart, but these drugs left the immune system so weakened that it could not fight off post-surgical infections. Eventually, a breakthrough came from an unexpected place – a Norwegian soil fungus.

https://www.flickr.com/photos/usdagov/38151055715

Sometimes medical breakthroughs come from unlikely places – like a Norwegian soil fungus.

While on vacation in Norway, a scientist collected a soil sample that would change the fate of organ transplants forever. The soil sample was taken to Sandoz Pharmaceutical Ltd. where Jean-Francois Borel worked diligently with a team of scientists to characterize an interesting compound found in the Norwegian soil: cyclosporine, which was made from a fungus.

Sandoz Pharmaceutical was interested in developing new antibiotics, but, cyclosporine did not prove to be an effective antibiotic. Luckily for future recipients of heart transplants, cyclosporine  did show promise as an immunosuppressant. Cyclosporine specifically inhibited white blood cells and T cells instead of killing them, thus preventing organ rejection while still allowing the immune system to fight off infections. Dr. Borel and his team faced several setbacks while studying cyclosporine, including pressure from Sandoz to discontinue the studies. However, they persisted until 1983 when the Food and Drug Administration approved cyclosporine as an immunosuppressant for all organ transplants. Many healthy hearts are beating today due to cyclosporine, and a heartfelt thanks goes out to the countless individuals who worked so hard to make these survival stories a reality.

Peer edited by Kaylee Helfrich.

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Cloned Monkeys: Another Human Creation

http://english.cas.cn/head/201801/t20180123_189488.shtml Image credited to Qiang Sun and Mu-ming Poo, Institute of Neuroscience of the Chinese Academy of Sciences

First cloned none-human primates: Zhong Zhong and Hua Hua (Image credited to Qiang Sun and Mu-ming Poo, Institute of Neuroscience of the Chinese Academy of Sciences)

Cloned primates are here! Over three decades have passed since the birth of Dolly, the sheep, scientists have now tackled cloning mammals that are even closer to us on the evolutionary tree: macaque monkeys. What does this mean for a society that witnesses dramatic changes day by day: computers are outperforming doctors in calling out heart abnormalities in patients; 3D-printed organs are bringing us one step closer to tissue restoration; genome sequencing has become an online product easily available for anyone curious about their ancestry, bodybuilding, or just simply wine tastes. Breakthroughs in science and technologies are so prevalent in our life that by now, we probably shouldn’t be surprised by any new discovery. Yet when the two cute, little, cloned monkeys were born, the whole world was, once again, shaken.

Published in Cell on January 24th, 2018, a study from a group of scientists in China reported their methods in generating two non-human primates that are genetically identical. To clone the two identical macaque monkeys, the scientists applied Somatic Cell Nuclear Transfer, the same method that generated Dolly in 1996. The key idea behind cloning is that a new organism, be it sheep or monkey, is generated without sexual reproduction. Asexual reproduction is not as uncommon as one would think, plenty of plants do so. For example, Bryophyllum shed plantlets from the edge of the leaves to produce new plants. Some insects, such as ants and bees, also exploit asexual reproduction to clone a huge working class army. Since asexual reproduction is essentially an organism duplicating itself, the offsprings are all genetically identical. Evolution, however, doesn’t favor asexual reproduction as identical offsprings don’t prevail in a fast changing environment. On the other hand, sexual reproduction combines different sperms and eggs to create diverse offsprings, of which some may survive. To combat challenges from the mother nature, higher organisms, such as mammals, almost exclusively reproduce sexually. This is why a cloned monkey, an anti-evolution human creation, is mind blowing.

https://commons.wikimedia.org/wiki/File:Kalanchoe_plantlets.JPG

The succulent, genus Kalanchoe, uses asexual reproduction to produce plantlets.

To clone mammals, scientists came up with the idea of transferring the nucleus of a somatic cell to an enucleated egg (an egg that lacks nucleus). Unlike  germ cells (sperm and eggs), somatic cells refer to any cells that don’t get passed onto the next generation. These cells have the full genome of an organism that is split equally in germ cells during sexual reproduction. Carrying half of the genome, sperm and egg need to fuse their genetic materials to make one viable embryo. Technically, the nucleus of a somatic cell holds all the genetic information an organism needs. Thus, by inserting the somatic cell nucleus into an egg, scientists could generate a functional embryo. But why not into a sperm? Evolution has trimmed mammalian sperm tremendously so that it can accomplish its only job better: swim faster to fertilize the egg. As a result, not much other than the sperm’s genetic information is incorporated into the fertilized egg and the embryo relies on the cellular machinery from the egg to finish development. Using this technology, the scientists generated over 300 “fertilized” embryos. Of these embryos, 260 were transferred to 63 surrogate mothers to finish developing. 28 surrogate mothers became pregnant, and from those pregnancies, only 2 healthy monkey babies were born. Although they were carried by different surrogate mothers, every single piece of their genetic code is the same as the the somatic nucleus provider, a real-life demonstration of primate-cloning. Followed by millions of people since their debut to the world, these two macaque superstars are the living samples of a revolutionary breakthrough in our science and technologies.

 

Despite the extremely low success rate, this technology erects another monument in the history of mankind’s creations. Carrying identical genetic information, cloned monkeys like these two can be a very powerful tool in biomedical research and diseases studies. Co-author Mu-ming Poo, director of the Chinese Academy of Sciences’ Institute of Neuroscience in Shanghai, said that these monkeys could be used to study complicated genetic diseases where environmental factors also play a significant role, such as Alzheimer’s and Parkinson’s diseases. While there are ethical concerns on this technology and its easy application to human cloning, it is worth noting that almost all human creations (explosives, GMO food, the internet, etc.) are double-sided swords. It is up to the hand that wields this sword to decide whether to do good or bad. It is wise to be cautious with the development of new technologies, but it’s also important not to constrain our creativity. After all, it is our creative minds that drive us toward creating a better life for everyone.

Peer edited by Cherise Glodowski.

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Why is the Flu such a Big Deal?

With each flu season comes a bombardment of new advertisements reminding people to get a flu vaccine. The vaccine is free to most and widely available, yet almost half of the United States chooses to forgo the vaccine.

When Ebola emerged, there was 24 hour news coverage and widespread panic, but the influenza virus (the flu) feels more familiar and much less fear inducing. This familiarity with the flu makes its threat easy to brush aside. Yet, every flu season is met with stern resolve from the medical community. What’s the big deal with the flu?

What makes the flu such a threat?

Influenza is a globetrotting virus: flu season in the northern hemisphere occurs from October to March and April to September in the southern hemisphere. This seasonality makes the flu a year round battle. The virus also evolves at a blistering pace, making it difficult to handle.

To understand why the flu is able to evolve so rapidly, its structure must be understood.The graphic to the right shows an illustration of the ball-shaped flu virus.

https://www.cdc.gov/flu/images/virus/fluvirus-antigentic-characterization-large.jpg

Illustration of flu structure

On the outside of the ball are molecules that let the virus slip into a person’s cells. These molecules are called hemagglutinin and neuraminidase, simply referred to as HA and NA. HA and NA are also used by our body’s immune system to identify and attack the virus, similar to how a license plate identifies a car.

These HA and NA molecules on the surface can chanAntigenic shift in the fluge through two processes. One such process is like changing one license plate number; this is known as antigenic drift. When the flu makes more of itself inside a person’s cells, the instructions for making the HA and NA molecules slightly change over time due to random mutations. When the instructions change, the way the molecules are constructed also changes. This allows the flu to sneak past our immune systems more easily by mixing up its license plate over time.

Another way the virus can evolve is known as antigenic shift. This type of evolution would be more like the virus license plate changing the state it’s from in addition to a majority of its numbers and letters, making the virus completely unidentifiable to our immune systems. Unlike antigenic drift, antigenic shift requires a few improbable factors to coalesce.  

Antigenic shift happens more regularly in the flu when compared to other viruses.For instance, one type of flu virus is able to jump from birds, to pigs, and then to people without the need for substantial change. This ability to jump between different animals enables antigenic shift to occur.

https://commons.wikimedia.org/wiki/File:AntigenicShift_HiRes_vector.svg

How antigenic shift occur in the flu

This cross species jumping raises the odds of two types of the virus to infect the same animal and then infect the same cell. When both types of the flu virus are in that cell, they mix-and-match parts, as can be seen in the picture to the right. When the new mixed-up flu virus bursts out of the cell, it has completely scrambled it’s HA and NA molecules,generating a new strain of flu.

Antigenic shift is rare, but in the case of the swine flu outbreak in 2009, this mixing-and-matching occured within a pig and gave rise to a new flu virus strain.

This rapid evolution enables many different types of the flu to be circulating at the same time and that they are all constantly changing. This persistent evolution results in the previous year’s flu vaccine losing efficacy against the current viruses in circulation. This is why new flu vaccines are needed yearly. Sometimes the flu changes and becomes particularly tough to prevent as was the case with swine flu. At its peak, the swine flu was classified by the World Health Organization (WHO) as a class 6 pandemic, which refers  to how far it had spread rather than its severity. Swine flu was able to easily infect people, fortunately it was not deadly. The constant concern of what the next flu mutation may hold keeps public health officials vigilant.

Why is there a flu season?

A paper by Eric Lofgren and colleagues from Tufts University grapples with the question “Why does a flu season happen?”. The authors highlight several prevailing theories that are believed to contribute to the ebb and flow of the flu.

One contributing factor to the existence of flu seasons is our reliance on air travel. When flu season in the Australia is coming to an end in September, an infected person can fly to Canada and infect several people there, kickstarting the flu season in Canada. This raises the question: why is flu season tied with winter?

The authors touch on this question. During the winter months, people tend to gather in close proximity allowing the flu access to many potential targets and limiting the distance the virus need to cover before infect another person. This gathering in confined areas likely contributes to the spread of flu during the winter, but another theory proposed in this paper is less obvious and centers around the impact of indoor heating.

Heating and recirculating dry air in homes and workplaces creates an ideal environment for viruses. The air is circulated throughout  a building without removing the virus particles from the air, improving the chances of the virus infecting someone. The flu virus is so miniscule that air filters are unable to effectively remove it from the air. The authors come to the conclusion that the seasonality of the flu is dependent on many factors and no single cause explains the complete picture.

What are people doing to fight the flu?

The flu is a global fight, fortunately the WHO tracks the active versions of the flu across the world. This monitoring system relies on coordination from physicians worldwide. When a patient with the flu visits a health clinic, a medical provider, performs a panel of tests to detect the type and subtype of flu present. This data is then submitted to the WHO flu database, which is publicly accessible.

This worldwide collaboration and data is invaluable to the WHO; it allows for flu tracking and informed decision making when formulating a vaccine. Factor in the rapidly evolving nature of the flu and making an effective vaccine seems like a monumental task. Yet, because of this worldwide collaboration twice a year, the WHO is able to issue changes to the formulation of the vaccine as an effort to best defend people from the flu that year.

Peer edited by Rachel Cherney and Blaide Woodburn.

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