I will now be on https://www.valeriebenti.com/
I’m still working out some kinks, so bear with me as I’m doing that, but in the meantime, I’ll stop posting here and start posting there. Thank you for following me so far!
I will now be on https://www.valeriebenti.com/
I’m still working out some kinks, so bear with me as I’m doing that, but in the meantime, I’ll stop posting here and start posting there. Thank you for following me so far!
It’s been two weeks.
Our fermentation vessel has been sitting at room temperature (~ 20°C or 68F) for two weeks.
It’s time to move some things around. Or move some liquid into some bottles, to be more precise.
In the bottles, we want some final fermentation to happen. This won’t really add any alcohol, but CO2. Perfect to create a bubbly beer! But there is one problem: all the sugar we put in the wort has been eaten up by the yeast in the fermentor.
So we have to add just enough sugar for the yeasts to convert to CO2 gas, but not too much (we don’t want the bottles to explode). We made up a sugar-water solution by boiling 2 cups (473 mL) and dissolving 4 oz (113 g) of sugar, which we mixed into the fermented almost-beer. We also needed to move the almost-beer into our bottling bucket – carefully, as to not add too much oxygen or contaminants!
Next step was to set up a bottling assembly line. Part one: filling the bottles up, leaving about an inch (2.5 cm) at the top.
Part 2: capping the bottle.
And there we are: a bottle of our very own, home-made beer!
About 40 bottles, actually.
Okay, we’re not quite ready. We need to give the yeast another week or two for the final fermentation. After a quick taste of the almost-beer, I kind of hope those two weeks will change the taste (and the bubbliness), because for now it tasted quite bland.
In addition, our special gravity measurement – which gives an indication of sugar content and can be used to estimate the alcohol content by comparing with the original value – wasn’t very promising. Our beer seems to be less than 3%.
But we’re not giving up hope yet! In two weeks, we’ll see what the final product is. I’ve also read that a few weeks of extra “ripening” can help with the taste as well. And we can always give brewing another go, keeping in mind what we’ve learned so far.
While we’re waiting for the yeast to do its thing, it may be useful to learn about what exactly fermentation is. Fermentation. You’ve heard it before, in the context of beer or kimchi or sourdough bread (or in a biochemistry class). But what does it mean? And why isn’t yogurt alcoholic?
Briefly, fermentation is a biochemical process where tiny organisms break down a complex molecule, such as starches or sugars, into a simpler molecule, an acid or an alcohol, while making some energy. This happens in an anaerobic environment – meaning it does not require oxygen. This contrary to aerobic processes, like what we humans do most of the time when we want to convert sugars into energy.*
Yeasts and bacteria are the two types of organisms that do this sugar breakdown. There are three different types of fermentation, depending on the end product.
Certain microorganisms are better at certain types of fermentation. That is way it is very crucial that the wort does not get contaminated by outside yeasts or bacteria: you only want the alcohol-making types, not the acid-making types. Unless you want to make a sour, that is.
It is also why, to make a sourdough starter, you just leave some sugars (starches actually to be more precise, in the form of some flower in water) out on the counter. The bacteria and yeasts floating around in the air are the ones you want for lactic acid fermentation – and to start up a sour dough culture.
Controlling the rate of fermentation and end products is a balance between making sure you have the right microorganisms (not all yeasts like being in alcohol – let alone making alcohol), balancing the water and sugars (is there enough food?), controlling the temperature (we prefer certain temperature, so to microorganisms) and waiting the right amount of time. That’s why fermentation is a bit of a science and also a bit of cooking. Though science and cooking are actually very similar to start with.
So to recap, fermentation is a process where yeasts and bacteria convert starches and sugars into alcohol and/or acids, with some by products. And yogurt isn’t alcoholic because the milk-loving bacteria are lactic acid fermenters, not alcohol fermenters.
Disaster has struck. We left the fermenter for one day and came back to this mess:
We had filled up the container too much, so once the yeast started munching away at the sugars, the extra build-up of foam caused the stop to come off. Oh no.
So we needed to clean up. We also siphoned out some of the liquid to avoid this from happening again. Hopefully, we did not expose the beer to external oxygen and yeasts and all during this process…
We put the S-stop back on the fermenter. This ensures that no gasses can come in, while gasses can go out. During fermentation, glucose (which is sugar) gets converted into alcohol and CO2. The latter is a gas and needs to go somewhere, so we let it go out.
This was last Monday. Since then, there seems to have been very little activity in the fermenter. The good news is that everything smells quite nice and beer-ferment-like, not sour, so we will move to STEP 7 sometime in the next few days: bottling!
We’re making a Northern Brown according to this recipe: https://www.brewersfriend.com/homebrew/recipe/view/564492/northern-nh-brown
Recommended reading: How to Brew
*I say most of the time because when we get muscle cramps, this is because we’ve been working too hard without providing our cells with enough oxygen to do aerobic respiration (the oxygen-needing-kind). In that case, our cells go into anaerobic respiration, which is very similar to fermentation actually. The result of anaerobic respiration is lactic acid (hey – go back and read about how that’s one type of end product for fermentation!) and some quick energy for your cells to use in the form of ATP. Anaerobic respiration is less efficient than the aerobic kind, but it can get us some quick energy in a pinch.
Source for little factoid is that one episode of the Magic School Bus that I remember where Ms Frizzle was doing a triathlon and her muscles started producing lactic acid so the students – who were obviously in a mini school bus inside Ms Frizzle (where else?) – let out the air of the tires so her muscles would have oxygen.
Next week is time for the local Jazz Festival, and to prepare I switch my background music back to Miles’ iconic album. In addition, I have been made aware that I seem to be making blue my go-to color. On a slightly related note, it turns out that blue is a very hard color to make.
It seems weird that blue would be hard to make. It’s so prominent in nature. The sky is blue. The ocean is blue. Blue jays are blue. Blue eyes are blue.
But as it turns out, blue pigment is very rare. Butterflies and birds with a blue color aren’t blue because their wings or feathers contain blue pigment, but because of nanostructures that reflect and diffract light in such a way that interference amplifies blue wavelengths, while cancelling out the others.
A blue pigment however, absorbs all wavelengths except blue. Light absorption occurs when a photon supplies an electron with enough energy to jump to a higher energy band. As red light has the lowest energy, only electrons with a narrow energy gap can be excited. Only a few molecules have the right structure for this to happen. Absorption of red light is crucial for a blue pigment, and therefore it’s a rare thing.
Because of their natural rarity, the design of synthetic blue pigments is of high interest for science and industry. The bluest blue was created by accident, by Mas Subramanian, a solid state chemist who wanted to create a material with the combination of electronic and magnetic properties for microchips. One of his ideas didn’t lead to anything particularly useful for fast computers, but it was very blue.
Where did this quest for blue originate? Blue is most people’s favorite color; it symbolizes depth, stability and serenity; and as it is the color of the sky and the sea, painters love it. True blue flowers are non-existent (violets are purple, people), even though horticulturists and scientists have tried endlessly. And even though blue food is unconsciously associated with toxins and spoilt food, some scientists’ life goal is to create true blue food coloring, rather than current food coloring that seems more green.
While artists, foodies, and flower lovers dream of the truest blue, I’ll go back to some sweet tunes and feeling slightly melancholic. I mean… Blue.
Read more about blue in this Science feature.
It’s no big secret that I think penguins are pretty cool. So I want to tell you some of my favorite penguin factoids. To be honest, mostly because lists are pretty easy to do (dixit the lazy blogger) and I did most of the research for this while tweeting for the Science For Progress RoCur (lazy blogger, remember?). Anyway, despite my evident laziness, penguins are actually awesome, and here are some reasons why:
Factoid number one:
Penguins have an amazing sense of style. They always look like they’re dressed for a party, rockin’ the tux look.
There are 26 “types” of penguins (due to the fact that a lot of types are geographically isolated from each other, it is not clear how many species there are). The largest type of penguin is the Emperor penguin (Aptenodytes forsteri – extra fact: Emperor penguins are the only bird species that never set foot on land!) The smallest penguins are little penguins (who would have guessed), including Eudyptula minor minor, in case you want to emphasize how tiny they are.
My favorite penguin, however, is the Macaroni penguin because they have the best. featherdo. ever. They kind of look like Einstein had a hair-coloring accident but decided to go out in a tux anyway. They get their name from 18th century English men who wore feather-adorned hats that were known as “Macaronis”.
Factoid numero trois:
A nest of penguin eggs in called a clutch.
Most penguin species are pretty good parents. Often, both parents take turns incubating the eggs. In some species, daycares are organized so some birds can go hunting while others take care of the fluffs.
While on parenthood, there are a number of examples of same-sex penguin couples taking very good care of penguins babies. Makes me wonder if they occur in nature. Perhaps they occur but don’t last when the couple realizes they can’t have any eggs. The examples are anecdotal in zoos, where the couple either gets an egg from the handlers or goes stealing eggs. Anyhow, there are plenty of examples from all over the world, including New York, Edinburgh, Sydney, and Denmark.
Walking like a penguin is a pretty efficient way to walk on ice without falling on your butt. And I’m a walking hazard without the ice. Also, my butt is higher up and has fewer feathers for cushioning. (#TMI)
I’ll leave you with this amazing video of a brave little Adélie penguin that went viral a few weeks ago:
Shoutout to my follower @drpenguinone for obvious reasons.
Edit: I’ve added links to this amazing video because I can and it’s hilarious.
Exactly a century ago, D’Arcy Thompson published his book On Growth and Form.
I’ve spoken about Mr. D’Arcy before, but as it is the 100-year anniversary of his masterwork, I feel it fitting to revisit the topic. Since mentioning him last, I have finished reading his book, and have also started to write up my thesis. I bring up my thesis because my work is related to D’Arcy’s work in the sense that I have been trying to bridge the gap between biology and physics, and I predict that some of my reading will inspire me to write more (hopefully more of my thesis but presumably also more on the general topic of bio-meets-phys).
Mr. D’Arcy wrote On Growth and Form to collect his observations on the mathematical principles of nature. He explains how biological phenomena of form and growth closely resemble physical and mathematical principles. Especially for some of the more simple examples (e.g. the shape and size of single or doublets of cells) the similarities between biology and physics (e.g. single and doublets of bubbles) are almost uncanny. These simple systems can easily be described using simple formulas, and he suggests that even more complex systems can be explained in a similar way (though he remarks that it will take a lot of formulas and paper space, luckily we have computers now). In 1917, this idea was pioneering, to say the least. Bio-mathematics and biophysics were nowhere near being the hot topics they are today.
One of the events organised for the anniversary of On Growth and Form, was the exhibition A Sketch of the Universe at the City Art Gallery in Edinburgh, showcasing works of art that were inspired by the book, or by the idea that mathematics and biology are closely intertwined. The exhibition is closed now, but this weekend I did get the chance to go visit it.
So, I present to you, some of the highlights that I found interesting or cool-looking:
“I know that in the study of material things number, order and position are threefold clue to the exact knowledge; and that these three, in the mathematician’s hands, furnish the first outlines for a sketch of the Universe.” (D’Arcy Thompson, On Growth and Form)
“For the harmony of the world is made manifest in Form and Number, and the heart and the soul and all the poetry of Natural Philosophy are ebmodied in the concept of mathematical beauty.” (D’Arcy Thompson, On Growth and Form)
“The waves of the sea, the little ripples of the shore, the sweeping curve of the sandy bay between the headlands, the outline of the hills, the shape of the clouds, all these are so many riddles of form, so many problems of morphology.” (D’Arcy Thompson, On Growth and Form)
You can read more about D’Arcy Thompson, On Growth and Form and some of the events being organised this year in honour of the 100 year anniversary, here. And presumably in the near future on this very blog.
[Note: Again, I realise that D’Arcy Thompson’s last name is “Thompson” so “Mr. Thompson” would be a more appropriate title (or Prof. Thompson) but I just cannot resist his practically Austenesque first name.]
Two weeks ago, I told you that physics and cancer are, perhaps counterintuitively, intermingled and that this relationship has biological and clinical implications. I outlined how mechanical forces act on cells and tissue, and perhaps are responsible for one of the many ways of cancer progression.
In this post, I’d like to tell you about how being able to detect mechanical properties of tissue can help with diagnosing diseases. So while the previous post was more about how physics can influence the biology of a tissue, this time I’d like to focus on how biology can dictate physical properties of a tissue.
A very important issue to point out, before going into the differences between healthy tissue/cells and cancer, is the size scale we are considering. Depending on whether we are talking about cells (µm size range) or tissues (100s of µm to mm), we can make quite opposite conclusions: several studies have shown that tumour cells are softer than healthy cells (of the same tissue type), while tumour tissue is stiffer than healthy tissue.
First the cells. Experiments such as Atomic Force Microscopy (which I mention because I have used it myself) show that especially metastatic tumour cells are softer than healthy cells. If we consider what cells do during metastasis, this actually makes sense. (Metastasis is the process where cells migrate away from the initial tumour and spread to other parts of the body.) A softer cell is able to squeeze through other cells, and through the wall of a blood vessel, allowing it to travel to elsewhere in the body. This different mechanical property allows it to behave in its particular way. Knowing this property allows us to predict the aggressiveness (or invasiveness) of a certain cancer. If the tumour has cells that are much softer than other, it is usually a more aggressive type of cancer.
This difference in mechanical properties not only makes sense if we consider the behaviour of the cells, it can also help make prognoses and decide on what type of treatments to use.
Next, on a larger scale, tumours are stiffer than healthy tissue. This is exactly what we feel when we are “looking for lumps”. A bit of tissue feels different, namely stiffer, than what it should be. The reason tumours are stiffer is not actually due to the (softer) cells it contains, but due to what sits in between the cells: the extracellular matrix. The extracellular matrix is a very structured meshwork of structural proteins that acts as a scaffold for the cells: it provides the tissue with structural integrity, cell organisation and mechanical strength. For example, there are a lot of extracellular matrix proteins in our skin, which is why it is, well, our skin (hurray for circular reasoning): a sturdy barrier between the outside and the inside of our body. In healthy tissue, the extracellular matrix is usually very well organised. The fibers making up the matrix are regularly cross-linked and have and neatly organised. However, the matrix in tumourous tissue is chaotic. In essence, was “built” too quickly. In this fast-growing bit of tissue, the scaffolding had to be assembled fast to support the rapidly dividing cells. As a result, the fibres are not well organised and the crosslinking is random. It is as if the scaffolding of a building was built too quickly, so rather than nicely structured, there are random beams sticking out in all directions. As a result, pushing down on the matrix does not compress it as much, and it feels stiffer.
At a tissue level, these differences in mechanical properties are very useful for diagnosing cancer. Because of different mechanical properties, we can feel lumps, but we can also image it using techniques such as ultrasound, MRI and other imaging techniques. Due to different physical properties, the cancerous tissues interacts differently with whatever wave (light, sound, …) we are using to try and detect it. Thank you physics!
To wrap this up: the physics of cancer is important, and useful, and interesting, and cool and definitely worth researching. And this is why interdisciplinary research is not only a fancy buzzword, it can also increase our understanding certain phenomena and come up with better diagnoses and treatments by approaching the problem from a completely different perspective.
This subject was the topic of my second FameLab performance (Scottish regionals), which ended in a little song (to the tune of “What a Wonderful World” by Sam Cooke), in which I wanted to highlight the importance of interdisciplinary research and how studying diseases from a physics perspective can only be productive:
You know, cancer’s about biology
And perhaps a bit of chemistry
But I’m telling you there’s physics too
There’s physics happening inside you
With one subject you can never be sure
Put them together, and we might find a cure
And what a wonderful world that would be…
Some references I used to verify that my thoughts on this subject were not completely unsubstantiated:
Baker EL, Lu J, Yu D, Bonnecaze RT, Zaman MH. Cancer Cell Stiffness: Integrated Roles of Three-Dimensional Matrix Stiffness and Transforming Potential. Biophysical Journal. 2010;99(7):2048-2057. doi:10.1016/j.bpj.2010.07.051.
Suresh S. Biomechanics and biophysics of cancer cells. Acta biomaterialia. 2007;3(4):413-438. doi:10.1016/j.actbio.2007.04.002.
Kumar S, Weaver VM. Mechanics, malignancy, and metastasis: The force journey of a tumor cell. Cancer metastasis reviews. 2009;28(1-2):113-127. doi:10.1007/s10555-008-9173-4.
Plodinec M, Loparic M, Monnier CA, Oberman EC, Zanetti-Dallenback R, Oertle P, Hyotyla JT, Aebi U, Bentires-Alj M, Lim RYH, Schoenenberger C-A. The nanomechanical signature of breast cancer. Nature Nanotechnology. 2012; (7):7 57–765. doi:10.1038/nnano.2012.167
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.
(Yes, the only reason for this post was to brag about my new cool nickname.)
Wouldn’t we all like to be immortal?
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)