Dagl1

Thanks! That sounds really cool (and currently way too complex to really understand. There is something specific I can work towards to understand). If anyone else comes along and wants to add some information, I find it quite interesting that gravity waves could travel at a speed lower than c (even if the wave interacts with itself, shouldn't whatever (particle??, graviton?) the wave is, travel at c at all times since is mass-less(?). Even light in a medium only has 'apparent' reduced speeds due to interaction/absorption with atoms right? Thanks again for the interesting answer! -Dagl

Thanks Swanson, Just to be sure, in general I should, open a new thread myself if I feel like it will require it to be split? Sorry for being lazy hahaha;p

This may require a split, but I have two questions that came up when reading this thread: Are gravitational waves affected by gravitational lensing, I found some random (not very sciency) websites talking about how gravitational waves will affect light (by changing the amounts of gravitational lensing). However I was wondering, will these waves also change 'apparent' direction (light goes in a straight path but it is space-time that is curved, which we see as 'apparent' curved paths, right?)? @Markus Hanke Could you attempt to explain how wave-tails emerge from non-linear interactions (at 1.5 post newtonian?). I looked up some articles about it, but realise this is currently quite far outside what I can easily understand. https://arxiv.org/abs/1607.07601 Thanks in advance! Dagl

Hi there, Please see the following paragraph of the Book [I don't want to bias anyone so I can't post its name, will do after a few answers], and the relevant radiation-related claims in the research article (https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1432-0436.1991.tb00872.x): I tried looking up sources for gamma-radiation-mediated enucleation, but can't find any. And in the articles he/they don't talk about "absence of genes' or 'DNA destroyed'. I think I have enough (lack) of evidence to say that the Book is misinterpreting/spinning the story, but wanted to check here just to be sure, before I accuse the Author of doing so.Because this is the main argument of the first 'scientific' chapter in the book. Thanks in advance -Dagl

I think it is because you are given sources, but then do not watch them, while still talking about 'alleged' temperature changes, as if that's not kind of shown at this point? Questions are fine, but it may be good to first fully consider the answers given.

I have only a superficial understanding of this, so it may be wrong. But as far as I understand, there is no medium needed for particle/wave functions as they are not true waves. Or possibly, but again, this is just me guessing, the medium is the field(s) from which the particle(s) arise? Interesting question, hopefully the physicists around here will know!

An simple example I could think of is on the level of (brown)fat production. Brown fat produces a lot more heat than ATP, when compared with the usual fat oxidation (I think?) mechanics. Having mutations in genes with as a result increased brown fat production, that person would most likely also have increased metabolic rate. When we look at people with overactive thyroids, we see that they use a lot more energy, so any gene that is involved in the thyroids function will possibly change basal metabolic function. On the cellular level, any mutation that leads to a less energy efficient enzyme, or less/more energy production will also affect basal rates. If you want to know specific genes, you will have to search the GWAS studies/data yourself, or maybe someone will feel like reading them and tell you, but I think the question is quite complex and a lot of genes will slightly affect metabolic rate, so its difficult to find causal relationships or even strong correlations. -Dagl

I completed that 6 years ago (it was my high school math curriculum), so back then I understood/knew most of it. Now is a different story. I think from the other replies and the videos/sources I found, that I understand it well enough (for now). Thanks though!

I have a question, do you recognise that people have attempted to explain that particular thing to you? Is it A that you don't accept their answers, B that you don't understand their answers or C you just ignore them intentionally? If it is not C, then its maybe a good idea to go back to figuring out where your thinking is in opposition, and how you could potentially learn more about, instead of immediately saying everything has failed. Honestly, you are doing a horrible job at learning anything, you don't seem to grasp or are intentionally ignoring a lot of explanations and instead you keep asserting whatever you think to be right...

Alright thanks!

One last question, since I see the standard deviation mentioned a lot, if I am just using erf(x), the standard deviation is constant (or does not matter?)?

Probably going to be quite difficult to find individual genes, although you could take a look at GWAS studies regarding basal energy expenditure. GWAS studies are a way of correlating genes to specific traits, as in cases such as metabolic rate/energy expenditure, the trait is too complex to have a single or a few genes which are important. Additionally it could be that variant X of gene1 increases energy expenditure in people with variant Y of gene2 but decreases expenditure in people with variant Z of gene2. This is probably less likely to happen than compounding effects, but since cellular networks are highly dynamic/complex, it is likely that it happens sometimes and it makes it a lot more difficult to search for specific genes/mutations that affect a complex/emergent trait. I did quick search and found some articles, but I haven't checked them for relevancy (only their titles appear relevant at the moment). I hope this helps or at least gets you started in your literature search (if you can't open an article, remember that sci-hub exists (although check whether or not you want to acquire your PDF there (legality/piracy reasons)), or send the authors an email, they will most likely send you their paper for free if you ask. Kind regards, Dagl https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381071/pdf/40608_2017_Article_145.pdf DOI 10.1186/s40608-017-0145-5 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6072034/pdf/pone.0201555.pdf https://doi.org/10.1371/journal.pone.0201555 http://apjcn.nhri.org.tw/server/APJCN/28/1/35.pdf doi: 10.6133/apjcn.201903_28(1).0006 https://www.sciencedirect.com/topics/medicine-and-dentistry/resting-energy-expenditure https://e-nrp.org/DOIx.php?id=10.4162/nrp.2016.10.1.115 https://doi.org/10.4162/nrp.2016.10.1.115 https://www.tandfonline.com/doi/abs/10.1080/10408399309527631 https://doi.org/10.1080/10408399309527631

Thanks, I get it now, just to re-iterate, in an example of length, I could ask: what is the chance of finding someone x away from the mean? I feel like I may have simplified it too much now, but still think I get it, gonna play around a little with the python as well, thank you a lot!

Thanks a lot @studiot! My (applied) and all other types of math is I suppose just slightly above that of high-school students (that is of course horribly defined as a lot of different school systems exist, here is the curriculum of the type of math that I think I can still all use https://www.examenblad.nl/examenstof/syllabus-2016-wiskunde-b-vwo-nader/2016/f=/wiskunde_B_def_versie_vwo_2016_2_versie_voor_hervaststelling_8-9-2015.pdf (it is in Dutch however, so I presume not very useful, but at least you got an answer haha)). Additionally I use (and to a degree understand) statistical tests that I use and what they are based on (one-way ANOVA's, "post-hoc" corrections and odds ratio tests). I think I also have a pretty good grasp of what exactly P-values are, but that is about all my mathematical skills. I will read your answer a few times the coming days, as not all of it is making sense to me (but also I don't think all of the information is relevant for the level of understanding I want (especially regarding that "it is finite", and therefore very useful). I do have 1 question still, I understand how this function is connected to statistics (as it's derived(?) from a gaussian distribution right?) but I still can't see how I would use it. While I am learning python just because I have this book and want to do coding, I assumed that this specific function would come back a lot if I would apply my python skills in a future biomed PhD (so let's say in interpreting quantifiable results of different treatments), could you give me a tangible example of where and how this function would be used. I am missing some fundamental "aha" moment, so the less abstract the better;p @Huckleberry of Yore I understand that you can set whatever x is by changing the value to your mean; but I still don't entirely get the application, could you show the code that does this, and what it does (the function still eludes me). @timo Okay so I am answering/reading these a bit in a different order, but what you said made something click, maybe. Now I also understand why we are taking the integral of the distribution (the "sum" stuff you said was made it click). So just to be very sure: This function is useful if I already know the mean/deviation of my standard distribution and with this I can calculate the likelyhood of finding a variable somewhere on that graph (that somewhere being defined by x in erf(x)?)? So it is just like a confidence interval but in reverse (that's a horrible description, ehh: A confidence interval gives me, for example, two points between, with 95% confidence (or whatever number we choose) I will find new values for samples from that same group/population. And this function gives me the chance that a given value is somewhere between 2 points. @Sensei Thanks for the reply, your answer shows how I can use a (pseudo)random number generators to get such a Random Variable, and that it doesn't have to be stuck between 0, and 1 (that is the last line about right?), thanks! But my question, although possibly a bit badly worded, was wondering more what value the Random Variable (as I thought this would be constant) would have when throwing 6 sided dice. Which I may now understand, but I am not entirely sure. Oh I just started coding (again), if your code does something else and does answer my question, my apologies but then I don't get this stuff yet. Thanks everyone for the answers!

Hi there, I have just started going through a python programming book and one of the functions presented is the error function. I understand it is not very necessary for me to understand the mathematics behind it, but I would just like to. Now from looking at, reading a bit about it and watching a video how it is derived, it is my current understanding that the function computes the probability that a Random Variable (if assumptions of normal distribution, standard deviation and expected value are all met) can be found within [-x, x]. I think two things are unclear for me, firstly: what exactly is a Random Variable, the wiki article and some other websites talk about it as if it just any variable that is determined by chance, such as the rolling of dice (I presume this cannot be used in error functions due to the lack of normal distributions). However I don't understand how this could be used (so most likely I am misinterpreting the explanations on the internet). Let's say I measure how tall some people are, and the people I choose are randomly picked with no bias in selection. That Random Variable's value would be.... what? Secondly I don't understand the usage of x in this case (erf(x)). The functions domain is - infinity to infinity, but from values of x that are around -3 or 3, we already have almost a 100% chance of finding our Random Variable. In my imagination those numbers would be arbitrary, and I can't see how one could use it (let's say we measure length in centimetres, why is the chance that the Random Variable will always be present when we do erf(3) = 0.9999978? I hope the explanation of my thought process and (possibly false) assumptions is enough for someone to point out the faults in my reasoning. I would like to know how I could apply this function and when this is useful. On Wikipedia is written: "this is useful, for example, in determining the bit error rate of a digital communication system." But that doesn't (yet) make it clear for me;/ Hope someone can help, and please forgive my ignorance on the subject. -Dagl

A lot of instinctional fears are encoded in our genome, it seems not too absurd to assume that, a stimulus+fear response may use the already-existing instinctional fear machinery present in the brain. One reason why it is difficult to give a clear answer is that your genes and epigenetics only encode for what each cell does, but when looking at behavior, we observe a network of cells all working together, thus finding non-abstract/non-generalised answers is difficult. Let's take some biology-based fictional example I just came up with; Receptor X is comprised of 4 different unique subunits, of which 20 types are encoded by the genome. Strong fear response changes the subunit pattern to a higher amount of type 3-5-5-16 instead of the regular 3-5-5-12 (the numbers are just the subunit types we currently have for this receptor). These changes will be epigenetic: histone modifications, DNA methylation, RNA-mediated etc. Now only the neurons in your brain that contain were activated (strongly) during the fear response, will contain more 3-5-5-16 instead of the rest of the neurons (of the same type) that were not involved in this fear response. Now the receptor just activates slightly faster or slower (or whatever, its a bit different but not in any major way). But this can have enormous differences in behaviour. Now imagine that something also changes in the germ cells (they get more of a specific type of RNA, which remains (or is actively maintained) throughout the life of the new offspring. The mouse/organism may already instinctionally have strong responses to specific tastes, colours (think of specific male fish that attack everything that is red, because other they have evolved to do that) or sounds/smells or even shapes (we apes are pretty scared of snakes, which is not a learned-behaviour). The epigenetic changes may just lead to a different subunit composition later in the life, which as a result (how, is very difficult to really say in a causal/per cell/per molecule basis) now fears the specific stimulus. In this case, having a good understanding of genetics, epigenetics, general cellular adaption and which types of behavior is already encoded within an organism, may make it easier to wrap your head around how this works. -Dagl

It might help, if you @Angelo would first, in an objective tone, lay out exactly what you believe Tyson's argument to be, and the steps in his reasoning (as far as they are provided and assuming they are truthful). As far as I understand the simulation hypothesis, is that it is based on chance and likelihoods coupled with some very specific assumptions; however the things you say, and the way you ask your questions and/or comment on other peoples posts, to me seems to indicate that you (at best) don't know the full reasoning behind the simulation hypothesis (or you do understand it, but are wilfully creating strawmens). Additionally, it would be great to present the strongest argument(s) for the simulation hypothesis, and not immediately assume that Tyson and other people agree on everything. If he has some illogical reasoning or assumptions you don't agree with, then it may be good to find a better version of the argument, instead of immediately disregarding the entire hypothesis. If you are really interested in understanding Tyson's and other people's point of view on this, it would help to start with a detailed summary/explanation of the hypothesis, because I could explain it (as far as I understand it), but I doubt the explanation is similar to what you think it is. And if you aren't sure on WHAT people belief, then it is very strange to already think of it as nonsense, therefore (assuming you have good reason to think of it as nonsense) it should be easy for you to explain it (in your own words, please don't just link something, that doesn't test your current understanding). Kind regards, Dagl

Epigenetics covers a lot of topics (I find that regulatory RNA's or RNA modification are also epigenetic, although of generally much smaller timelengths), the two most well known (researched) mechanisms would be DNA methylation (mostly CpG islands in promoter regions) and histone modifcations (the simplest concept, but not the only mechanism by which histone modificaitons work is to think of DNA as a string of negative charge. This string is wrapped around proteins (histones) like beads on a string, it just wraps around a little less than 1.5 times, so only a small portion (147 basepairs) of the total string is around each protein. To "read" (transcribe) a gene, a ring has to go over the string; if the string is wrapped tightly, it may not be able to due to friction with the histone, but if you make the histone negative, it will repel the negatively charged DNA, allowing for more room between the DNA and the histone, making it easier for this part of the genome to be transcribed.

I'm no expert on filters, but I am almost certain that any enclosed space with a HEPA filter will be much less polluted than a similar room filled with plants. I would be careful with interpreting %'s, especially when comparing those numbers with, for instance plants. A HEPA filter is a specialised piece of equipment, and as such will most likely do a much better job than a plant of the same size. But the surface area of a HEPA filter will be many more times that of a plant of similiar size, so in what way do you mean "effectively" in your question. Does 1 HEPA filter, work as effectively as 1 plant, or do we compare surface area? Do you give different weights to different types of particles? Maybe plants filter larger or smaller things at different efficiencies, and some may be more dangerous for human health than others. Your question is too vague to answer in one go I think, it is also not clear how you plan to use them. Will your house be sealed and all fresh air will enter through a filter? In that case it will by definition be better than plants, cause you just cant put enough plants in between the source of new air and you/your parents. On the other hand, one could, theoretically (and realistically it isn't that hard) create an environment that constantly recycles its own air by using plants, just need to make sure the O2 and CO2 production are in equilibrium around the optimal levels for human consumption. In that case you would only need small amounts of outside air to combat leakage etc. In that case I would assume the air in your eventually becomes cleaner than using a HEPA filter (assuming plants and the surrounding support-(micro)biome don't produce new airborne particles that are unhealthy etc). -Dagl

I am not entirely sure how "model organisms" is (meant to be) used here, but research in well understood model animals (flies, worms, mice etc) enables faster and more complex understanding because of how much we have already researched them. Model organisms have many (specific) uses, and understanding their limitations is obviously important. But let's look at the Seahare (Aplysia Californica); it has possibly one of the simplest learned/inducable reflexes that we can research, and the fundamental cellular machinery is in many ways quite close to that of humans (and in many ways far off, so its important to choose the right sort of model for the right type of question). By producing/breeding specific mutations into the Seahare and then observing the differences induced, we can see effects of genetic/genomic changes on "behaviour" (even if its a very simple reflex). This type of research gives us a lot of insight into what specific regions of the genome are responsible for. Additionally, a lot of the genome is much less understood and doesn't code for proteins, instead having regulatory functions. Highly controlled models will of course make it easier to find subtle differences that are the result of mutations in the non-protein parts of the DNA. Hope this is interesting information, even if it may not be exactly what you wanted to know. -Dagl

I like books by Smullyan, such as "The lady, or the tiger?". https://www.amazon.com/LADY-TIGER-Raymond-M-Smullyan/dp/0394514661 Reading "Thinking fast and slow" will give you a better insight in how you think, potentially improving your decision making. https://www.amazon.com/Thinking-Fast-Slow-Daniel-Kahneman/dp/0374533555/ref=sr_1_1?crid=1KC9WKEPZKSOW&keywords=thinking+fast+and+slow&qid=1577018204&s=books&sprefix=thinking+fast%2Cstripbooks-intl-ship%2C222&sr=1-1 If your into or willing to try meditation, there's a book that guides you with meditation practices to improve your focus, but I am not really sure if that works. https://www.amazon.com/Attention-Revolution-Unlocking-Power-Focused/dp/0861712765/ref=sr_1_1?crid=3CEV6S14XD8ZQ&keywords=attention+revolution+alan+wallace&qid=1577018129&s=books&sprefix=attention+rev%2Cstripbooks-intl-ship%2C226&sr=1-1 "A mind for numbers" is nice i suppose. https://www.amazon.com/Mind-Numbers-Science-Flunked-Algebra/dp/039916524X/ref=sr_1_1?crid=2Y220INEUBMDA&keywords=a+mind+for+numbers&qid=1577018115&s=books&sprefix=a+mind+for+number%2Cstripbooks-intl-ship%2C225&sr=1-1 Not straight up logic or memory, but still something that could improve decision making: Superforecasting. https://www.amazon.com/Superforecasting-Science-Prediction-Philip-Tetlock/dp/0804136718

I personally don't feel like a question is valid if you have to find the most right answer among those that are all wrong. Regarding 5, while that might be the case, the question is: which of these statements is true, and the answer, that catalytic reactions mediated by enzymes follow saturation kinetics, or am I misunderstanding your comment. I think as a student you have a lot of ground to complain and demand proper questions on tests.

Regarding the questions (after Charon's comment I hope i'm not too wrong): 1. More permeable = cis-unsaturated phospholipids (http://bio1510.biology.gatech.edu/module-3-molecules-membranes-and-metabolism/02-membranes/ I presume this is right, didn't look into it mucm) 2. Hypotonic 3. Can't immediately find a source. 4. Don't think either of those answers has something to do with Km but I hope someone can correct me if I am wrong, but Km is just a substrate concentration needed for 1/2 Vmax (catalytic activity), but the Km concentration does not tell us anything about what value Vmax has right? 5. not sure what the first answer here says. but I think the second answer (saturation kinetics) is right? "enzyme-catalysed reactions display saturation kinetics." https://en.wikipedia.org/wiki/Enzyme_kinetics 6. I think 60 but no clue really 7.That question is strange, I suppose it is Photosystem 1 Cytochrome B, but I think the question is bad, as none of those enzymes (as far as I know) have anything to do with the "higher energy levels of photons". ehh I skip the rest. @CharonY Do you not think the question/answers of 4 and 7 are strange? And is the wiki quote I posted at question 5 incorrect or? Maybe I have to brush up my enzyme kinetics;p

Hi, As the question says, I am wondering if eukaryotic (mammalian) cells such as endothelial cells (or whatever really) have intra-cellular defences against viral infection. I mean specifically if 1 cell infected with viral stuff (protein, RNA, DNA), can it neutralise this threat and continue to live and function afterwards. I am aware of TLR's being able to increase Interferon production, but that influences the viral response of the body as far as I understand, not the survival chance of the individual cell. Apoptosis is of course not what I mean, nor is the slowdown/shutdown of translation through kinases that recognise viral RNA/DNA. I suppose something with a similar final result as CRISPR/Cas in bacteria, although possibly through other means. Is there possibly targeted microRNA-like things that are produced similar to how RNA-induced silencing (RITS) uses the targeted mRNA for production of new siRNA? (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC544066/ RNA-dependent RNA polymerase is an essential component of a self-enforcing loop coupling heterochromatin assembly to siRNA production) Thank you in advance! -Dagl

Yes but if encased and it doesn't circulate for too long, it shouldn't be too much of a problem, as it then (should) enter the bacteria right?