AP Biology class blog for discussing current research in Biology

Why don’t Naked Mole Rats Feel Pain?

This question is currently being researched because of the mole rats amazing inability to feel pain the way that most animals do. The reason lies in sensory nerves. An ion channel is sensitized when molecules bind themselves to receptors which is TRPV1. Scientists performed a test to see what exactly what makes these animals different than others.

They tested the thermal hyperalgesia of both the common rat and the naked mole rat at TRPV1. What do you think the difference is? From this experiment and by looking at the DNA of other animals as well, they concluded that the switch of 1 to 3 amino acids has a great effect on the naked mole rat. This change causes the receptors to be less sensitive to pain. This unique receptor may be the reason that they are able to survive better than other animals with genetic mutations. Also because they do feel as uncomfortable in the heat compared to others, they are able to live in small tightly packed spaces underground.

This topic is very important because it shows how a small genetic difference can be the basis for a species. It is proven that through evolution, they have a slow metabolic rate and that they do not have anything that is not necessary for their survival, including extra pain receptors. More research is being done on this topic to help us better understand why some animals feel pain and some do not.   

Beauty is Pain: and naked mole rats have neither

The naked mole rat is the ugly duckling of the rodent family. These small rodents can live up to 32 years, are virtually resistant to cancer, and have evolved to become immune to certain types of pain. Beneath its wrinkled, fleshy surface, the naked mole rat is the closest animal we have to an indestructible species.

A new study published October 11 in Cell Reports offers some reasons behind the rodent’s abilities. Minor evolutionary changes to the amino acids in their pain receptors make the naked mole rat highly insensitive to pain after birth.”We think evolution has selected for this tweak just subtly enough so that the pain signaling becomes non-functional, but not strong enough that it becomes a danger for the animal,” says lead author Gary R. Lewin, a professor at the Max-Delbruck Center for Molecular Medicine in Berlin, Germany.

Much of this is due to the environment and behaviors present in the mole rats life. Naked mole rats often live in large colonies, with up to 300 members. The constant digging of tunnels and over crowding should leave the mole rat in great discomfort, and highly prone to a condition called thermal hyperalgesia. Humans have the same condition, which we generally call heat sensitivity. Imagine entering a hot bathtub with a bad sun burn. When this happens, it’s because sensory receptors on your skin have been chemically “sensitized” by inflammation or high temperatures. Once those receptors are sensitized, even the smallest amount of heat will cause sensory nerves to send signals to the  brain that register this as painful. Naked mole rats lack this reaction.

Through a series of calculated and carefully designed experiments, Lewid and his team were able to pin point what differentiates naked mole rats from all other rodents- a change in their TrkA receptor. They discovered a switch of just one to three amino acid changes on one section of the naked mole rat TrkA receptor that make it less sensitive.

“Even though the naked mole rat’s version of the TrkA receptor is almost identical to that of a mouse or a rat, it has a very significant effect on the animal’s ability to feel pain,” says Lewin. The naked mole rat is built for efficiency. It’s an animal built to survive the toughest of conditions. Evolution has shut down everything that is not necessary in the naked mole rat, including nerve receptors.

In my opinion, the naked mole rat is pretty cool. It has learned to evolve in order to survive. Maybe this trait is why the this species of rodent in particular outlives all of its fellow rodents by over 25 years. My one question would be, “Is the ability to not feel pain always an advantage? Or can this sometimes lead an animal into dangerous situations?” Whatever the answer, the naked mole rat is an evolutionary success.



A Brand New Dinosaur? Just When You Thought There Were No More Dinosaurs.


Yep, you read that correctly, a brand new dinosaur(…’s skull) has been found in the Patagonia region of south America. Its amazing that after millions and millions of years new dinosaur fossils are still being discovered which can lead to the recognition of a whole new species of dinosaur. In this case, the dinosaur was part of the pterosaurs group, which is a extinct group of “flying reptiles”. This brand new type of dinosaur was named Brain Ancient; just kidding, its name translates to “brain ancient” its really called “Allkauren Koî”. But why was the dinosaur named this? These two additional websites may help answer that as well as show what the dinosaur might have possibly looked like. The name was probably given to this extinct animal because all that was found of it was an ancient brain(in reality the skull and part of the backbone and vertebrae was found). This find shows just how interesting the world used to be and it still amazes me that we are able to find remains of the beasts that ruled the world before humans.




Here is the fossil of a close relative of this newly found dinosaur (this dinosaur is in the same group, pterosaurs). S.W. Williston’s reconstruction of Ornithostoma ingens, a synonym of P. longiceps


To clarify, if you would like to see pictures, that can’t be shown on this article due to copyright issues, of what this new dinosaur Allkauren Koî might have looked like, you can use these two links that are shown below.




1930’s Dust Bowl (MARS EDITION)


Mars has experienced dust storms for years now, so a simple one is nothing new; however, by October 29th of this year, the dust storms will be at their all time high according to NASA. The dust storms on Mars are so strong that back in 2007 (the most recent larger one), the storm dimmed the sun, reducing the solar power available to two rovers on different sides of the planet. This continues to be an issue as the storms increase, limiting the power available to the rovers, and leaving them alone. Not only do dust storms threaten rovers, but astronauts too. Future astronauts will have to face tremendous winds, extreme dust, and lack of solar energy like the rovers. Furthermore, research from the past will now to indicate a pattern to predict future storms as the storms have thus far indicated a cycle and with further observation will continue to prove true.

I chose to write about the mars dust storm because besides the fact that I am utterly obsessed with space, the dust storms and the recent water finding on mars bring us closer to finding a planet just like ours, and thusly in the far future a refuge planet in the event of disaster on earth. By creating a history of dust storms we can evaluate the safety and conditions of this planet as we continue to learn about it.



NASA develops model to predict global dust storms on Mars


What’s Causing Your Migraine? The Answer May Be Inside Your Mouth.

photo by user "taennit" on on

photo by user taennit on on

Have you ever been going about your day and suddenly you’re hit with the feeling of needles ricocheting against the walls of your skull? Frustration grows inside you as you ponder what could’ve possibly triggered your migraine this time. Millions of Americans are struck with similar pain and turmoil every day, which makes the cause of migraines an in-depth and on-going research topic. Though the cause of migraines remains a bit blurry, it is believed that neurotransmitters, like serotonin, are involved in the development of a migraine. Known triggers of this hindering head pain are hormonal changes, stress, and our diets. Author Tim Newman’s article Could Migraines Be Caused by the Bacteria in Our Mouths?, published on, suggests that migraines can be caused by the nitrate-filled foods millions of people consume on a daily basis.

Though you may resort to a glass of wine or piece of chocolate for relaxation after a hectic day, these two things can ultimately make your day into an all but relaxing evening. Both chocolate and wine possess high nitrate levels, as do processed meats and leafy, green vegetables. When nitrate is consumed through food, bacteria in the mouth converts nitrate into nitrite. Nitrites then enter the body and can be formed into nitric oxide which is helpful in reducing blood pressure and boosting cardiovascular health as a whole. Because of the benefits these forms of nitrate can have on the body, many people are given drugs containing nitrate in order to help with their health problems. Author Antonio Gonzales and programmer analyst Rob Knight found that four in five of the people that take these drugs also experience extreme headaches or migraines as a side effect. With this information, both Gonzales and Knight used information collected by the American Gut Project to further inspect the links between oral bacteria, diets, and migraines.

When someone takes drugs filled with nitrate or eat nitrate-sufficient food, their body must produce the necessary amount of bacteria or enzymes to break up the nitrate and turn it into nitrite or nitric oxide. Both Gonzales and Knight noted that people with migraines tend to have a significantly higher amount of nitrate-related bacteria located in the mouth, thus increasing the chance that the amount of nitrate-related bacteria in the mouth may correlate with the increased occurrence of intense headaches and/or migraines.

That all being said, the world of migraines is still a bit fuzzy to all of us and all we can do is continue to research the mysteries of this painful phenomenon. I won’t say that the results of these studies should be totally cast aside, but what I will say is that until nitrate-filled food and the presence of oral bacteria are a blatant cause of migraines, you shouldn’t flush those leafy, green vegetables, throw away the chocolate, or pour all the wine down the drain just quite yet.







Don’t BEE Hating on BEES (Bees and Emotion)

Have you ever stepped on a bee or crushed it out of anger because it was bothering you?  Little did you probably realize that there is scientific evidence that bees, do in fact, experience emotion.  Biologist Clint Perry, University of London demonstrated this phenomenon in his bee experiment.  In order to see if bees really did experience emotion he ran a test with a blue flower and a green flower.  The blue flower had a 30 percent sugar solution, ultimately causing the bees to associate blue flowers with a sweet treat.

After this he created another experiment in which 50% of his bees were given sugar water and the other half were not.  He set up colored flowers and in his experiment found that the bees given a 60% sugar water solution to drink flew more quickly to the flower they were trained to go to (in this case the blue one), compared to the bees that were not given sugar water.  This sugar seemed to have “amped up the bees into a positive emotional state, making them more optimistic that the flower would contain a sugary treat.”  The author of this article compared this to humans and how after eating a sweat treat are in a better emotional state and feel happy.  Another experiment done was with a drug that disrupted receptors of dopamine, causing the preference and motivation to disappear.  This proves the importance of the chemical dopamine in the brain.  Dopamine is ultimately what is giving the bees emotion.  It is important to understand that biologist Clint Perry did not prove that bees have feelings, because feelings are different than emotion. “Emotions are the body’s adaptive response to external events or stimuli.  Feelings are subjective to experience of them.”  In this experiment emotions were tested because it tested the bees response to something rather than past experience.

Now that we know bees have emotion is it possible that eventually they may acquire feelings?  Maybe you will think twice the next time you swat a bee away!

Other helpful links

Are Politics Playing a Role in the Fate of the Great Barrier Reef?

The Great Barrier Reef is one of the Seven Wonders of the World, but that does not mean that it is invincible. In fact, it has been in grave danger for some time now. A new study, written about in ScienceMag, explains how the Australian government is stepping up to initiate protocols to protect the Great Barrier Reef. They focus a lot on short-term goals. This seems to be because, in the public’s eye, the Australian government is supposed to be doing something to fix this problem, so they are, but not enough to truly guarantee the safety of the reef. One main reason that the Australian government is getting involved at all is to insure that tourism doesn’t get negatively affected.


But would if really be a bad thing if tourism to the Great Barrier Reef were negatively affected?


The answer isn’t so clear-cut. It really depends on one’s perspective. From the point of view of someone truly interested in keeping the Great Barrier Reef alive, a decline in tourism at the reef would be much preferred. This is because the unprecedented number of people entering the reef disrupts the reef’s ecosystem. The foot traffic, fuel pollution, and anchor damage inflicted by tourism on the reef is a big reason for the steady decline in the reef’s life.


Tourism isn’t all to blame, though. A huge factor in the death of the Great Barrier Reef is global warming. Now this is where the Australian government stays silent in regards to the reef. Global Warming is responsible for the long-term death of the Great Barrier Reef. The increase in water temperature, even if it is just by a degree or two, is not good for the survival of the coral. If water temperatures don’t return to their lower temperature, there may be nothing that can be done to save the Great Barrier Reef.


But for now, people are just happy that something is being done to save the reef, even if it is counterproductive in the long run.

A Second Theory: Is the RNA World Hypothesis Wrong?


Prior to recent research, scientists strongly supported the “RNA world” hypothesis, a theory that claims that DNA derived from RNA, and that RNA therefore provided the basis for life as we know it. The evidence of this new study under scientists at The Scripps Research Institute leads to an alternate theory that challenges this previous mode of thinking. This study is intriguing not only because it challenges what has mostly been accepted as factual truth by most scientists, but also because it attempts to solve the question of where and how first life developed.

Background: The “RNA world” hypothesis

The “RNA world” hypothesis dates back to over 30 years ago. Proposed independently by Carl Woese, Francis Crick, and Leslie Orgel, it essentially is a theory that states that RNA existed before modern cells, and stored genetic information and catalyzed chemical reactions within earlier cells. This theory further claims that DNA came later and only then contained the genetic material. It also infers that proteins served as a catalyst much later, only fulfilling this role once RNA evolved. The evidence that supports this theory lies with the chemical differences that distinguish RNA from DNA. RNA can be formed from formaldehyde (HCHO) which is chemically simple, especially in comparison to the much more complicated sugar deoxyribose. In a reaction catalyzed by a specific enzyme, deoxyribose is produced from ribose which also indicates the possibility that DNA comes directly after the structurally more simple and single helix RNA.

Recent Studies

Researchers believe that if this theory is correct, RNA nucleotides and DNA backbones would have mixed to create “heterogeneous” (or a product resulting from differing “parents” with unique charateristics) strands. The resulting “chimeras” (an organism composed of cells from different zygotes leading to subtle variations in form) would be an intermediate step in the transition to RNA if stable, however the study shows a decrease in stability (specifically in thermal stability or the ability to function at high temperatures) when the backbone is shared between the two nucleic acids. The researchers attribute this instability to a slight difference between the sugar in RNA and the sugar in DNA. As a result, if the RNA theory had been true, the chimeras would have died off. This proves that evolution has lead to a system where enzymes have developed to maintain the system of “homogenous” molecules, keeping RNA and DNA separate since they function much better separate from one another. Since these enzymes are fairly “new” in terms of the span of the existence of DNA and RNA, it is highly unlikely that RNA was able to transition to newly developed DNA. Without any mechanisms to keep DNA and RNA separate, it is logical to conclude that RNA does not predicate DNA. This concept is reminiscent of the endosymbiont theory that discusses the possible reason for the unique qualities of mitochondria and chloroplasts in that both theories rely on existing knowledge about these unique structures and how each component might contribute to a different function. Similar to the endosymbiont theory, there is no exact answer as to whether this theory is correct, however through challenging the theory and conducting experiments, we can further develop our understanding of certain biological phenomena.


This alternate theory, on the other hand, proposes a different view that RNA and DNA have coexisted and that one therefore did not develop from the other. While this theory is not completely new, these recent findings regarding instability for a backbone shared between the two nucleic acids provide more evidence for this secondary theory (to the RNA world theory). If this theory is accurate, DNA could have developed its homogenous system much earlier than scientists have predicted up until this point. According to this second theory, after RNA first interacted with DNA it still could have evolved to create DNA. Although scientists will never be able to discover life’s exact origin, these findings can provide insights for biology overall.


Is There a Limit to How Old Humans Will Get?

In the 1900s, the life expectancy for humans in the United States was approximately 50 years. Since then, the age to which humans can live has only grown. In 1997, a woman by the name of Jeanne Calment died at the age of 122- an astounding increase from the life expectancy less than a hundred years ago. A new study written about in the New York Times explains that Dr. Vijg, an expert on aging at the Albert Einstein College of Medicine, feels that we have now reached our “ceiling. From now on, this is it: Humans will never get older than 115.” Dr. Vijg and his graduate students published their pessimistic study in the journal Nature, presenting the evidence for their claim.

For their study, Dr. Vijg and his colleagues looked at how many people of varying ages were alive in a given year. Then they compared the figures from year to year, in order to calculate how fast the population grew at each age. For a while, it looked as though the fastest-growing group was constantly becoming older; “By the 1990s, the fastest growing group of Frenchwomen was the 102-year-olds. If that trend had continued, the fastest-growing group today might well be the 110-year-olds.” (NY Times Article). Instead, the increases slowed and eventually stopped, leading Dr. Vijg and his colleagues to conclude that humans have finally hit an upper limit to their longevity. Further research into the International Database of Longevity seemed to validate their findings; No one, except in rare cases like Ms. Calment, had lived beyond the age of 115. It appears as though human beings have hit the ceiling of longevity.

There was a varied mix of responses to the study. Some, like Leonard P. Guarente, a biology professor at MIT, praised it, saying “it confirms an intuition he has developed over decades of research on aging.” Others, like James W. Vaupel, the director of the Max-Planck Odense Center on the Biodemography of Aging, called the new study a travesty and said, “It is disheartening how many times the same mistake can be made in science and published in respectable journals.”

This study is by no means conclusive. It is simply one more piece of research in the ongoing debate over whether human beings will continue to live longer, and will continue to be debated by many experts in the field.

However, one must wonder whether living longer should be the goal. After all, as Dr. Vijg pointed out, “aging is the accumulation of damage to DNA and other molecules. Our bodies can slow the process by repairing some of this damage. But in the end, it’s too much to fix. At some point, everything goes wrong, and you collapse.” While morbid, he makes a valid observation: Humans can only go so long until necessary bodily functions begin to break down. Rather than worrying about whether we will live to an extraordinary age such as Ms. Calment, I concur with Dr. Vijg; the focus should be on living the most amount of healthy years and taking care of our bodies. While it may seem like a great idea to live to the age of 125, what good would that do if you aren’t able to continue with the activities you enjoy because your body is breaking down?


Other Relevant Articles:

In Depth Explanation of Longevity:

A brief summary of Dr. Vijg’s findings (a bit shorter than the NY Times article):

An interesting article about an entrepreneur’s quest to make people live even longer:


Brand New INSANE Trick To Maintain HUGE TELOMERES!!!

Do YOU want to learn the secret to having BIG, LONG telomeres?


Do you know what Telomeres are?


you might not know what they are, but I’m pretty sure you’re gonna want long ones,

and a few scientists lead by Eli Puterman, an assistant professor of kinesiology at the University of British Columbia in Vancouver, just made a huge breakthrough regarding telomeres.

let me explain.

New research done on Data collected in University of Michigan’s Health and Retirement study and reported on by TheScientist, has found that A.) accumulation of stressful events over the course of a lifetime are associated strongly with shorter telomeres later in life and B.) stressful experiences during childhood have a far greater effect on the shortening of Telomeres in adults than those that occur later in life.

First of all back up. What are Telomeres? And when it comes to Telomeres, does length really matter?

I’ll tell you.

(spoiler alert: length always matters)

Telomeres are caps that go on the end of our DNA. You can think of them like aglets on the end of shoelaces. Telomeres work to protect DNA from becoming damaged, and with that preventing the functionality of DNA from becoming compromised. They’re exactly like that little plastic bit on your shoelaces prevents your lace from becoming frayed, and ruining your shoelace, and your day, and your life.


(the pinks parts are the telomeres)

And a moment of thanks, to the great man who invented aglets.

Harvey Kennnedy,

Thank you.

Back to your telomeres. As we know cells are constantly copying themselves, creating new cells, and every time this happens the telomeres on the end of our DNA become shorter and shorter, before eventually they fail to adequately protect the DNA, causing our cells to lose functionality, and on a larger scale, causing you to age faster. Essentially throughout our lives our telomeres get shorter and shorter, like a candle thats burning lower and lower, it’s a marker for our aging process. A constant reminder of our mortality as humans. A literal ticking clock. We’re all gonna die. Life is meaningless.

You know what’s not meaningless though… BIOLOGY! So while we can never escape the grim reality that our lives are nothing more than the blink of an eye on a fleck of dust that’s drifting through an empty abyss of nothingness, why not try to extend that blink of an eye for as long as we can, so that we can read about research findings in the world of biology! speaking of which…

In the study, a group of 4,598 Americans that had an average age of 69 were asked to identify stressful incidents that occurred in both their youth and later adulthood. They then had their telomere lengths measured from cells from saliva samples. In the study, Part of the study’s findings were that “Each additional adverse event during childhood was associated with an 11 percent-increased odd of shorter telomeres”. These results are staggering to be sure, but are not totally out of the blue. One Judith Carroll who researches the links between behavior and health at UCLA said after the study had been completed “The findings are consistent with other reports suggesting that early life is a particularly vulnerable time when the body is rapidly growing and adapting to its surroundings”.

These results were very strong, however some have taken issue with extrapolating stressful incidents to higher mortality. While it is acknowledged that the shortening of telomeres is associated with aging, some wished the study had gone a step further, and examined whether these shorter telomeres really do result in earlier death. As it is said by Iris Hovatta, a scientist at the University of Helsinki (in Finland)(a country I have never been to, so I can’t confirm whether or not it actually exists)(which is neither here nor there)(whether or not ‘there’ really does exist) “this study did not address the effect of stress on health or lifespan and whether individuals with shorter telomeres have an increased mortality” It’s a fair criticism, but as far as we know now, shortening of telomeres causes aging, and this study puts forth strong evidence of an association between stressful events over the course of a lifetime, especially during youth, and shortening of telomeres.

So what does this mean?

if you don’t want to age, avoid stressful events during your youth.

avoid stuff like forgetting when your blog post was due, then staying up until 3 in the morning to finish it.

Then again biology its pretty much all I have to live for.

give and take I guess, we all have to find a balance that works.


New Dinosaurs Identified from the Jurassic Period

  Just a few days ago, a new species of British Ichthyosaur was identified from a complete set of skeletal remains.  After years of of being on display at the University of Bristol’s School of Earth Sciences in Bristol, England, the fossil remains were finally studied in an advanced research project. The six year long research project was led by the University of Manchester and geared to identify the large British Ichthyosaurs skeletal structure as a new species because of sudden differences in the bone structure. The group was able to solidify the differences and announced this specimen as a new species.   The group examined the differences in the endoskeleton skull and the fins in the species.  

ichthyosaurus_sp_2Another species of Ichthosaurus Photographer: User:Ballista from Dinosaurland, Lyme Regis, England

  Honorary Scientist, Dean Lomax, and Professor Judy Massare, from a college in New York led this study.  Lomax said: “It’s quite amazing – hundreds of people must walk past this skeleton every day, yet its secrets have only just been uncovered.”  The two scientists named the new species Ichthyosaurs Larkini after a paleontologist Nigel Larkin.  Incidentally, Larkin literally translates to ‘fierce’, a word used to describe the habits of the dinosaur.  

unknownTemnodontosaurus burgundiae attack Stenopterygius hauffianus. Lias of Germany

The reptile lived nearly 195 million years ago in the early Jurassic Period and was an ocean dwelling specimen. Research shows that Britain was a small chain of islands at that point in time.  Today it would most resemble dolphins and sharks.  The species could grow up to 15 meters long and were fierce predators and could move very quickly.

ichthyosaur_vs_dolphin-svgExamples of distinct features shared both by dolphins and derived ichthyopterygians 

The specimen fossil was given the University of Bristol in the 1930’s by the City Museum.  It is the complete skeletal remains of a large Ichthyosaurs Larkini, referenced as ‘Specimen 25300’ before its identification.  The fossil of this species is now on display in the Wills Memorial Building, which is part of the University of Bristol School of Earth Sciences Collection.




The Resurrection of “Dead” Bacteria

Many kinds of bacteria have the capacity to radically alter their metabolism in order to switch into a dormant state. This allows them to survive without any possibility of growth. One reason this might be advantageous to bacteria is if their microbes do not have a substantial amount of food. The cells’ revival process follows a strict genetic timetable. This is an important survival strategy.

One of the oldest types of bacteria are cyanobacteria – going back more than 3 billion years. Their activity released oxygen into the atmosphere, therefore enabling life on earth in its current state. When nitrogen, one of their major nutrients, is lacking, these cyanobacteria cease their growth and enter a dormant state. They dismantle their photosynthesis apparatus and lose their color. This allows them to survive long periods without requiring nutrients. If they become exposed to an accessible supply of nitrogen, they return to normal life within 48 hours. It is intriguing because the cells appear dead and then out of nowhere they return back to normal.


Diagram of Cyanobacteria

Through various experiments it was found that the cell revival process began almost immediately once nitrate was added. This is a highly organized process.

Phase One: Bacteria suppress all remaining photosynthesis activity and tap into reserves to obtain energy quickly

At First: Intake and processing of nitrogen. The production of protein synthesizing mechanisms are activated.

12-16 Hours Later: Photosynthesis begins

48 Hours Later: Full capacity reached. Cells begin to grow and divide again


There are copies of DNA that are not translated into proteins found in sections of uncoded RNA. These are important switches in the awakening process. This genetically coded program allows cyanobacteria to colonize environments where the nitrogen supply is inconstant. It also allows them to survive environmental stress and survive over three billion years of evolution. This is not the only bacteria that is capable of this phenomena. This can help scientists better control the spread of dangerous bacteria.



Other Resources (For More Information on This Topic):

Understanding how bacteria come back from the dead

Yawning and Brain Size


Recently, scientists discovered a correlation between yawning and brains: the longer the average duration of a specie’s yawn, the bigger that specie’s brain size,  as measured by brain weight and total number of cortical neurons.

The study was conducted on 109 individuals from across 19 different species, including cats, humans, mice, camels, and more. The investigators found that the duration of yawns was shortest in mice, who averaged 0.8 seconds, and longest in humans, who averaged 6.5 seconds. The scientists plan on investigating whether this correlation holds true amongst individual members of a species.

The study was created in response to the ideas set forth in Gallup’s 2007 paper on the thermoregulatory theory of yawning, one of the strongest theories about why we yawn (we do not yet definitively know the biological purpose of yawning). The thermoregulatory theory indicates that yawning cools down the brain in homeotherms via three potential mechanisms. But whether or not this brain-cooling is simply a side effect or the primary function of yawning is up for debate.

Based on Gallup’s paper, the investigators of this study hypothesized that longer yawns would produce greater physiological responses, in terms of blood flow and circulation to the brain– which would be evolutionarily necessary for species with larger, more complex brains.

There are other theories about why we yawn, such as a 2014 paper stating that yawning stimulates cerebrospinal fluid circulation, which in turn increases species’ alertness. A common theory that yawning increases blood oxygen levels has largely been disproved. How would such alternate theories have different implications for the discovered correlation between yawning and brain size?

23 Chromosomes. One Unique You.

This weekend, my parents told me we were trying a new product from a company called 23andme. When I first saw the words ”Welcome to you, DNA Collection Kit” written on the box, I thought it was another one of my Dad’s SkyMall purchases that is thrown away a week after buying it. This one was more intriguing than most, so I decided to investigate on-line. I am amazed that he actually purchased something of use.

23andme is a new company that analyzes your DNA and compares it to millions of others to determine your unique traits. While human DNA is about 99.5% identical between people, there are small differences called variants. These variants come from your parents, your parent’s parents, and so on. Within a month of submitting your DNA, I will get results that will tell me a number of things relating to my genetic make-up including possible health conditions that I have now or will get in the future, traits and my ancestry groups. I can’t wait.

To start the process, 23andme provides a tube with instructions. I had to spit inside the tube and my saliva was mixed with a clear liquid when I sealed the tube.  The tube is then shipped to 23andme, where they will take the saliva sample and extract and process the DNA on a genotyping chip that reads hundreds of thousands of variants in your genome. Genotyping is a method to extract and analyze the DNA found in your saliva. The lab will read the variants in my DNA versus other people’s DNA and generate personalized reports based on well-established scientific and medical research.

I’m pretty nervous about what the DNA test will tell me!

First, I will learn about my ancestry – where did I come from? What percent of my ancestry is European and what percent is Cuban? Who are my relatives? Is Yoenis Cespedes my real father? All of these questions will be answered along with contact information for my DNA relatives around the world- I think this means season tickets too!

Secondly, I will find out if I am a carrier for certain inherited conditions. Being a carrier means I have the variant for a condition which I can pass down, but I don’t have the condition. This is where potential controversies arise because people may or may not want to know if they are carriers  for harmful diseases. I am not sure I want to know! They test for over 35 conditions.

Thirdly, I will get a report that explains how my DNA impacts my health and my traits. Some of these include hair color, my chances of having a unibrow,  if I’m going to go bald (and when!), and if I have a preference for sweet vs. salty foods (I actually like both so good luck with that!).

I’m particularly excited for my results because I was born with a syndrome called Beckwith-Wiedemann syndrome, which results from the abnormal regulation of genes in a certain region of chromosome 11. I’m very interested to see if they are able to tell me more about this syndrome.

As 23andme gets more popular, there will be more data to compare with, which will expand the limits of what we can find out! I can not wait to meet all of my DNA relatives. Results will be in by the end of November, hopefully just in time for bring your Father to school day!




Transgender- Science Behind Sexual Identity

Stop Homophobia - NUS Sports Gay Protests, London

Darren Johnson Image Link

Transgender concepts have been a prevalent issue. It has been seen on a celebrity level with Caitlyn Jenner but on smaller levels as well. Schools are struggling to make decisions of whether to make bathrooms same-sex or unisex. While administrative figures are struggling to make accommodations for the increasing number and popularity of LBGT rights, society is also struggling to determine whether trans-gender identity is a social or biological doing.

One recent finding has shown that anatomical sex- gender identity and orientation- is determined in the womb. However, once the anatomy is settled, there is about a six month lag before the brain masculinizes or feminizes. Research has concluded that through some combination of genetics, hormones and the uterine environment, sometime between six months and delivery the sexual orientation is set in the brain. The only question that rises is what happens when the brain does not match the genitals.

Genetics has been proved to play a role in transgender identity. Researches studied a group of twins where either one or both were transgender.  In identical twins, 39% were both transgender. Of the fraternal twins, there were zero pairs where both were transgender. In fact a study in the Journal Biological Psychiatry, researchers found a gene variant that was associated with being a trans woman.

For the 61% of identical twins where only one is transgender, the prenatal environment, or womb, had a key role. While identical twins share genetic codes, the genes that get expressed or remain unexpressed differ. Identical twins have separate umbilical cords , separate amniotic sacs, and develop in separate locations of the womb. All these things can have an affect in the mixing of chemicals and the sexual identity process.

Lastly, the structure of the brain also plays a role. A 2014 study from the Journal of Neuroscience found that “differences in the brain’s white matter tracts [fall] along a perfect spectrum of gender identity with cisgender men and women at the ends and trans men and women in the middle.”


Dolly’s Legacy and the Healthy State of Sheep Clones

Over the past two decades, there has been much discussion around Dolly in the scientific community.  No, not Dolly Parton (although her name served as an inspiration), but Dolly the cloned sheep.  In 1996, researchers at the Roslin Institute, an animal sciences research center at the University of Edinburgh, made history by cloning the first mammal from an adult somatic cell via nuclear transfer.  The cell utilized for the cloning was from a mammary gland, and Dolly’s successful birth and 6 year longevity signified that cells other than gametes and germ cells could recreate an organism.  However, scientists and laymen alike have expressed concern regarding Dolly’s short lifespan in respective to the overage sheep’s of 10-12 years.  Does this mean clones are unhealthier versions of their “natural” predecessors?

dolly_face_closeupPhoto of Dolly’s taxidermied remains by Toni Barros, source

According to research conducted by Kevin Sinclair of the University of Nottingham, the answer is no.  Monitoring four sheep derived from the same mammary gland cells as Dolly in addition to nine cloned sheep of other breeds, Sinclair has dug up no evidence to suggest that the clones are less healthy than sheep born of natural processes.  In fact, all 13 of the sheep are now older than nine (equivalent to 70 or 80 years in the lifespan of a human) and are as healthy as their non-cloned counterparts according to tests scanning their bones, blood glucose levels, and blood pressure.

And so the question is posed, why did Dolly die young?  Scientists who interacted with Dolly claim that her life was taken by a contagious illness that ravaged the flock- not some defect as a result of her being a clone.  To address Dolly’s severe amounts of arthritis at the time of her death, geneticist Helen Sang from the Roslin Institute points to her indoor captivity and the excessive amounts of treats she was given.

While cloning might not be as efficient as traditional modes of breeding, this study exhibits that cloned animals which survive gestation and are relatively healthy during their infancy have the same chances of thriving and living to expected longevity as any other animal of the breed.  Additionally, cloning allows scientists to generate embryonic stem cells for further scientific research and to produce “high-value livestock”.  These advantages begin to show the importance of clowning and how beneficial it can become if it is accepted as an integral part of scientific studies. What animals are next to be cloned?  What impacts would cloning humans have on our society?

How Did Our Baby Learn That Word?!?!

Jason Sudeikis’ character is hosting a nice dinner party with his wife played by Jennifer Aniston, and all seems to be going great. Then, all of a sudden, their 12- month-old baby blurts out a curse word! “How could our baby learn such a thing?” In a flashback 8 months earlier, we see the less-experienced parenting pair blurt out some pretty R-rated things in a fit of frustration on the road with their baby in the backseat. And so the punch line sinks in.

In modern day parenting comedies, scenes like this fabricated one are a dime a dozen. But these humorous takes on life always get at least one thing right: babies are sponges. Let’s take a look at why on a cellular level.

image source:

Prior to birth, most neurons migrate to the frontal lobe of the brain where, during postnatal development, they link together and forge connections, allowing a baby to learn proper responses to stimuli. The “circuits” formed by the neural connections are incredibly flexible during the early months of development (roughly the first 6 months) and can quickly be formed or severed, resulting in a remarkable neonatal human ability to rapidly pick up new knowledge about our surroundings. But how are they so malleable?!

Researchers at the University of California, San Francisco may have the answer! In a study coauthored by neuropathologist Eric Huang, they found neurons forming a chain moving towards the frontal lobe from the sub ventricular zone, a layer inside the brain where nerve cells are formed, in infants up to 7 months old!

This research seems to point to the idea that these new brain cells form connections with the pre-existing neurons in the frontal lobe later in the infant’s development, resulting in more cognitive flexibility for a longer period of time.

To quote the original article by Laurel Hamers, what the new neurons are doing is analogous to “replenishing the frontal lobe’s supply of building blocks midway through construction”.

Huang’s team observed postmortem infant brain tissue under an electron microscope and discovered a group of neurons synthesizing migration proteins, but the real major discovery came with the observation of rare tissue acquired moments after death. The team injected viruses tagged with glowing proteins into the neurons (thus making the nerve cells glow) in the sample and tracked their movement. While infants up to 7 months old were observed with migrating neurons, the researchers recorded the number of migrating cells at its highest at 1.5 months old and saw it diminish thereafter. The migrating neurons usually become inhibitory interneurons which, to quote the original article, are “like stoplights for other neurons, keeping signaling in check”.

So there you have it! To make sure your baby doesn’t learn that bad word, just suck up all the migrating neurons from its brain!

All jokes aside, this research presents an amazing window into the brain development of the most intelligent species on earth! It’s fascinating how it breaks down psychological mysteries using cellular evidence. And it raises new questions about these mobile neurons: When are they created and how long does it take them to move to the frontal lobe?

How do you think this new research will influence our understanding of the creation of social biases? Do you think this will lead to breakthroughs in research on the foundation of Autism spectrum disorders?  Do you have any funny baby stories? Let me know in the comments.

Our Appetite Uncovered

Researchers in Korea have just taken a major step in the journey towards understanding the patterns of our eating behavior. Scientists at the Daegu Gyeongbuk Institute of Science and Technology have recently discovered the dynamics of the enzyme in our brains that controls our appetite.


Previous research has uncovered that the hypothalamus region in our brain detects levels of glucose and hormones in our blood in order to manage our food intake. To extend these findings, the recent research done in Korea has shown that having low amounts of glucose in the bloodstream activates an enzyme, called adenosine monophosphate-activated protein kinase (AMPK). This enzyme alters the properties of neuropeptides, small protein molecules used by neurons to communicate with each other, using autophagy.

Copyright Nevit Dilmen

Credit Nevit Dilmen

How it Works

When decreased amounts of glucose in the bloodstream are detected, AMPK is stimulated, which diminished the levels of two neurohormones in the brain, neuropeptide Y (NPY) and pro-opiomelanocortin-alpha (POMC). The levels of NPY and POMC are reduced by the process of autophagy, the natural self-destruction mechanism in the body. Decreased amounts of NPY and POMC have been strongly linked to an increase in food intake and obesity.


Research Methods

In orders to trace the complex pathways between the brain and the body to come to these conclusions, researchers conducted experiments using cell lines in vitro and mice. Using the cell lines, researchers were able to record the presence of autophagy under different levels of glucose and activated certain pathways to find the links between the brain and the body. In the mice, researchers injected a virus that eliminated AMPK in the mice’s brains. As a result, the mice ate significantly less than others not injected with the virus.


Combining the results from the cell and mice experiments confirmed that AMPK altered the levels of NPY and POMC, therefore affecting one’s appetite. While these findings are preliminary, they are a significant step in the direction towards completely understanding our eating behavior and may one day lead to solving the obesity epidemic we face today.


More Info:


What is happening to bees?

The media has been buzzing lately about bees! Pesticides and fungicides have long been thought to be problematic for our yellow, fuzzy, pollinator friends, but never more-so then now; 7 species of bees have been officially placed on the US Endangered Species List. In fact, a UN sponsored report revealed that over 40% of pollinator species such as bees and butterflies are facing extinction. This is an incredibly dangerous statistic, as 75% of the world’s food supply depends at least partly on pollination.

This rapid decline is forcing scientists to reexamine the use of pesticides on crops and bee colonies, and begin to think holistically. It’s a concept reminiscent of cancer research, calculating the “exposome,” or the net amount of pesticides an organism is exposed to over its lifetime.

When investigating the health of bees it is important to consider the colony as a single “super-organism” led by the queen bee, rather than individuals. On average, a queen bee will live for around two years, but lately queens haven’t been making it through a single season. Sometimes, the colony is able to replace her, but often they cannot. The loss of a queen can end in death for the entire colony.

Why is this happening?

After following almost a hundred colonies owned by three different beekeepers, for a full agricultural season, researchers from the University of Maryland found a total of 93 different pesticide compounds that came in contact with the bees. Some of these accumulated in wax, pollen and even the bodies of Nurse Bees. After further tests, they found between 5 and 20 different pesticide residues in every sample that exceeded the “hazard quotient”, or amount of a toxin an organism can handle. One surprising finding concerns fungicides, an alternative long thought to have been bee-friendly. In fact, these fungicides tended to have even more deadly effects on Queen Bees.

What can we do?

Ultimately, these findings, coupled with the rapid decline of bee population nationally shows us that we as humans are undeniably at least partly responsible for the decline of bee population. Bees are crucial to our way of life, and we should do everything we can to protect them. By supporting sustainable agriculture practices, and farms that use alternative forms of pest and fungus control, you too can do your part to save the bees.



Tardigrades: the Superheroes of Biology

What is a Tardigrade?

Tardigrades are microscopic caterpillar-like creatures, sometimes called water bears, that are known to survive the extremes. Unfortunately, they look nothing like the Sea Bear from Spongebob, and a lot more like Rufus the Naked Mole Rat from Kim Possible.

Tardigrade (water bear)

Tardigrades are biological superheroes, capable of withstanding near total dehydration and even space vacuums. Tardigrades do something called cryptobiosis– a state in which metabolic activities are slowed and proteins and sugars are synthesized to protect the organism’s cells. This makes it possible for Tardigrades to live in extreme environments where other life forms fail to survive, such as deserts and polar regions.

Why do we care?

Scientists recently discovered a new Tardigrade superpower: Resistance to X-Ray radiation. This survival skill is due to one of the proteins synthesized during cryptobiosis: Dsup. A molecular biologist from the University of Tokyo (Takekazu Kunieda) led an experiment in which cultures of human cells were manipulated to have similar qualities to Tardigrade cells. These new cells were able to reduce radiation damage by 40%.

These new findings open the doors for improving the resistance to radiation in humans. One day, it could be safe for people to withstand extreme radiation, temperatures, or dehydration just like the Tardigrade does. Who would have thought that such a tiny organism had the potential to solve so many problems?


Page 1 of 28

Powered by WordPress & Theme by Anders Norén

Skip to toolbar