Author: jmckenna

Life Finds A Way

Welcome to Jurassic Park! Or welcome to 2022 Australia where we are simultaneously expanding our fossil fuel projects to the equivalent of 200 new coal power stations and trying to bring back the Tasmanian Tiger (Thylacine) from extinction. Quite the paradox, isn’t it?

Big, grand ideas like de-extinction divert us from the terrors of the world and make us reminisce about happier past times – whether they’re realistic or not. Science is remarkable in that it constantly walks the uphill battle of convincing people that we ARE capable of doing the impossible. To reach the unreachable. People laughed when we dreamed of going to the moon or curing polio – until we did precisely that. A little bit of faith (and A LOT of money) can go a long way. 

So, could we make our Jurassic Park dreams a reality? What if we could bring Thylacine back from the dead? How would we do it? Or, a better question… Should we? Well, hold onto your butts, because I’m about to dive into de-extinction and whether I *think* we can and should bring Thylacine back from the dead.

The Jurassic Park Method
You’re probably all quite familiar with de-extinction thanks to Jurassic Park, but there are a few different iterations and techniques involved with bringing something back from the dead. The Jurassic Park method involves extracting DNA from dinosaur blood sucked up by a mosquito (which was conveniently frozen/preserved in fossilised amber) and then combining that DNA with frog DNA to ‘fill in the gaps’, then implanting that frog/dinosaur hybrid DNA into an ostrich egg.

Sound simple? Although I love #simplescience, this is highly, highly unlikely to create a living, breathing dinosaur. Anybody experienced with DNA extraction, purification and amplification will tell you that, in reality, these processes are incredibly sensitive, and geneticists are scared to even breathe near a sample in fear of contaminating it with their own DNA (but that’s Hollywood!). So, there are definitely some limitations with what they’ve claimed, but, hey, that’s science fiction – They’re supposed to stretch what is scientifically possible, so we can’t fault them for having an imagination, but I’m going to anyway.

Firstly, the DNA that the scientists would have extracted would only be a tiny fraction of the DNA that’s inside that mosquito. Imagine how many other dinosaurs that mosquito had bitten, and how many times the blood was mixed with that of other dinosaurs or even different species of dinosaurs, not to mention the mosquito’s own DNA complicating things. Ever tried to pick out just the carrot from a bolognese? Or just the salt from a chicken soup?

It’s incredibly unlikely that the DNA is pure enough to represent a single dinosaur species reliably. But, for argument’s sake, let’s assume the DNA they extracted was pure velociraptor DNA. Why did they mix it with frog DNA? Well, enter problem number two.

To bring an animal back from the dead, you need a complete genome. However, more often than not (and in the case of Jurassic Park), the recovered/extracted DNA is incomplete or damaged. So, you can either use the DNA of the same species (ideal) or a closely related species to fill in the gaps/replace the damaged parts – but a frog? Really? How closely related are frogs to dinosaurs? Not very.

We’ve known for quite a while now that modern-day birds are actually the closest living relatives of dinosaurs. I mean, look at that cassowary – does that NOT look like a dinosaur? Dr Wu and his Jurassic Park scientists must have some rhyme and reason for using frogs instead of birds, but maybe they forgot about birds. Wait, no, they didn’t. Because after creating a dinosaur-frog hybrid, they then implanted that DNA into an ostrich egg… Why did they use frog DNA (besides apparently allowing the female dinosaurs to change sex/breed) instead of ostrich DNA? Beats me…

Anyway, coming back to this mixing of DNA. While filling in the gaps of damaged or missing DNA is a completely valid technique, the odds that the velociraptor DNA they’re playing with isn’t completely degraded after the ~80MILLION years of being stuck inside a mosquito is probably the biggest bone I have to pick with Dr Wu (we’ll leave John Hammond out of this, because you can’t be mad at the guy).

Over time, the hydrogen bonds that hold DNA bases together break down, making it very difficult to read and interpret. So, the ‘gaps’ they’re talking about are more like yearning chasms of missing/damaged DNA instead of a few potholes in the road. How do we know where the DNA that’s missing fits into the genome, and in what order? Well, without an appropriate template to compare against, we don’t. Imagine trying to piece back a book that’s been through the shredder; the pieces are there, but the order is almost impossible to figure out.

SO. Impure DNA samples, large areas of missing/damaged DNA, and inappropriate template species DNA are working in tandem to NOT bring back a velociraptor (sad face). So, a science-fiction movie is exactly that… Science fiction (no surprises there). But how does this relate to Thylacine? Could we use the same ideas from Jurassic Park with modern-day science tech to make it a reality? Possibly.

Thylacine History
The last known living Thylacine died less than 100 years ago in 1936 in Beaumaris Zoo, Tasmania. Excessive hunting and poaching drove the already at-risk species to extinction, but other factors like urbanisation and disease may have also played a role in the iconic species’ demise. So, once again, it’s our fault that something beautiful is no longer around.

However, in evolutionary terms, 100 years is a minor blip. Thylacine’s extinction is so recent, that scientists have managed to collect quite a lot of very valuable tissue from several different animals, and kept it in pretty good condition, too.

Thylacine was also an apex predator that filled an extremely important niche in the food chain and helped provide balance and stability to the local ecosystems. Since their extinction, the habitat in Tasmania has remained relatively unchanged – meaning reintroduction may not be so farfetched and it may be able to reoccupy its niche.

So, we’ve got some well-preserved tissue, we’ve sort of got the environment for it to go back into, but do we have the tech? Not quite, but we’re well on our way to having it.

How Will We Bring Them Back?
Well, very similar to how the dinosaurs were fictitiously brought back! Find some good quality DNA, tweak it with that of a closely related species, and then transfer that DNA into a host species egg (an ostrich in Jurassic Park, more like a Tasmanian Devil for Thylacine) for it to grow and gestate – Once again, sounds simple, doesn’t it? Remember, #scienceisneverthatsimple.

A research lab at the University of Melbourne is leading the way in bringing Thylacine back from extinction and has already made some headway in defining some of those very complex protocols and techniques. Essentially, the team have broken it down into 3 broad steps: 1) Fully sequence the Thylacine genome and one of its closest relatives (in this case, that’s the fat-tailed dunnart), 2) define protocols to grow and culture Thylacine stem cells, and 3) develop the reproductive techniques like enucleating oocytes, embryo culture and transfers to put the icing on the de-extinction cake. These are all very standard laboratory techniques, but marsupials present with some extremely unique biology and hurdles to overcome when it comes to reproduction.

Thankfully, scientists have already ticked off the first step of sequencing Thylacine and dunnart genomes, and are currently working on ways to grow and culture marsupial stem cells. But, unfortunately, that is where the story ends… for now. But this gives us a chance to ponder and reflect if this is something we should be doing in the first place.

What’s the Right Choice?
I definitely don’t pretend to be an ethicist/bioethicist, and it is a lot more complicated than I, and many others, give it credit for. But, it’s hard not to think about other research or different conservation efforts that we could be working on and funding instead of bringing back a species that we killed off. After all, “genomes don’t save species, only habitat and protection do.”

Would it not be more prudent to prevent other, extant species from going extinct instead of putting all of our extremely valuable time and resources into an immensely difficult endeavour that may not be the *right* decision for conservation/ecology? Let’s say we do bring back a Thylacine, and we get some adorable stripey babies and the world oohs and aahs over how cute they are and what an incredible achievement it is for science. Well, we’ve actually done this before in different species… And it didn’t really go down very well.

The Pyrenean Ibex was brought back from extinction about 20 years ago and, and was the first species in the world to have been de-extincted – and then, 7 minutes later, re-extincted itself again. We’ve also cloned several different animal species before. The most famous of which would be Dolly the sheep, but we’ve also cloned mice from tissue frozen for more than 16 years, and black-footed ferrets from tissue frozen for more than 35 years – genuinely incredible stuff. However, while cloning and de-extinction are similar, they are not exactly the same, and we know a HECK of a lot more about mouse genetics and biology than we do about an already-extinct Thylacine.

Let’s say we do bring Thylacine back, and they do live a long, healthy life. What do we do with one animal? To be a reproductively viable and ecologically impactful species, you need ~500-1000 individuals (or 40 generations worth), and how in the world are we going to make that many unique individuals? How long would that take, and is this really how we should approach conservation issues – Being reactive instead of proactive? If de-extinction does work, and we can bring species back from the dead, we will risk becoming ambivalent to species extinction because we can simply bring them back later, rather than fixing the environmental or societal pressures that led to their demise in the first place.

I’ve been pretty doom and gloom so far about how ‘experimental’ research like this got funded, how difficult it will be to bring them back, and how to manage them once/if they ARE Back. But, I’ll briefly play devil’s advocate for my own arguments…

What isn’t experimental research? How do we know what will & won’t work until it’s done? The very essence of science is going where nobody has gone before – whether the likelihood of success is high or low is irrelevant. Also, the process of de-extincting a species does not happen in isolation; research is inherently collaborative and de-extinction is no different with geneticists, evolutionary biologists, immunologists, and reproductive biologists all having a say and a role to play. That means knowledge sharing, honing of techniques, and expertise developed; aspects of research that are beneficial not just for this singular species, but for other, related species as well. And, at the end of the day, if we have the staff, equipment, and funding to attempt de-extinction… why not try?

While we don’t quite have the answers yet, that’s why science and nature are so fascinating. They are in a constant state of motion: continually evolving and adjusting to deal with whatever the world has to throw at them. We may not have the answers to these complex questions now, but we will soon. After all, if there is anything evolution has taught us, it’s that life is resilient. Malleable. Sometimes, life, uh, finds a way.

Fantastic Phalluses and Where to Find Them

Mother nature has a way of creating a mind-boggling amount of diversity, and animal genitalia is no exception. So, yes, this blog is going to be all about the male appendage: THE PENIS. Big ones, small ones, spikey ones, the four-headed ones – nothing is off-limits.

The idea behind this article actually stems from the second year of my PhD during our weekly (very boring) meetings where we took turns presenting our own or a new piece of relevant research. Instead of talking about the spatiotemporal expression of Interleukin-11 and Forkhead Box Protein 1 throughout the murine endometrium, I decided to talk about penis diversity (naturally).

Hopefully, by talking about penises in a somewhat scientific way, you can come away having learned something about evolution and biology. So, grab the popcorn, sit back, and try to contain the giggles because there will be pictures and there will be puns.

Let’s get the big ones out of the way. The obvious contenders for the largest penises in the natural world are the whales, and coming in at first place is a tie between blue whales and humpback whales at a shuddering 3 METRES long making it as long as a Christmas tree is tall…

Let’s now bring in some of the largest land mammals: Gorillas. Weighing in around 180-250kg, gorillas got pretty shafted in the penis world sporting a 1-2inch penis – maybe good things come in small packages?

The next animals on the list of mighty members are barnacles. Yup. Barnacles. Barnacles spend their entire life sucked onto a rock, a boat, or even a whale, making it pretty hard to find a mate. Unless of course you have the longest penis to body size ratio of any species on the planet. In which case, it’s not so bad. With a penis about 8 times the length of their body, that would make a blue whale’s penis around 220m long or about the size of a 60-70 story building. Clearly, that would be a pretty impractical prick, but for a barnacle, it’s the perfect sexual adaption to its environment. This is called environmental or phenotypical plasticity where animals evolve to live and function better in their environment. Go, barnacle boy!

However, this isn’t the only way animals can evolve. Another cool evolutionary tidbit is something called convergent evolution – where two distantly related animals independently evolve similar traits to adapt to a similar necessity, e.g sex.

Convergent evolution – Baculums
Lucky for you, I’ve got two pretty crude penis examples of this (you’re welcome).

The series of white structures are called baculums, or colloquially known as penis bones (where the term boner came from!). Quite a lot of animals have baculums and they span through almost the entire animal kingdom: Mice, bats, walruses, and even the mighty gorilla with its 1-inch member. So, what’s the point? Why on Earth would mice and gorillas both need a penis bone? No, it’s not an evolutionary cock-up. Animals evolve out of necessity, not by mistake.

It’s actually quite a big area of research and scientists have pumped out a tonne of papers trying to explain why constantly having morning wood is better than turning it on and off again.

There are 3 main theories out there:
– Protect the penis from damage
– To allow for longer mating durations, thus less time for other males to mate with the lucky female
– Overcome issues with blood pressure or ‘not getting it up’

All seem to make quite a bit of sense, and all do solve some sort of issue within each species – it just turns out that evolving to have a penis bone was the solution. That wasn’t so hard now, was it?

Convergent evolution – Penile spines
Yes, those are penises, and, also yes, those are spines on the shaft. OUCH.

If anybody is wincing at the idea of spikey penis sex, you’re not alone. But, like penis bones, penile spines have their own bizarre purpose in the world of animal sex. Felids, wombats, and some snakes have penile spines and there are a few theories, but, to be honest, they’re largely misunderstood little pricks.

However, we do know why and how they work in felids, and why queens (love how that’s the actual term for a female cat) often scream, hiss, and fight their way away from a male during mating. Seminal research in cats proved they are induced ovulators, which means mating is required for queens to ovulate. I.E those penile spines prick the superficial layer of the vagina and send a signal to the brain and ovaries to release an egg – can’t have one without the other. So what about wombats and snakes? Well, it could be that those spines scrape out a rival’s sperm or copulatory plugs (coagulated semen) to increase the chance of ‘reproductive success’ – but we’re still not entirely sure.

So that’s an intro into the confusing, but wonderful world of animal penises. But it’s nothing compared to what I’ve got coming up next… Let’s get into the REALLY WEIRD penises.

Two sides of the coin

I would be remiss if I didn’t at least mention the female side of things. Penises, although hilariously diverse, are only half the conversation, and there are some astounding differences in female reproductive tracts throughout the animal kingdom, too. However, I’m going to leave that one up to all of you, because my search history is already a bit iffy after googling penis a dozen different ways and reading papers all about how penises work (my recommended ads are very interesting, I can assure you).

If you’re up to the challenge, have a read about the kangaroo’s three vaginas, the two (but only one functional) uterine horns and ovaries of the platypus, or even the elephant vagina, which is about ~1.5METRES away from the vulva.

FASCINATING.

Crisp Genes

Imagine we had the power to use genetic technologies to stop one of humanity’s most dangerous predators. What is that predator? Sharks? Crocodiles? Snakes? Think far, far smaller. It is in fact, the mosquito.

Mosquitos cause all sorts of nasty diseases like the Zika Virus, Dengue Fever, Yellow Fever, and Malaria. While nobody really wants to contract any of those diseases, and they’ll all make you pretty miserable, they’re nothing compared to the frankly hellacious Malaria being one of the single biggest killers of humans in history.

Well, plot twist, we actually do have the technology and it comes in the form of some genetic machinery discovered in bacteria: CRISPR-Cas9 (or CRISPR for short).

What is CRISPR-CAS9?

Basically, there’s a protein that acts like pair of scissors able to cut DNA (the CAS9 part), and a length of RNA that directs the protein to any point in the genome that you want (the CRISPR part).

Once that cut is made, the DNA can either stitch itself back together with the cut section of the DNA now removed from the genome (called homologous end joining), or that break can be filled by a new sequence of DNA by providing the cell with a template or a recipe so it can make the new gene the scientists are interested in. Essentially, CRISPR is a mix of cutting and pasting that happens inside our cells instead of Microsoft Word.

So, we just need to CRISPR some mosquitos and they won’t be able to carry the malaria-causing parasite (called plasmodium); problem solved. Well, obviously it’s not that simple, and that’s because of the way genes are inherited.

Thanks, meiosis.

Here comes a crash course in meiosis and gene inheritance (thanks for getting me through undergrad, Hank Green). Most genes have two copies (one inherited from each parent), so when those genes are passed down from one generation to another, there’s only a 50:50 chance that a given gene variant (called an allele) will be expressed by the offspring. In essence, if you CRISPR a mosquito (the white mosquito in the image) so it can’t carry plasmodium, statistically, half of its offspring will still be able to carry it, and half won’t. In just two generations, the plasmodium-immune mosquitos only represent 25% of the population. Back to the drawing board, scientists!

Well, it would be if they didn’t already have a solution to this problem: Insert gene drive.

Gene drive forces the new allele to become dominant over the other allele, thus making inheritance of the plasmodium-immunity allele 99.5% rather than 50% – Tada!

While CRISPR tech has only been around for roughly a decade, gene drive was actually proven to work with 100% efficacy in a 2018 study. So, I hear you asking… Why haven’t we done it yet? Why do we still have Malaria?

Playing God

The COVID-19 pandemic has proven to the world how quickly science can move when given the proper funding, resources, and attention. However, the ethics and policies behind a lot of scientific discoveries and applications often lag far behind.

Also, humans have never edited the genome of another living organism on this scale before, and once we do it, there’s no going back. So, should we even do this? What are the implications of using CRISPR on mosquitos? Will plasmodium evolve into an even scarier, more deadly version of itself, or will it just find another host? Well, scientists are optimistic as the change to the mosquito genome is very minor, and mosquitos breed so rapidly that plasmodium won’t have time to evolve. We hope…

Scientific modelling can provide a lot of guesses on what could or is likely to happen, but we just won’t know until it’s done. Clearly, there’s still a lot of debate and uncertainty out there, and technology as powerful as gene drive needs to be handled with a lot of care and its ethical considerations heavily scrutinised. However, we also have to ask ourselves if it’s unethical to not use this technology while it’s available when 1,000 children die every day from the disease.

So, until the world can come up with a decision, for now, at least, scientists have their scissors locked away in the top drawer until they’re safe enough to use.

Wormholes: The Ubers Of The Universe

It’s no secret that Albert Einstein was a pretty smart dude. His theory of general relativity flipped physics on its head and changed the way we think about the fundamental concepts of the universe. While he proposed a lot of solutions with this theory, he also left us with some pretty big questions and mysteries. One of those mysteries was wormholes. While they may be ‘theoretically possible’, do they actually exist? Just because something is theoretically possible, doesn’t mean that it actually has to happen, or ever will happen. After all, it’s theoretically possible for me to hit a hole-in-one every time I play golf, but do I? No. Have I ever? Also no.

Either way, let’s delve into what wormholes are, how they’re made, and where we might find them.

General relativity
Einstein’s theory states that the universe is made up of an interwoven fabric of space and time together (called spacetime); you can’t have one without the other. If I wanted to meet my friends at a bar on Friday night, I would need to know where (the space aspect) and when to meet up (the time aspect), otherwise we’ll never meet and I’ll end up drinking alone.

Einstein also argued that anything with mass will warp or bend the spacetime around it. Let’s use a bowling ball as an example. Imagine putting a bowling ball on a waterbed. The ball would ‘sink’ into the bed, bending the fabric of the waterbed around it and anything in the vicinity would fall towards the bowling ball – this is how gravity works according to this theory, but check out this video if you’re more of a visual learner like myself. So that’s Einstein’s incredibly complex theory of general relativity explained in two paragraphs. However, there are some other possible outcomes to this theory that were completely mysterious and are still quite mysterious to this day. One of those answers is black holes (I promise this will all make sense soon).

Black holes
They’re the most powerful and some of the most misunderstood things in the universe. Black holes are areas in space where there is so much mass concentrated in one area, that spacetime is warped so much that literally nothing can escape, not even light (hence why they appear black).

Black holes are formed after a star dies and has exploded its guts throughout the universe (called a supernova). Whatever’s left, is pulled so rapidly, and so violently towards the star’s core (at about 1/4 the speed of light), that, if the star is massive enough, a black hole will form. To help understand how dense black holes are, as an example, if a black hole were to form with the mass of the earth, it would be no wider than 2cm in diameter (gasp!). But black holes can, very scarily, be far, FAR bigger than this…

The tricky thing with studying black holes is that we can’t exactly peer inside of them very easily. After you cross a certain distance away from the core of the black hole, an area called the event horizon, there is no turning back. This makes finding out what’s past that point almost impossible. Again, I’ll point to the visual scicomm kings, kurzgesagt in a nutshell, for a video on the life and death of black holes.

So what’s this got to do with wormholes? Well, just as black holes are possible within the laws of general relativity, there are also theoretically white holes, too. Scientists can get so creative with names, can’t they? If a black hole is a point where spacetime is warped so much that nothing can escape, then a white hole is a point where nothing can enter – essentially an area where gravity is flipped and pushes things away, rather than sucks them in. And this is where we may have our potential source of a wormhole.

Einstein-Rosen Bridge
In the 1930s, Einstein teamed up with another physicist, Nathan Rosen, to expand on this theory of black and white holes and proposed the existence of bridges between the two from one point in the universe to another – which they called Einstein-Rosen Bridges. These bridges quickly became colloquially known as wormholes where one end sucks you in from point A, the other spits you out at point B.

So, if we jump inside of a black hole (which I couldn’t recommend less unless you would like to be ‘spaghettified’ – it’s a real word scientists use, trust me), and we reach the wormhole, what’s next? Can I just meander on through until the white hole pulls me through the other side to the bar where my friends are waiting for me? Well, probably not. General relativity also says that wormholes are incredibly unstable and would collapse very quickly compressing us completely out of existence. So, how could we keep them open?

Riding the worm
I just want to say physics is very hard and confusing, so if you’ve kept up with me so far, thank you for your persistence. But, I’m also sorry because I’m about to make it a bit more confusing by introducing something SUPER weird: Exotic matter. Unlike everything else in the universe, exotic matter (if it even exists) has negative mass and negative gravity. This means exotic matter is inherently repulsive and may be able to prevent gravity from closing the wormhole (or from people getting in my personal space, which I’m a fan of). So, we grab some exotic matter, strap it to the inside of a wormhole, and jump in. Then what? Well, that’s where the science sort of stops, and the science fiction begins (if it hasn’t already). If the wormhole can safely connect two points within our universe, then I guess I’m never taking an uber again. But if it opens a pathway between two universes (yup, there could be more than one), well then who knows what could be on the other side – spoiler alert, it’s probably death.

So, until we can find a real-life wormhole, they’ll exist only in theory and in the movies where Matthew McConaughey falls through blackholes ending up in interdimensional time libraries – Personally, I’d prefer the bar.

Why Is There Still No Cure For Cancer?

Cancer: The sexiest of the diseases.
No, I don’t mean literally, but if anybody says they work in cancer research, you’re almost obligated to reply with a ‘wooow that’s amazing.’ As opposed to renal disease, asthma, or diabetes which get a rather underwhelming ‘oh, that’s cool.’

Over about a century of research, billions of dollars have been poured into finding the cure for cancer, so why don’t we have one? We could make COVID-19 vaccines in less than a year, so why don’t we have a ‘cancer vaccine’? Are scientists just hoarding our hard-earned tax dollars and making sharks with friggin laser beams attached to their friggin heads instead? Hopefully, you’ve picked up on my sarcasm by now, but the answer is unequivocally and unquestionably no.

The unfortunate reality is, cancer is responsible for one in six deaths globally, and is unlike any other disease we know of. It presents in hundreds of different forms, and is incredibly difficult to understand, study, and treat.

So, what is cancer, and what makes a cell cancerous?

Cancer, unlike many other diseases, is not a foreign pathogen invading the body using you as their pawn in the evolutionary war of ‘which superbug will reign supreme?’ Cancer is actually a mass of our own cells that, for one reason or another, have uncontrolled cell growth and division, inadequate or non-functioning cell death mechanisms, and the ability to rapidly acquire genetic mutations. Amazingly, cancerous cells can mutate so rapidly, that there is more genetic variation between two types of cancers (lung vs kidney, for example), than there are between two people – so much for one disease, one cure, right?

Cell biology, being the wondrously and at times incomprehensibly complicated field, has proven there are countless ways DNA could be damaged or mutated, meaning there are many, many different ways a tumour could form. Being a very individual-specific disease, those DNA mutations could have arisen through a completely different pathway between two people, even though they have the same type of cancer. Also, there are only about 2-5 genes (called oncogenes) that actually make us susceptible to cancer out of the roughly 20,000 that make up the human genome. So if only 0.01% of our genes make us susceptible to cancer, why does it happen so frequently, and how in the world do we treat or prevent it from happening?

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Our cells replicate and divide throughout our entire life, and it’s not a perfect process. Mutations accumulate pretty frequently but are often recognised by the cell itself, or by the immune system. If those mutations are harmful, those cells are targeted for destruction (apoptosis), but if they’re harmless, then the cell may continue to function normally. However, when it goes unchecked, that’s when cancer can form.

Thankfully, we know quite a lot about the path from genetic mutation to tumour growth – lung cancer is a great example. A lot of lung cancer-causing mutations are tightly linked to smoking cigarettes, and some of the treatment options can be tailored quite ‘easily’ depending on your smoking history.

Chemotherapy, a form of systemic cancer treatment, is a common treatment method for various types of cancers. By targeting rapidly diving cells, which cancer definitely is, chemo (for the most part) targets cancer cells, leaving the majority of your cells happy and intact. Of course, I say this with a degree of caution, because chemo has plenty of side effects, and often targets other non-cancerous, rapidly diving cells such as hair follicles and germ cells. And that’s the tradeoff with chemotherapy – it’s about finding the right Achilles heel for the right cancer in the right patient.

Another treatment option is to target the protein, that the mutated cancer gene produced. Here’s the theory: If gene X codes for protein X, and protein X prevents the cell from undergoing apoptosis, then perhaps a vaccine targeting and inhibiting protein X will prevent those cells from becoming cancerous. Research is ongoing in this area, and some inhibitors have been found, which are currently undergoing clinical trials.

While oncologists have several treatment options, they are hardly as cancer-specific as we’d like them to be. If we remind ourselves of how rapidly cancers can divide and mutate, they can also move throughout the body (a process known as metastasis; check out this great TED-ed talk on metastasis), which can then change the treatment regime. Once the cancer has moved from say the ovary to the liver, this may require a different cocktail of chemotherapy and pharmaceuticals to target the new mutations and new form of cancer – cancer precision medicine is cutting edge stuff, and clearly very, very difficult (maybe oncologists do deserve an oh wowww).

While we may be able to stop some cancers from getting out of control once you have it, preventing it from happening in the first place or killing the cancerous cells without killing your own and before it has metastasised is the tricky part.

Have we gotten anywhere?
I’ve been pretty doom and gloom so far, and I apologise. Because it isn’t all doom and gloom, and we’ve learned an extraordinary amount about this extremely complicated, evasive disease. For example, in the past 50 years, breast cancer survival rates have skyrocketed. In 1975, there was a bleak 15-20% survival rate within 5-years of diagnosis, whereas in 2018 it sits closer to 90%, and overall cancer survival in the UK has doubled in 40 years from 25% to 50% – how incredible is science?

This is thanks to the amazing oncologists around the globe studying cancers but also the inherently collaborative nature of research. While cancer can generally be described as a localised disease (unless metastasised), we also need to understand everything we can about the healthy tissues or organs the cancerous cells stem from. This is why oncology overlaps with just about every other biological/medical field there is, and why underlying organ function can significantly influence cancer survival rates.

So, will we ever get a cure?
Here I go being doomy and gloomy again, but it’s very unlikely to be any time soon. Technically, we’ve only cured (eradicated completely) two diseases, and both are the result of vaccine development (smallpox and rinderpest).

Cancer researchers have picked a very difficult career filled with experimental and clinical strife. However, scientists have a remarkable ability to stay resolved and committed to their research, even in times of hardship. And, as I said earlier, science is inherently collaborative and the solutions to our problems may not be in the most obvious of places.

For example, have you heard of Peto’s paradox? Essentially, as larger animals have more cells than smaller ones, they should be much more prone to cancer than smaller animals. Makes sense, right? More cells = higher probability of genetic mutations = higher probability of cancer.

But, here’s where the paradox comes in. Large animals get cancer far, far less than they ‘should’. In fact, blue whales don’t really seem to get cancer at all…Why? Is the cure for cancer hidden in a blue whale’s stomach? Well, there are two main theories here: Evolution and hypertumours. Put simply, larger animals may have evolved to naturally have a higher number of tumour-suppressive genes, and therefore require more mutations for cancer to develop. They’re not ‘immune’, but it’s just very, very rare.

Now the more sinister-sounding theory, hypertumours, employs a cancer cell’s own mutative speed against them. Over time, some of those cells in the tumour can break away and form their own, genetically distinct tumour, which then competes with the original tumour for resources (the whale). This fight to the death between tumours may ironically leave the whale relatively unscathed, just like how Mr Burns got every disease known to man and was ‘indestructible’. So, in a weird way, the hypertumour situation keeps all the tumours in check, preventing them from getting large enough to be noticeable or troublesome for the animal. After all, a 2g tumour to a mouse is roughly 10% of its body weight, 0.002% of a human, and 0.000002% of a blue whale – see my point?

For a more in-depth, animated version of the Peto’s paradox, I highly recommend checking out a video by Kurzgesagt – In a Nutshell.

So, what have we learned?
Cancer is impressively difficult to kill, extremely virulent, and can come in hundreds of different forms with each requiring its own unique treatment regime.

We’ve come a long way in cancer research, and cancer survival rates have never been so high. But where to next? Are blue whales the ‘next big thing’ in cancer research? Are the tumour-suppresive genes inside a blue whale the key to a cancer cure? The only thing I can say with confidence is wooow, that’s amazing.

What Good is a Menstruating Mouse?

About 8–12% of couples of reproductive age suffer from infertility, and roughly 15% of all pregnancies end in miscarriage.

The underlying mechanisms of human pregnancy are still poorly understood. In part, this is because pregnancy works quite differently in most mammals.

Read more: Miscarriages affect 1 in 6 pregnancies. We need better investigations and treatments

However, recent research indicates the Egyptian spiny mouse, which menstruates like humans do, could offer an excellent model for research. Our new study, published in Scientific Reports, shows the lining of the mouse’s uterus, or endometrium, also grows in a human-like way to prepare for embryo implantation.

Why animal models are important
There are many reasons for miscarriage and other pregnancy complications, ranging from hormonal and vitamin imbalances to failure of placental development and impaired embryo implantation. To understand these conditions, researchers need to do experiments – but doing experiments on humans poses serious ethical, practical and financial challenges.

That’s why researchers try to “model” the conditions in suitable laboratory animals. Animal models (using rodents in particular) have helped explain many aspects of human reproduction, but they are limited by fundamental differences between human reproduction and that of other species.

Read more: We mightn’t like it, but there are ethical reasons to use animals in medical research

Less than 2% of all mammal species menstruate, with most instead having an oestrus cycle (“going on heat”). Aside from humans, most menstruating species are great apes or old-world monkeys.

Non-human primates like these would be the most biologically appropriate animals for modelling human reproduction. But their large size, complex welfare requirements and high costs have prevented their adoption as laboratory animals.

So, to study and manage human pregnancy more effectively, we need a more appropriate menstruating animal model of female reproduction.

The menstruating spiny mouse
The Egyptian spiny mouse (Acomys cahirinus) was recently shown to have human-like menstruation. This had never been seen before in any rodent, and the discovery gives researchers an unprecedented non-primate model for studying menstrual and gynaecological disorders.

Researchers from Monash University have since delved deeper into the mystery of spiny mouse reproductive biology. The researchers have provided an in-depth characterisation of the menstrual cycle, identified PMS-like behaviour and, most recently, early embryo implantation and pregnancy.

Endometrial growth
In our study published in Scientific Reports, we discovered that the lining of the spiny mouse’s uterus displays similar patterns of growth and receptivity to embryo implantation as other menstruating species.

Before an embryo can implant, the uterus lining must more than double in size and begin secreting the required proteins to encourage an embryo to implant correctly. This study demonstrated simultaneous increases in thickness and receptivity of the spiny mouse endometrium before embryo implantation, closely reflecting the events in other menstruating species.

A fluorescent image of the spiny mouse uterus just before embryo implantation. The green chunk is the muscle of the uterus, and the thinner green structures are the uterine arteries. Blue shapes are cell nuclei, and the red dots within the arteries are blood cells, and red outside the arteries is either blood cells or protein. 

Spiral arteries
In all menstruating species, spiral-shaped arteries grow in the uterine lining.

These spring-like arteries are vital to provide nutrients for a growing placenta, and poorly functioning spiral arteries are associated with several pregnancy complications such as pre-eclampsia and intra-uterine growth restriction.

Read more: Explainer: what is pre-eclampsia, and how does it affect mums and babies?

In our study, we observed the growth of spiral arteries prior to embryo implantation, but also changes to their structure and function soon after. This also occurs during early pregnancy in other menstruating species including gorillas, chimpanzees and humans.

Looking to the future
Although our knowledge of spiny mouse reproductive biology is in its infancy, what we do know is very encouraging.

This study is further proof for the unique reproduction of the spiny mouse and adds to the growing list of reproductive traits we share with this fascinating species. Not only do spiny mice have human-like menstruation, but this recent study demonstrates similarities of endometrial growth, receptivity and the critical role of spiral arteries during early pregnancy of menstrual species.

Further research into spiny mouse reproductive biology may reveal new treatment options for pregnancy complications. In turn, this could change how we treat and monitor pregnancy and lead to better outcomes.

An edited version of original publication by The Conversation.

The Power of Assisted Reproduction

While most people are aware of the threats posed by climate change, few know of just how drastic those threats are to biodiversity. According to the World Wildlife Fund (WWF), the Earth loses roughly 10,000 species every year, roughly 5,000 times higher than the natural extinction rate.

​While zoos are an effective way to house endangered or threatened species, the reproductive biology of these animals is largely unexplored but is becoming increasingly important for species conservation. Two of the most pressing issues facing zoos today are space and lack of genetic diversity. Even when zoos are well-managed and internationally connected, zoo populations rarely contain large enough animal populations for long-term sustainability. Moreover, when new animals are brought in to revitalise captive population genetics, the logistics of moving animals between zoos can be extremely challenging (imagine the logistics and costs of moving an elephant or giraffe from New Zealand to New York). This is where assisted reproduction can play a significant role.

What is assisted reproduction?

Broadly speaking, assisted reproduction involves managing an animal’s reproductive cycle or manipulating gametes to achieve fertilisation and a subsequent pregnancy/live birth. Some of the most common assisted reproductive techniques in our arsenal are gamete cryopreservation, artificial insemination, and in-vitro fertilisation (IVF). Assisted reproductive techniques have become very well defined in humans that, since the birth of the world’s first IVF baby in 1979, around 8 million children have been born from assisted reproductive techniques globally. Assisted reproductive techniques have also become so commonplace in laboratory rodents and farm species that we often forget the incredible difficulty in defining the fundamentals of a novel species’ reproductive biology. Unfortunately, this is exactly the case with many endangered or threatened species. Even artificial insemination, one of the more basic assisted reproductive techniques, requires an in-depth understanding of male and female reproductive physiology before we can even think of making an attempt. Although daunting, once even simple techniques like AI or reproductive cycle management are defined, assisted reproductive techniques can be incredibly useful in supporting captive breeding efforts.

Frozen Zoos

As I mentioned earlier, the difficulty of transporting some animals between zoos (let alone continents) is extremely challenging. Sperm cryopreservation is an effective procedure for many species, where semen is collected either voluntarily or through electroejaculation and frozen without dramatically affecting sperm viability. Similarly, even cells from wild individuals can be collected, frozen, and used in captive breeding programs. Cells frozen correctly can (in theory) remain viable forever and be shipped around the world far more cheaply and simply compared to shipping an entire animal. Several institutes around Australia, including the Taronga Conservation Society and Monash University, have adopted this idea and have established the futuristic concept of a ‘Frozen zoo.’ Frozen zoos store cells from endangered animals and plants in liquid nitrogen until they’re needed for future genetic reintroduction programs into captive or wild populations through techniques such as artificial insemination or IVF.

I think it needs to be clearly stated that assisted reproductive techniques never intend to (or I think ever will) replace captive breeding. Assisted reproductive techniques are tools that scientists, conservationists, and zoo staff can use to more effectively increase captive animal numbers without replacing traditional breeding methods.

Have frozen zoos and assisted reproductive techniques been useful before? 

In practice, assisted reproductive techniques are rarely used in captive settings due to their technical complexity and perceived costs. However, assisted reproduction continues to make headlines in scientific literature and the media, including artificial insemination in giant pandas and jaguars, cryopreservation in coral and fish species, and, most recently, the cloning of black-footed ferrets from cells frozen over 30 years ago. While it may seem drastic to start cloning rhinos or freezing sperm from lions, climate change poses incredible threats to species biodiversity, which we are doing a terrible job in mitigating. The Earth is losing roughly 10 million hectares of forest every year, and, as a result, animal populations are becoming increasingly fragmented and isolated, limiting gene-flow between populations. By not having enough genetic diversity between populations, a species can suffer from inbreeding depression: the reduced biological ‘fitness’ of a species and their ability to reproduce and survive in the wild. Reliable techniques for preserving and transporting species genetics between captive settings (or from the wild to captive settings) enable better management of genetic diversity while increasing that species’ biological fitness.

So, what does the future of assisted reproduction look like?

While assisted reproductive techniques have clear immediate and future benefits to species conservation, their use is unfortunately not up to the conservationists and scientists but up to funding bodies and political big wigs.

The importance of assisted reproductive techniques in the future of species conservation cannot be understated, and researchers continue to build the case for assisted reproductive techniques as reliable, effective tools for the protection of biodiversity. Conservationists and assisted reproductive biologists have chosen a difficult career, often restricted by funding issues and a pervasive misunderstanding of the importance of biodiversity in the general population. Although everybody loves the trailblazing, revolutionary discoveries, or achievements in science, these discoveries are only possible after decades of fundamental research. Without the proper funding or public interest in biodiversity, species conservation will remain an incredibly tough, arduous field. That being said, although progress may seem slow, if we continue to fight the uphill battle against climate change, we will be glad we invested in assisted reproduction science when we had the chance.

Originally published by Bolded Science