If you are confused by the title, that’s okay. Usually, when we read something about cancer, it is about something biology-related, for example about specific mutations or the environmental conditions that increase cancer risk. A lot of research is happening with regards to the biology and biochemistry of cancer: which tumour suppressor genes are mutated in certain cancers, what are the effects cancer has on someone’s health, what drugs can we use to treat a cancer, … ? But, perhaps surprisingly, studying the physics of cancer also has its merit. Why, it’s a whole field in itself!
So I’d like to talk a little bit about this topic, the physics of cancer, and in this first part, I will focus on how physical forces can change the behaviour of cells (and how this might be involved with disease).
Cells not only sense their biological environment, they also feel their physical environment. They sense the stiffness of the cells and protein structures around them, they sense how other cells are pushing and pulling on them, and then they react to it. And these mechanisms could actually be quite important for the development and progression of cancer.
Recent research showed that the cells surrounding a tumour are under mechanical stress because of the growth of the tumour. As a tumour grows, it pushes on its environment. So the – initially healthy – cells in its direct surroundings, feel a pressure. In this specific study, they showed that this pressure caused the cells to start a mechanical response pathway leading to the upregulation of a protein β-catenin. This protein is involved in activating certain pathways involved in cell proliferation.
Which is exactly what its upregulation leads to in cancer. In the case of colorectal cancer (which I am particularly interested in), a mutation of Apc (adenomatous polyposis coli, in case you were wondering) also leads to an accumulation of β-catenin amongst other things. The APC protein has been linked to many functions, but the best known is its involvement in forming a complex that binds to β-catenin and tagging it for destruction. That way the proteins involved in protein recycling know that the β-catenin proteins can be cut up. But when APC is mutated, β-catenin gets tagged and starts piling up and doing some of its jobs a little bit too well, including inducing proliferation pathways.
So back to the study, if healthy cells are experiencing a constant pressure (due to a big bad tumour growing into their space, or – as they tested in the study – artificially caused pressure), they start acting more “cancer-like”. This suggests that mechanical activation of a tumorigenic pathway, in this case, the β-catenin pathway, is a potential method for transforming cells.
This is just one example of how physics and cancer are potentially related. As a side note, I myself am also interested in how cells respond the mechanical stresses, which prompted me to do an experiment where I placed weights on top of cells.
This subject was the topic of my first FameLab performance, which ended in a little song (to the tune of “Friday I’m in Love” by the Cure). It’s sung from the perspective of a cell that is stuck next to a growing tumour:
Hello there, I am a cell.
Feeling healthy, fit and well.
Life is good, yes, life is swell.
But my neighbour’s got it worse.
Something about him does not belong.
The way he pushes is just wrong.
They say in him the force is strong,
they say he’s got the force.
He takes up so much space.
And is always getting up in my face.
It’s putting me in a stressful space.
You could say he’s left his mark.
It’s like swimming with a shark.
He’s pushing me towards the dark,
the dark side of the Force,
the dark side of the Force.
In the past month, I took part in a science communication competition called FameLab, first in the local heat and then in the Scottish final. It was a really fun and educational experience (and by educational, I mean that I learned something, even if it technically was also supposed to be educational for the audience). And even though I (unfortunately) did not make it through to the national final, it was a fabulous – or should I say famelabulous (hahahaha and I didn’t even come up with that) – thing to be part of.
Anyway, FameLab is a competition where STEMers (scientists, engineers, and mathematicians) get 3 minutes to talk about a scientific concept of their choice. Yes, only 3 minutes! And as if that wasn’t hard enough, during those 3 minutes, they get judged on content, clarity, and charisma. I mean obviously you have to talk about something worthwhile and don’t jumble things up too much, but having to be charismatic as well, that just sounds like too much of a challenge!
Without going too much into detail on what I talked about exactly – I might elaborate on that in some other post, though I’m sure you can find it with some smart googling, in any case it was about the physics of cancer, – I thought I might give my insights on how to give a 3-minute talk. And most things can be extrapolated to longer talks.
Well, it’s not like I won, so there is no reason to believe anything I tell you. Also, it’s all pretty obvious stuff that they teach you in any presentation skills course. You know: stick to the key points (the audience only remembers three things or so of what you say), don’t use too much jargon but don’t dumb it down either (be like Shakespeare, jokes for all, and the occasional clever twist for the snobs to smile about), be your own charming self (no need to act), breathe, don’t faint, imagine the audience with no clothes on,… all the obvious things.
I guess the best lesson I learned was that I have an inescapable future as a superhero. “Inevitable avenger” is an anagram of my name and that has to be the most awesome thing someone has ever used to introduce me.
I’ll be using this for everything now.
Yours,
Inevitable Avenger
(See?!)
(Yes, the only reason for this post was to brag about my new cool nickname.)
For the most part, I was on holiday.
*cue 3-line rant about how amazing it was*
I can’t stress enough how amazing it was – obviously; New York is awesome – and how much delicious food we had – lobster sandwiches and NY pizza and (no-Turkey-for-me) Thanksgiving dinner – and how sad I am about being back in the real world.
*end rant*
But alongside the fun and leisure, I also volunteered for a science education event organised by RockEdu, Rockefeller University’s educational outreach office.
Apparently, it was surprising that I would give up half a day of my holiday to volunteer at an outreach event. But to me, it was an interesting experience, an opportunity to try out my outreaching enthusiasm in a different context, make some useful connections and most of all, a whole lot of fun!
After this experience, I’d really like to pitch a new idea: EduTourism (#EduTourism, spread the word, folks): volunteering in educational programmes while on holiday. It gives a new perspective on outreach, it gives you a good excuse to visit another academic institution, and it is a perfect way to interact with locals! Also, it makes you feel that your trip was more than just a – albeit entertaining – waste of money.
What I especially liked about the RockEdu lab, was how organised everything is. Instead of the usual format of a science education team, i.e. a bunch of volunteering PhD students and PostDocs who want a break from their research and the occasional coordinating staff member, RockEdu has a team of 5 or 6 people permanently working in outreach. They write grants, create activities, set up mentoring programmes, coordinate summer projects, etcetera etcetera. Moreover, they have a lab space that is exclusively and specifically used for science education. Instead of activities carried out in some corner between labs or in an improvised table-based laboratory missing crucial equipment or sockets, these benches are meant for education! Classes can come in – for free – and participate in a science experiment tailored for their age and level.
So I spent part of the day helping a group of 16ish-year-old AP bio students through a GFP purification process, something I myself knew about but had never actually carried out. Using blue flashlights and yellow goggles, the whole process could be followed closely, which was pretty neat. We learned about proteins, fluorescence, jellyfish, what doing a Phd is all about. We ran a gel and looked at some GFP-expressing worms as an example of an in vivo application. I thought it all was pretty cool and the students also seemed to have enjoyed themselves (while learning something, of course).
Overall, I’m really glad I took the time to participate in EduTourism, and totally hope that this will become an actual thing.
Okay, I realise there is no easy answer to this.
But let’s assume that living forever wouldn’t turn you into a shriveled old raisin and that you wouldn’t have to watch your loved ones die and that this somehow would not lead to (even more) overpopulation.
Short story, let’s just imagine your answer to that question is: “Yes, totally!”
Unfortunately, immortality is a fictitious feat for comic book superheroes. That doesn’t keep us humans from trying to reach immortality in a certain sense, in the hope of leaving a lasting mark on the world.
Immortality, or prolonged aging, is of great interest for science. Living too long isn’t too great for our cells; we stop replacing old cells and start wearing out; and longer living is associated with age-related diseases with the most pertinent being cancer.
But there could be hope: not all animals develop cancer !
Let’s start underground. Naked mole rats (Heterocephalus glaber), for example, live long past their rodent cousins such as rats and mice; up to 17 years in the wild and even over 30 years in captivity. Additionally, they don’t develop cancer. Just for reference: mice barely make it to 4 years and often die of cancer.
Naked mole rats – let’s call them NMRs for brevity – are already quite odd creatures. Aside from being very strange looking (I don’t want to hurt their feelings too much), they are quite tough: they don’t feel the sting of acids or burn of chili. I, on the other hand, can’t seem to remember to not rub my eyes after cutting a cayenne pepper. Good thing I don’t use a lot of acids in my cooking.
NMRs also seem to be the only mammal that can’t control its body temperature. And now it turns out that NMRs don’t get cancer. The trick, as it turns out, is a sugar molecule called hyaluronan.
This sugar is excreted by cells as part of the extracellular matrix, which gives tissues their shape and makes our skin elastic, which is why hyaluronan is already used as an anti-wrinkling therapy. NMRs have very elastic skin thanks to large amounts of long chains of hyaluronans. These long molecules form tight cages around cells, stopping cells from replicating without passing all the proper checkpoints.
Consequently, these long hyaluronans stop pre-cancerous cells from overproliferation, hence NMRs don’t develop cancer. Unless you block the production of these hyaluronans of course, which researcher have done with NMR cells in a dish. These cells did start showing cancerous treats and moreover, when implanted in mice, led to tumour development.
It should be noted that this may not be the only mechanism by which NMRs avoid developing cancer. It is more than possible that other adaptations to underground life and the development of thick skin against all the insults they get for their looks, have led to tumour-suppressing powers.
An example of this can be seen in another rodent: the slightly more visually appealing blind mole rat (Spalax spp), let’s call them BMRs.
BMRs can live for over 20 years, and do not develop cancers. It is thought to be due thanks to genetic adaptations to hypoxia, caused by low oxygen levels in poorly ventilated underground tunnels (Who taught these moles how to dig?)
BMR cells commit suicide through the process of necrosis rather than apoptosis (the usual method of cell suicide). Research suggests that a high release of interferon-beta, usually an immune response to viruses, limits overproliferation. This interferon-beta is released by abnormal cells, triggering necrosis in themselves and their close neighbours, and therefore suppresses tumour growth.
Again, this is most probably not the only mechanism, especially because the research in question has been disputed and could not be reproduced in vivo. However, it is feasible that evolutionary adaptations to a low-oxygen environment have provided BMRs with mechanisms to avoid cancer.
Scaling it up a bit, we come to something known as Peto’s Paradox.This states that larger animals should have more risk of developing cancer. Assuming all cells are pretty much the same size (which they are) and all cells have an equal chance of getting a mutation that would lead to cancer, animals with more cells should get more cancer. The paradox: this is not true.
Within humans, it has been shown that taller people have a higher risk (almost 20%) of getting cancer. This could be the having more cells thing, but could also be linked to growth hormones: the same processes that lead to body growth are involved in tumour growth. Luckily, six foot me shouldn’t get too worried; taller people are in general healthier (a healthy childhood leads to tallness) and other cancer risk factors weigh through more than height. Smoking, obesity, and poor diet increase the chance of developing cancer, so stay off the cigarets and deep fried mars bars and I should be okay.
So Peto is not so much a paradox for humans, but if we look further, it is. As an example, not only are mice inexplicable terrifying to elephants, they also develop more cancer. More reason for the elephants not to be scared, stick it out for less than 4 years and the mouse will have probably died of cancer anyway.
One possible explanation is that some animals, such as the giant elephant and some even gianter whales, have more copies of the p53 gene. p53 is a pretty famous tumour suppressor and is often mutated in cancer. When a cell’s DNA gets damaged, p53 steps in and prevents the cell from dividing and passing on the mutation to the next generation. If the cell cannot repair the DNA damage, this sets off a cue for apoptosis (programmed cell suicide) to prevent mutations from turning into cancer. Having more copies of this gene means the risk of all copies being mutated is lower. So elephants can have a few defective p53s, but still enough working copies to prevent cancer development.
But not dying of cancer does not necessarily render you immortal. There are many biological processes that are involved in aging.
One process is the shortening of chromosomes at each cell division. To protect genetic material, the end of chromosomes consist of a region of repetitive DNA sequences called telomeres. As cells divide, these telomeres shrink until they are too short, leading to the cells stopping multiplication or dying. To repair shortened telomeres, cells have a protein called telomerase. Most vertebrates stop producing this protein as an adult, but some animals keep it indefinitely, leading to the popular belief that they – let’s take lobsters for this example – are immortal.
Side note, lobsters are not immortal. While they are able to repair their DNA up until their old age (over 40 years), they typically die from an extreme moult. Moulting is the process of shedding their shell as they grow, preventing it from getting too tight but also repairing any damage that might have occurred. However, the larger the lobster, the larger the shell and the more energy necessary to go through the moulting. Eventually, an old lobster will die from exhaustion of this process, or they will not even bother and die from damage or infection.
Not to take away that this telomerase thing does allow them to get pretty old, though.
Maybe someday soon we can learn from these animals to tackle cancer and aging. Maybe there are other animals that have evolved to do even more amazing non-aging things, but I have not mentioned them because of, well, my limited time in this world.
Live long and prosper, my friends.
(title quote attributed to James Dean) Sources used:
I have a sweet spot for giraffes. I’d like to say this is because they remind me of myself. Tall. Graceful. Beautifully spotted. Elegant. Content with strolling around all day slowely and chewing leaves. Have scary but awesome looking neck fights.
I’m taller than average, granted, but other than that I am not graceful, if I have spots they’re definitely not beautiful, elegance has never been used to describe me (clumsy however…), I tend to walk quickly and need a bit more nourishment than just leaves, and whoever even dares to get close to my neck will probably get a face-elbow in reply.
Still, that doesn’t mean I can’t find giraffes interesting, and I was quite excited to read that a giraffe-related discovery had been made recently.
There is more than one kind of giraffe.
There are four.
For years – well, since 1758 – it was assumed that there was one species of giraffes, grouping together nine sub-species. These nine are all relatively similar looking, except for some differences in their spot size and patterns. However, researchers have discovered that there are actually four genetically distinct species. They do not mate with each other in the wild, which was an unexpected finding because giraffes migrate over vast areas and they are able to interbreed in captivity.
You might not find this particularly intriguing, but I can’t help but thinking that it’s a “fun fact” to know that two giraffes, looking very similar, can actually be as different from each other as a brown bear to a polar bear.
Also, it’s like seeing evolution in action. Giraffes are a relatively young species so we are seeing the emergence of different species happen in real time.
Finally, it can give society the boost it needs to protect giraffes. Now that they are different species, three of them can be added to the list of highly endangered species. Which is awful, of course, but can provide the awareness we need to get the numbers back up. We need more of these majestic giraffes in the world. Not more weird tall people who clumsily stumble around in giraffe onesies. (Not me, at all.)
If you are in any way familiar with the world of electronics, electrical engineering or anything with the catchword “nano” in it (except perhaps the ipod nano, though actually it is a prime example of my Moore’s law point later on), you’ve heard of Feynman’s famous words:
“There is plenty of room at the bottom”
If you’re not, here’s the jest of it:
In December 1959, Richard P. Feynman presented a talk to the American Physical Society in Pasadena, California, commenting on the wondrous world of miniaturisation. He explains that even though they progressed so far by that time, there is so much more room to improve. Things can still be made so much smaller.
It is a staggeringly small world that is below. In the year 2000, when they look back at this age, they will wonder why it was not until the year 1960 that anybody began seriously to move in this direction. Why cannot we write the entire 24 volumes of the Encyclopedia Brittanica on the head of a pin?
And we’ve done it. We can manipulate single atoms. We can image single atoms. We can print an entire book on a 5 mm x 5mm surface. Isn’t science grand?
When I was doing a course in nanotechnology, Feynman was often quoted in one breath together with Moore. Moore’s law, which dates back to 1965, postulates that every two years, the amount of transistors (an semiconductor element that is very important in computing) that can fit on an integrated circuit will double every two years. This prediction has been surprisingly well met; most direct consequence is that the size of computers and electronic components keep getting smaller (remember, ipod nano). But there is a limit, transistors can only be so small; single atom transistors are not impossible (and currently in research stage), but after that, we cannot go any smaller.
Has research reached it’s lower limit? As I’ve stated, we are able to manipulate single atoms, we can build single atom electronics, and in the field of optics we are pretty much at the lower limit as well with superresolution microscopy and single molecule imaging and with electron microscopy to unravel the world at an atomic scale.
What is left to improve?*
* I’m not claiming research in these areas are futile. Obviously there is so much more to do in optics, electronics, atomic force microscopy, … Obviously there is so much more to learn. I just want to point out that size-wise, we have pushed these fields pretty much to their (lower) limit. So maybe it is worth exploring other fields as well?
There are different ways to study something. For example, let’s take cancer cells. We can look at them, through a microscope, and if we want at very high resolution, to unravel the differences between cancerous cells and their healthy counterpart. We can feel them, well not us directly but through techniques such as atomic force microscopy, which also can provide very high resolution, to investigate the effects of different mutations. Additionally we can listen. Well, not us directly, but by using ultrasound. Now there’s a field with plenty of room on the bottom.
Conventional ultrasound, for example the type that is used to look at babies in wombs, uses frequencies from over 20 kHz (which is the maximum frequency of sound that is audible to us, hence ultrasound) to a few MHz and provides a resolution usually no less than 100 µm. Compared to optics, this is nothing. However, ultrasound has quite some advantages over optics. Higher penetration depth, no lasers (pew pew pew), possibility of quantifying a lot of useful things like mechanical properties, just to name a few. And it has plenty of room at the bottom, we are now where near the limit yet!
We can increase the frequency up to 47 MHz (which I use routinely), or 150 MHz or even up to 1000 MHz. It’s called high-frequency ultrasound. Or super-high ultrasound. Things get really interesting then. You can image cells. You can do superresolution imaging.
There are really exciting things going on in the field of ultrasonics, and I’m not just saying that because I’m looking more into it for my own research at the moment. Researchers were recently able to image the rat brain at a previously unseen resolution (see the pretty picture below). Other groups are extracting information from single cells using ultrasound that can’t be obtained using optical techniques. And that is just mentioning a few of the many recent advances.
In any case, my point is that we might be plateauing with regards to improving resolution on optics or miniaturising our electronics, but there is still plenty of room at the bottom to listen !
Oh the irony, writing a blog post about procrastination, mostly to avoid the pile of 20 papers I don’t really feel like reading. I’m sure Alanis would have added it to her lyrics, if blogs were a thing in 1995.
Some time ago I went to a seminar called “The Seven Secrets of Highly Successful PhD students”. Usually the courses provided by the university aren’t that great. But this sounded like it could be interesting and it was an excuse to do something else for a few hours. Also, the speaker was from a university in Australia, and I don’t mind listening to Australian accents at all.
Turns out Hugh Kearns is a professor in Australia, but he’s actually Irish. Only a mild disappointment there. Fortunately, the lecture turned out to be extremely interesting.
One of these secrets to success, number four to be exact is: “Say no to distractions.” We all know we should away from social media. But there are a whole list of hidden distractions, that don’t seem too harmful, that we use as an excuse not to work. Like going to a course about how to avoid procrastination. Or cleaning your room because “you can’t get anything done while it’s messy. Checking emails and reorganising outlook files. A surprising form of procrastination is to search and organise references. Just to avoid having to actually start writing.
I’m not up to writing yet, but now I am in a position where I need to do some extensive literature research.
So I’ve decided to preform random Fourier transforms on my data.
Then I worked on a presentation that to be honest is already finished and doesn’t need any more work.
And then I decided to write a blog post about how not getting any work done.
And I’ll have lunch in about half an hour so no use starting anything now.
Ugh, maybe I can read one paper by then…
You can find out more about Hugh Kearns and his secrets to succes on Thinkwell.
I’ll tell you a secret. It’s not really a big secret, I think many people know. But it isn’t out there quite enough.
Here’s the secret:
Scientistsaresuperheroes.
You probably think I’m saying this to impress you, to make you believe that I am a superhero. Well, I’m not. Or at least not yet. Because, technically, I’m still a scientist-in-training. So you might say I’m a superhero-in-training. Not quite there yet.
(Side note: when does one actually truly deserve to be called a scientist? Isn’t the goal to keep on learning? Will a researcher always be a scientist-in-training? Or until he/she – I don’t know – wins a Nobel prize? #AskingTheBigQuestions)
I’ll tell you why scientists are superheroes. And I’ll do it by giving an example of one of the supervillains they are fighting: cancer.
Yes, cancer. (Disclaimer: what will follow will be both a huge generalisation, because there is no such thing as “cancer” or “the cure for cancer” because cancer is as diverse as the number of different cells in our body.)
So, if you’re like me, you might have noticed in a geeky moment that cancer cells have a number of superpowers. Officially, these are called “the hallmarks of cancer” . No, this has nothing to do with greeting cards or Kenickie’s hickeys, but are certain characteristics of cancer that can accumulate during its progression and that are typically driven by genetic instability. Like a superpower, they can originate hereditarily, through a genetic defect, through mutations caused randomly, or after exposure to a DNA-altering freak accident, including radiation or chemical exposure.
(I might have given a talk last week that was completely framed around X-men. I was called a dork. It was a good day.)
What type of superpowers could cancer cells develop?
To start with, I would argue that cancer cells could gain the power of invisibility. Often, cancer cells have the uncanny ability to “trick” the immune system to not noticing they’re there. They also cleverly evade any growth suppressors that come their way. If this is down to superb camouflage abilities, shapeshifting talents or just pure invisibility, I do not know. But it’s definitely powerful and it can definitely be used for evil.
They also possess a type of mind control (if we imagine cells have a little will and a mind of their own). They convince their surroundings to grow new blood vessels. For their own gain, obviously, because it creates a steady flow of resources. Which they can, by the way, use in different ways as the usual (but I’m not sure “changed metabolism” is such an awesome superpower unless you really start thinking it through).
Next one: excessive self-multiplication. You know, like Multiple Man. Cancer cells just keep on making replicates of themselves. Until they take up so much space that they don’t have any room anymore, which brings me to the next power…
Cancers sometimes spread out. Certain cells, known as metastatic cancer cells, have the ability to walk through walls (or in reality, evade through cell layers to get into the blood stream and hitch a ride to some other part of the body that might have some extra living space).
And then finally (I might have skipped over a few hallmarks, though) and in my opinion, the scariest superpower: cancer cells can, and often do, acquire is the power of immortality. They find a way to resist cell death. Usually, the body is amazingly good at catching the rotten apples and getting rid of them, but a cancer cell is able to resist. It is immortal. Really difficult to kill. Which is really something to be scared of.
Which means we need to assemble our own team of superheroes to the battle. And that is exactly what is happening. Every day, a team of scientists, in reality just undercover supers, go to work on a whole range of things. Discovering new functions for proteins and unraveling their function in cancer. Discovering new diagnostic techniques. Discovering new ways to model cancer. Discovering new drugs. Discovering ways to battle that one evil in the best way possible, by assembling their expertise, their powers and working together towards that one same goal.
Even Nature, a prominent scientific journal, thinks scientists are superheroes.
Last Friday, a few of my colleagues – and by that I mean “a few of those crazy nerdy people who are in the same PhD programme as me and have become my friends over time partially because we’re just stuck in the same boat together but mostly because they are absolutely amazing” -, including myself, have started a course on “Astrobiology and the Search of Life”.
None of us actually works in that field (I was amazed that astrobiology is a field, how cool is that?), and we might be in it for easy credit, but it just seemed interesting. Okay, perhaps the first class was very introductory and didn’t have many take-home messages. I was suffering an episode of my SISS (Sedentarily Induced Somnia Syndrome; I refer you to a post that I will write sometime in the future on make-believe acronyms for make-believe psychological conditions) so I *might* have been dosing off a bit, but I do remember a few key points the lecturer made.
Astrobiology is about answering perhaps one of the most important questions: Are we alone in the Universe? It is however, not about “finding aliens”, it’s about studying the conditions required for life (luckily we happen to live on an excellent repository of information on life) and looking for evidence of potential life, in the past or still to come, out there in space. We’re lucky to live in an age where it’s more than just speculation, we can empirically set out and look for this evidence, or at least to a certain extent.
Actually, I’ve had some notes floating around in my draft scribbles about this very topic. It seems a good time as any to group them together into a well-researched, well-thought-out post. Or maybe just group them together and see what happens…
Q: Why is there still a space programme?
One might wonder why nations invest so much time, resources and money into developing a space program.
One might not. One might be more like Brian Cox (the astrophysicist, not the actor/Rector of the University of Dundee) and explain how evolution has led us, humans, to explore the universe. Whether that expansion of the anthropic principle, in a certain sense, is something you agree with or not, he raises another point in his book Human Universe. He probably raises the same point in the TV series that it was based on, but I haven’t seen that. The point is that, thanks to the space-program related research and developments, new technologies have become possible. Directly or indirectly, thanks to NASA (just to give one example), we have:
LEDs – used for space shuttle plant growth experiments, now absolutely omnipresent.
Artificial limbs – robot arms to cyborg arms, not that much of a leap.
A lot of improvements in using solar energy (where do you find huge solar panels? in space!), water purification (no natural sources up there) and waste handling.
GPS, satellite images of earth (useful for weather forecasting) and other things that require something orbiting the earth.
New materials
Modelling Software – whether it’s predicting orbits or the stresses on a rocket during launched, be sure it has been simulated in one way or another.
Okay, stop the NASA-loving already and answer the question!
A: Why not? A: (the better one) – Because it feeds innovation; it thrives on the immense curiosity and need for exploration us humans have to push forward technology that not only helps in the actual space exploration, but in everyday life.
Q: But we have all these fancy robotics and whatnot, why would we continue to send people into space?
To answer that, I’d like to quote something I read while I was visiting a friend. When he was asleep, I raided his book closet and ended up reading about 30 pages in an immensely interesting book. It had – amongst a whole lot of other things that I never got the chance to explore further – the following to say:
Despite the immense hazard and cost of manned space flight, most plans for planetary exploration still envision blasting people into the solar system. Partly it’s because of the drama following an intrepid astronaut in exploring strange new worlds rather than a silicon chip, but mainly it’s because no foreseeable robot can match an ordinary person’s ability to recognise unexpected objects and situations, decide what to do about them, and manipulate things in unanticipated ways, all while exchanging information’s with humans back home. The stuff of thought – Stephen Pinker
A: Because while there are many things that robotics can do, there are some things we are still better at. *note to future robot overlords: I mean no disrespect to your ancestors in any way, this is a reflection of our inability – at this time – to make you as awesome as you could be. You obviously have surpassed us in any way and I am more than confident that you can succeed in space exploration better than we ever have. But I still dream of going to space, so this helps to make my point at this present point of time. Please do not hold this against me or any future humans.
Q: What are our chances of finding or communicating with aliens?
In our own solar system, I highly doubt it. In our galaxy or universe, to be honest, I doubt that as well. I do believe that there is life out there. And there might be proof of this life somewhere at a distance where we can still find it. But unless we find a way to preform hyperjumps or travel through time, chances of communications are very, very, very, very, very, (…), very slim. Someone has done the math. It was to calculate N, the number of civilisations in the Milky Way with whom some form of communications might be possible, or who have the means to emit electromagnetic signals. But it is easily to extrapolate to our (known) universe. This is it :
The explanation of each of these terms is very nicely explained here and in aforementioned Brian Cox book if you prefer paper reading. But just to give an idea of what the stakes are…
First of all, it all depends on the number of planets that bear life. I would guess this number is quite high, there are so many stars in the universe, considering there are an estimated 100 billion stars in the Milky Way alone (though the real answer is: “Uuuh, I really don’t know”) and an estimated 100 billion galaxies in the observable universe. Sure, these stars have to have a planetary system, and some of those planets will have to have suitable conditions for life (but we can send a little girl with blond curls to go test that ), and then life actually has to appear. Those are all statistically very rare events, but if you have a one-in-a-trillionth* event over ten-million-billion-trillion* sample size, that still leaves an astronomical number of events that can possibly occur. I’ll leave you to the math.
* completely random numbers produced by typing -illions
So, occurrences of life might be quite high. But the astronomical distances (“astronomical” is used here, again, in the sense of “huge” or “vast”, in case you got confused) pose a problem. Even if life is out there somewhere right at this moment, and they have the intelligence and technology for interstellar communication, by the time any communication signal will reach them, they could be extinct. Or they would send a signal back and we wouldn’t get it until after our sun has already exploded. Simultaneous means nothing when the distances are so, I’ll use it again, astronomical.
What’s the point then? Well, we could find proof of intelligent life perhaps. We can travel (or send our robot overlords) to distant planets that have the right conditions of life, and see if these conditions have ever sustained life, or if they have the possibility to do sometime. And, we can hope that perhaps, maybe, ten million light years from us, an amazing civilisation sent out a signal 10 million years ago. And that we would be able to detect it. We won’t be able to communicate, but it might be enough just to know that we’re not alone (or have proof, at the least). A: Finding, perhaps. Communicating, I wouldn’t count on it.
Q: But then why… A: You know what, you cares? It’s space. SPACE. It doesn’t need an explanation, it needs exploring.
It might have become clear that I have a slight fascination with outer space. Not to say that I am utterly obsessed. One might say I am ‘astronuts’. Completely Bonkers for space. But who can blame me?
Over the past two months I have collected pictures, taken with my not-always-so-smart phone, of views on the Tay Bridge from the top floor of my building. I mainly wanted to characterise the different types of suspended water particles based on how limited the resulting view was. However, in the mean time, the clouds have lifted, or at least occasionally, so I was unable to gather all the reference pictures needed for my mist-classification project. It was going to range from “I cannot even see the church tower” to “wooooow”. Instead, I was treated on some colourful sunrises. Hardly something to complain about.
Here is a mini subcollection of those pictures, including one from yesterday showing the hint of snow we have received:
So, before January ends and I sound like a complete div: Happy New Year. May it be filled with beautiful sunrises and other things people wish each other.