Caving at Riverbend Cave (Horne Lake)

Last week-end, armed with a helmet, a head lamp, and wrapped in fleece, I visited Riverbend Cave at Horne Lake Provincial Park on Vancouver Island. The “Extreme Rappel Tour” took us 5 hrs into the cave, where we had to crawl through some very tight spaces, rappel down a seven-story shaft (the Rain Barrel, as it is called), and … little did I know, rock-climb back up the cliff on the way back out.


A few sensations to note about being in a cave... First, it’s cold – is was about 8 degree Celsius on the day we were there. And dark – the only illumination comes from your head lamp, so bring a spare. And surprisingly, it is so damp that the water vapour from our breath stayed floating in the air. Many of the pictures have speckles of water vapour in the frame. A very memorable experience came when we reached the end of the cave, turned off our lamps, and remained silent. We “experienced the cave”; its sounds, smells, feels, and, well, lack of sights. I’ve only ever experienced that level of pitch darkness once before, and that was at the end of a copper mine I visited.

I was rather anxious of the crawling through tight spaces (read: narrow tunnels), but I felt like a kid again and enjoyed that the most. I did come back rather bruised (particularly around the knees) – but I don’t remember making any of these, so it doesn’t matter. Saw a few impressive calcite formations (see pictures – one is of the bacon strips on the ceiling, and the other of me posing at the bottom of the Rain Barrel (the cliff from which we rappelled)). Notably, one was called the “Starship Enterprise”, but seeing the object for which it was named required a lot of imagination. Apparently the delicate cave structures have survived three major earthquakes, which is reassuring given the recent media coverage about how the region is more prone to mega-thrust earthquake than previously suspected.


Few animals to note: just a few insects. The guide told us that he’s seen salamanders a few times, but I did not see them. Apparently the cave used to house bats, but they have been scared away by cave visitors. Given that I am currently preparing a course on Infectious Diseases and that bats keep coming up as a vector or reservoir for many viral and bacterial species that can infect humans, I can’t say I was all too sad. Although, I did stumble upon an interesting article on White Nose Syndrome, a fungus that is infecting many bats in North America and is decimating the bat population. This fungus disrupts the hibernation pattern of bats and causes the bats to spend energy when they should be hibernating. It can even kill the poor little creatures. Upon learning about this disease, I decided that my Infectious Diseases course focused too much on human health. They’ll be a wildlife infectious diseases component now. Every adventure teaches me something that I can bring back to my class….

Infectious Cancers and Other Lessons in Animal Conservation

Tasmanian Devil Facial Tumour Disease

You may recall the Tasmanian devil (of Looney Tunes fame) from your childhood days. It may surprise you to learn that this character is based on a real animal that lives in Tasmania, a large island-state off the southeast coast of Australia. The Tasmanian devil is the world’s largest carnivorous marsupial. It feeds on small preys such as birds, snakes and even insects. They are also scavengers, feasting on carrion. As marsupials, the young develop in a protective pouch like the kangaroo. To me, the devil looks like a cross between a rat and a dog, and it weighs between 10-20 pounds. The animal gets its name for the ferocious cries and growls it emits and the threat displays it produces when faced with a predator, while fighting for mate, or defending a meal. Tasmanian devils often bite one another while fighting, particularly on the face and neck.

In 1996, conservation authorities in Tasmania noticed that some animals had peculiar ulcers on the face. Further investigation determined that the ulcers were cancerous in nature. The tumours grew relatively rapidly, eventually preventing the animal from eating and causing death. Alarmingly, many animals were affected, and now it is estimated that the population has been halved as animals die from this disease. It is estimated that the species could go extinct within the next 25-30 years.

Tasmanian devil with facial cancerBBC Natural History Unit

Infectious Cancer?

This later fact should trouble you for many reasons. First, from a conservation point of view, the disappearance of the largest carnivorous marsupial represents a loss of the biodiversity for the planet. When animals go extinct, they don’t come back. As a molecular biologist, this case concerns me for an entirely different reason. An animal population seems to be decimated by cancer. And not just any form of cancer, but the same type: facial cancer. But wait. How could this be? Cancer isn’t infectious, is it? How is it then that many animals are dying of facial cancer?

Let’s review what cancer is. Cancer could be described as one cell in the body deciding it’s had enough of working “for the good of the group” and becomes a selfish rogue. This cancer cell stops doing whatever its function was (e.g. if it was a lung cell, it stops helping to transport gases in and out of the body), and it starts replicating out of control. There are several other changes that must occur, notably being able to evade the immune system (note: cells in our bodies often become cancerous, but our immune system usually identifies these rogues and kills them before they can do any harm). Finally, cancerous cells detach from the tissue where they formed, and invade the body. If they find their way to the blood or lymph system, they can travel elsewhere in the body, and form tumours somewhere else where they lodge (this is metastasis). Note that there was one source of cancer cells, despite multiple occurrences of tumours in the body. The initial lung cell that became cancerous is now found in your liver, your brain, your stomach, and causes damage in all of these places. Ultimately, the body breaks down because the tumours are impeding the function of normal tissues.

The cancer process that I have described happens inside one animal. There is no transmission to another animal. Transmission between animals is where viruses and bacteria excel. Viruses and bacteria are very small foreign organisms that take over or impede your cells from functioning properly. You have experienced them as flus and cold and other infections. They infect one organism, replicate, and then spread to the next animal, where they cause identical symptoms. Looking at what is happening among the Tasmanian devils, it seems a bacterial or viral agent is at play. Yet when you look at what is causing the disease, it’s clearly cancer. What’s going on?

A solution to this enigma was first proposed in 2006 (1), when it was discovered that the cancerous cells found in the facial tumours of diseased devils all came from the same source. This was identified through chromosomal analysis which confirmed that the cancerous cells in all diseases animals were clones of one another (this was recently confirmed by another study (2)). How could this be? Well, in a way, cancerous cells are very good at replicating and invading other tissues, so it’s not that surprising. What is surprising is that they have spread to other animals. Let’s review a bit of the life history of Tasmanian devils. They often bite one another on the face in fights. Perhaps when an infected animal bit another it left some of its cancerous cells in the wound of the second. Those newly transferred cells then began to replicate and do what cancerous cells do, and the second animal developed cancer. Bingo: infectious cancer!

You should be very alarmed by now. If you have ever come in contact with someone with cancer, have you increased your risk of developing cancer yourself? In fact, in the scientific literature, there is one reported case of a surgeon who inadvertently cut himself while operating on a tumour and did get sick. There are also reports of organ recipients getting cancer from the organs they received, pregnant women transmitting cancer to their unborn child, and twins in the womb exchanging cancerous cells. There is also a report of an unusually infectious venereal cancer in dogs …But these are exceptions, and for a very good reason. Remember that the immune system is very good at recognizing cancerous cells. It’s also very good at recognizing “self” from “non-self” cells, i.e. cells that come from your own body and cells that do not. The general response when the immune system encounters a “non-self” cell is to destroy it. That’s why organs have to be typed and matched in organ donations. If the immune system of the organ recipient recognizes the organ cells as “non-self”, it will attack and destroy the transplanted organ. So, while it is theoretically possible for cancer to be passed between humans, many things have to go wrong for cancer to develop.

So what went wrong in the Tasmanian devils? One hypothesis was that Tasmanian devils are too similar to one another, and their immune system therefore has a hard time differentiating between self and non-self cells. In 2007 (3), a research group demonstrated that this was indeed the case. In the past, the devil population has gone through what is called a bottleneck, meaning that the population dwindled to a very small number. The animals that survived repopulated Tasmanian, but they had to do so with a substantial amount of inbreeding: close relatives were mating with one another. The problem with inbreeding is that the DNA of close relative tends to be very similar. There is not much variation. Effectively, it’s as though the current devil population are nearly identical clones. When a cancerous cell from another animal “infects” their body, their immune system is not able to tell it apart from their own cells, and they are prone to the disease.

So there you have it: the facial tumour disease probably developed in one animal around 1996. Ever since then, the cancerous cells from that one animal have been passed around. They are spread between animals through biting. All animals are vulnerable because they are too genetically similar and their immune system is not able to detect and defend against the cancerous cells.

Lessons Learned

So what are the lessons learned from this case?

First, cancers can be infectious. They don’t tend to be, but under specific sets of circumstances, they could be. Humans have a very diverse set of genes that control the “self” from “non-self” recognition system. In fact, it’s been suggested that the reason it is so diverse is to prevent infectious cancers. So you can rest soundly, this will probably not happen (but there are always exceptions!) in humans.

Second, given the low degree of genetic variability in the devil population, it’s unlikely that the devils will evolve a way to resist the infection. This is another reason why a large amount of animals need to be protected when establishing conservation strategies. If there aren’t enough animals protected and preserved, there is not enough genetic diversity, and inbreeding will cause this (and other) problems that threaten the viability of the species.

References

1. Pearse Am, and K Swift (2006). Transmission of devil facial-tumour disease. Nature 439:549.
2. Murchison Ep, Tovar C, Hsu A, et al (2010). The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer. Science 327:84-87.
3. Siddle HV, Kreiss A, Eldridge MDB et al (2007). Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial. PNAS 104(41): 16221-16226.

Silicon to be Replaced by Proteins?

I’m revamping my Molecular Biology course and have stumbled upon a few interesting nanotechnology topics that might be of interest to some people…

A few years ago, I attended a very interesting lecture about the use of biological molecules in building computers. Why, you might ask, would you want to use biological molecules to build computers? The answer is that biological molecules are small – typically on the order of nanoscale (one millionth of a millimeter), whereas most silicon-based chips are at the microscale (one thousands of a millimeter). Thus, if we could use proteins and DNA to build the logic gates and memory circuitry, we could miniaturize computers by at least 1,000 fold. This could have many applications, not the least of which are medical applications. Think of injecting small robots into your bloodstream that are autonomous and can direct themselves to the appropriate location, execute repairs, and leave your body without the intervention of surgeons. It gives a whole new meaning to “take two pills and call me in the morning”.

DNA seems a very likely candidate for building logic gates, and perhaps I’ll discuss them here soon. In the meantime, I just wanted to mention the potential of proteins in serving in memory chips. Proteins are the workhorses in your body. They do everything from digesting bread, to synthesizing fats from ingested sugars, to pigmenting your skin, to making up the bulk of your hair.

One protein in particular, rhodopsin, has attracted a lot of attention for its nanotechnology potential. Rhodopsin is a protein found in your eyes. It is found at the back of the eye and serves as a sensor for light of a specific wavelength (i.e. colour). When light of a specific colour strikes rhodopsin, it causes the protein to change its shape. This change generates a signal that your nervous system interprets as the perception of light or colour. The critical property of this protein is that it can exist in one of two forms, one when it has been hit by light of a certain colour, and another in the absence of light.

Now think of a small cube, maybe 1cm by 1 cm by 1cm that you fill with an ordered array of rhodopsin. You know where each molecule of rhodopsin is in this cube. Each molecule of rhodopsin is tiny – so tiny in fact that we know its atomic composition in great detail. Each molecule lives at a particular place in the cube, and it exists in one of two shapes. Since each rhodopsin lives at a certain fixed physical address, you can shine a laser (i.e. light of a specific wavelength) at that spot and change the shape of one specific rhodopsin molecule in the cube.

Does this start to sound a little bit like the memory of a computer? A memory chip (or a CD or DVD for that matter) is simply a material on which there are several “cells” that live at specific addresses and that exist in one of two states: ON or OFF, or another way of thinking about it is 1 and 0 (the famous binary code). Typically, each of these cells is microscopic.

Hopefully, you see the parallel with the cube of rhodopsin. It’s the same thing, except that the rhodopsin cube encodes the information at a 1,000 fold smaller scale. So for a similar sized disk, you could encode 1 meg of information with silicon technology, or 1 gig of information with biological nanotechnology.

A few issues remain to be worked out. How to “reset” the protein once you have changed its shape, for example. However, this technology is very promising…

Migratory Bird Watch

I know that I said that my next post would be about one of the many topics we discussed in my Molecular Biology course last month, however, something’s come up. Last Wednesday, I played hooky with the two resident ecologists at the University and we went to the George C. Reifel Migratory Bird Sanctuary in Delta, BC, Canada. My colleagues were investigating the area as a potential site for a field trip for their ecology course. My excuse was that I have to oversee everything for the life sciences courses (haha – what a thinly veiled excuse for playing hooky!). The snow geese were said to be in town, and lured by the prospect of a sighting or two (or a thousand), we headed to Delta.

It was a delightful day, not least of which was due to the fantastic weather we enjoyed. This was my third visit to the Reifel Sanctuary. This time, I was accompanied by bird watchers. If you have the opportunity, it’s really worthwhile to visit this site with people who love birds. Not only will they point out where the birds are (you are very likely to miss out if you are not an avid birder), but they will also tell you about the natural history of each species, and (this turned out to be important for my personal safety) which birds have a mean temper and that you should keep a safe distance from…

We saw many bird species. Bald eagles, sand hill cranes, snow geese, mallard ducks, more mallard ducks, still more mallard ducks, wood ducks, other ducks I could not name, blue herons, some other type of heron that was perched on a tree, chickadees, pigeons, coots, hawks, red robins, trumpet swans, and others I could not name. No owls (although we were told they were on site). And most impressive of all, the sky was FILLED with migrating birds. There’s a constant background noise made by the migrating flocks of birds that’s quite soothing.

All and all, a very good day, and I recommend it to all… I think Nobi and Mai have decided to bring their students there for their ecology courses in the coming months… I wonder if there’s any way to link this to Molecular Biology somehow? Why should they have all the fun?

Biology to return...soon

... Just posted a new entry on the MacLeans.ca OnCampus Blog , on the merits of using case study pedagogy in the science classroom (image to the left shows some of my students working through a case study).

As I now have some time to update my blogs (having recently finished teaching a Molecular Biology course), you can soon expect some entries in this blog on biological topics... I plan to do a little piece on phage therapy, golden rice, and HIV/AIDS, three topics that generates lots of discussion in my classroom...

Coming soon!

Community Day – The best way to freshen up a course is to cancel class

I was recently invited to contribute to a blog for MacLeans.ca On Campus. This blog, written by a group of 5 university professors, is a place where "A varied group of professors and education researchers come together to discuss their experiences teaching and how to improve the undergraduate experience." Yesterday, I made my first contribution.

Quest University had its first Community Day of the academic year yesterday, and I wanted to write about our experiences. My blog entry is reproduced here, for your reading pleasure...

One day each term, when the students least expect it, all classes are canceled at Quest University Canada. These days are called “Community Days”. We just had a Community Day today.

I would love to claim this was our idea, but it was inspired by a similar event that takes place at the Lester B. Pearson United World College of the Pacific near Victoria BC (an innovative international high school). What’s the goal of this Community Day? It’s threefold.

First, sometimes you just need a break. Quest teaches on the fast-paced block scheduling plan. Students take one course at a time, 3 hrs each day, for 3 ½ weeks. It is an intensive way to learn: students must stay on task and manage their time effectively because assignment due dates come up fast, and before you know it the course is over. You need a breather, a chance to revitalize, interact informally with all students and faculty, not just the ones in your 20-student class.

Second, it promotes student interactions. The morning schedule of a typical Community Day consists of team building and leadership exercises, preferably outdoors. Some of the activities today included trust exercises and the raising of a student-made Quest flag (we first had to dig a hole, then carry a tree log up a hill, then raise the log and stabilize it with ropes once it stood reasonably erect). Oh, I know – a lot of you are probably rolling your eyes, covering your mouth and thinking “and they call this a university? What’s the academic merit of doing that?”. I probably would have been right there with you a few years ago. Sure, it’s unorthodox. But having seen its effects in the classroom first hand, I am now a convert.

Do you know what happens when you set up a situation where students must bond, trust one another, exercise leadership abilities and have fun together? Do you know what happens when you then put them together in a 20-student classroom and ask them to contribute to a class discussion?

You cannot shut them up!

They feel comfortable with one another, they trust that their peers (and their teacher) will accept them, and they do not fear being ridiculed. A non-academic activity goes a long way towards improving the academic quality of my classroom. I’ll sacrifice a day of class any day if it means that the questions and insights that are shared and asked in my classroom are more numerous, more honest, more in-depth, and are contributed by a larger percentage of the students.

Third, the afternoons of a Community Day are generally spent asking for the students’ input on building this university. Quest opened its doors to students a mere 13 months ago. A lot of its policies, practices, and even its identity are currently being developed. The philosophy at Quest is that students wouldn’t be told what to do: study this course and that – they would be active participants in their own education. They are guided through the design of their own degree. They also contribute in building this university. Today, the topics under discussion were student admission, student retention, fundraising (since we are a private non-profit institution), energy-conservation on campus, and student life. It’s amazing what different perspectives students can have on an issue than faculty. It was very refreshing to hear their take on what matters. And they also provided tons of ideas for improving this place.

At the end of the day, when the Community Day is over, you get buy-in. You get the sense that Quest belongs to all of us. That we each have a hand in shaping it. That we are not a number but an important member of a community. That this place is special. It re-infuses energy into all students and faculty and into every classroom. And at the end of the day, we are all reminded that there is no other place we would rather be.

So now you decide – wasn’t a day of “fluff” a valuable part of a student’s education?

Sky Diving - Why Would a Brain Want to Do Such a Thing?

Sky diving was a very cool experience, and I suspect some more may be in my future (and yes, that's me jumping out at 10,000 feet).... But let's ask the question: why would anyone want to jump out of a flying plane, at 10,000 feet of altitude? The answer, of course, is complex. However, we do know something about the brain's reward circuitry. The reward centre of the brain (ventral tegmental area, nucleus accumbens, and others) are a part of the brain that functions to make an individual survive, and reward the person when he or she does something good for survival. Typically, this is sex or food, that kind of thing. Cells in this part of the brain talk to each other by releasing a chemical called dopamine. So whenever you do something good for survival, dopamine gets released in the reward centre, making a person "feel good", and that much more likely to repeat the behaviour that caused the release of dopamine in the first place.

Incidently, novel activities cause the releas of dopamine in that part of the brain. So we enjoy doing things that are new and different. We don't want to overload that system, but novelty is something we appreciate.

Drugs of addiction are addictive because they stimulate that part of the brain: they potentiate (increase) the release of dopamine in the reward centre. So drugs of addiction take over the control of a portion of the brain designed to reward an animal for certain behaviours. It's easy to see how such drugs become addictive: the brain "feels good" each time you take them and makes the person much more likely to repeat the behaviour (i.e. drug taking) that caused the release of dopamine in that part of the brain.

It turns out that some people are less sensitive to dopamine in that area of the brain. Some people have "mutant" D4DR dopamine receptors. By the way, this is not unusual in and of itself: we all have different varieties of different genes in our body - if we didn't, we would all be clones and look identical. However, what has been observed is that people who have the mutat D4DR receptor in the brain tend to score higher on sensation-seeking personality traits (Note: this is not a necessary relationship, it's only a "more likely" type of a relationship). In otherwords, we have noted a correlation between the "adrenaline junky" personality type and havingD4DR receptors in the brain. If you take a moment, you will realize that this makes sense. If you brain is a little insensitive to dopamine, it will take a larger stimulation for your brain to respond to the dopamine release. So a person with a D4DR dopamine receptor needs to experience "stronger sensations" to "fell as good" as a person with the "normal" version of the dopamine receptor to feel.

Incindently, people who score high on the novelty-seeking trait tend to also have a greater likelihood of developing a drug addiction. Part of the reason is that they are simply more likely to try the drug in the first place. Part of the reason is that if they have a brain that is insensitive to dopamine (D4DR receptors) , and they have access to a chemical that is likely to stimulate their brain to levels comparable to what other people experience daily for doing "simple" activities such as eating food and having sex. So in effect, these people are more likely to use drugs of addiction because it allows them to regulate ther dopamine levels and experience "feeling good" to levels comparable to those of controls. That's the theory, anyways.

Based on my past history of SCUBA diving and now sky diving, I suspect I have D4DR receptors in my brain. This is only a guess, based on the noted association between personality trait and dopamine receptor type. I don't know for sure.

If you want to see how you score on this persoanlity trait, you can take this Sensation-Seeking quiz at the BBC website. Obviously, this is not an "official" study of your brain, this is for recreational purposes only.

For those of you out here without this trait, I leave you with this video of my jump... Live vicariously through me!