Dagl1

Thanks Strange, you're an angel!! By the time I got back I couldn't edit my own post anymore

Alright, so I feel a bit (not a lot luckily) stupid, in the heat of the moment I thought my code was broken, but of course the else statement will show [3,1,2] once, before it finds the 1,2 sequence. I also see that for some reason (I suppose it is the command for Italic) the [ i ] in my Songs [ i ] has disappeared. I have manually checked my code a few more times and suppose it is working as intended, so my original question is now, once again, applicable I think: does this code really produce the right results. It feels very counter intuitive to me (but of course, it can just be that; a wrong feeling), that in a randomly shuffled list of 1000 songs, it was managed to be shuffled around 35-40% of the time in such a way that there are no sequential numbers...

Hi there, Edit: I spotted the mistake already, although i have to go now and have no time to change it completely!!! Please don't waste your time on it! I am (still) working my way through a python book and a question came up but I am not 100% if the answer I produce is correct (and the book does not have an answer to this particular question). The question is as follows: Music shuffling. You set your music player to shuffle mode. It plays each of the m songs before repeating any. Compose a program to estimate the likelihood that you will not hear any sequential pair of songs (that is, song 3 does not follow song 2, song 10 does not follow song 9, and so on). From: Sedgewick, Robert. Introduction to Programming in Python (p. 135). Pearson Education. Kindle Edition. I have the following code: # # 1.4.24 m = 1000 #number of songs n = 1000 #attempts counter = 0 Songs1 = stdarray.create1D(m,0) #create empty array with songs for i in range(len(Songs1)): # number each song Songs1 = i+1 for g in range(n): Songs = Songs1[:] #copy Songs1 so that we don't have to do the initialising within this part of the loop again for i in range(m-1): #randomly shuffle the songs r = random.randrange(i, m) temp = Songs[r] Songs[r] = Songs Songs = temp for i in range(m-1): if Songs[i+1]-(Songs[i]) == 1: #check if, after shuffling, the songs are in sequential order, if so add 1 to counter counter +=1 break # else: # print(Songs) # check if none-counted songs actually do not contain any things in sequential order print(100-counter/n*100) # calculate percentage I think, based on the checks I did, that this code should work. However I find the numbers (34-39%) quite high for the current numbers (n = 1000, m =1000), and therefore feel that I may have made a mistake. Thanks in advance Edit: I spotted the mistake already, although i have to go now and have no time to change it completely!!! the commented out else statement also shows [3, 1, 2] that is not counterd within the last if statement, i will figure it out later and come with an answer so that other people may learn from it!

First of, what are you trying to discuss? This is a discussion forum. Secondly, as you stated and implied multiple times, some things can be illusions or seem one way but are another. It seems that you are not applying this to your spirit/voices. There are medical conditions which lead to such believes. How are you able to say that your voice is real an not an illusion played upon you by your mind? You also state 'I knew it was not your average case because of what i was experiencing'. How do you know? Why is it not probable that you are (for a lack of a better word) just affected by some disorder that brings about voices in your head. For a lot of people they seem real and acoustic or visual hallucinations/delusions seem real to a lot of people. You must see the futility of going to a science forum, presenting a case of probable schizophrenia, then trying to convince us that because of what YOU experience(d), it is real? If another person with delusions comes along, equally convinced that his/her's are real, would you accept their 'evidence' upon hearing this story? What if their 'spirit' contradicts yours? Also, this free will thing? Causality and quantum mechanics (in my opinion, and my opinion only (can't speak for others)) already takes away any type of effect you could have on what path your life takes. Is this physical explanation not satisfactory? If not, what 'evidence' makes you now come to this conclusion?

You can always check addgene: https://www.addgene.org/59926/ (I think this one is okay but only quickly looked, please investigate before buying :)!) Thermofisher, sigma and origene also sell vectors or expression systems, however I couldn't easily find an eukaryotic expression vector there.

I would highly recommend reading up a little further... It is very important that you at least understand the basic mechanisms of memory before going off and trying to figure out how to do something that no one (as far as I know) has been able to do. I don't really agree with this article, yes the brain isn't a computer, but information IS stored in the form of a complex network of neuronal connections. And when we adjust such information, those connections have to be changed or a new pattern is produced and the old one is (partially) discarded. I have no evidence for that last part (what happens when we adjust information, but I feel those are the two options we have). The article describes that a newborn baby isn't born with data, but mentions reflexes and specific behavior. How is that not a form of data? I don't really understand the context of the article (in the end it seems a introduction to computing?), but on it's own I would say that while brains are certainly not computers, memory is stored in some form inside your brain. Additionally, things like the Default Mode Network (DMN) and other constant pathways do seem to at least on the face seem to imply some type of processing (but what it seems to me, definitely isn't truth). -Dagl

I wasn't very sure if what you said was true (cause it sounds very... broad;p) so I checked for a source, turns out that you are right and low frequency stimulation does seem to enhance episodic memory! https://www.frontiersin.org/articles/10.3389/fpsyg.2019.00993/full Quoted from the conclusion: The findings of the meta-analysis on younger adults revealed that frequency interacts with MTI as well as with stimulation timing. Specifically, both online and offline 1 Hz rTMS led to enhancing effects, which was driven by below-MTI stimulation. In addition, offline 20 Hz rTMS had enhancing effects whereas, online 20 Hz rTMS and 20 Hz rTMS at below-MTI led to impairing effects on episodic memory. A systematic review of the older adults and those with clinical disorders revealed a similar pattern of enhancing and attenuating effects of rTMS on episodic memory performance. However, important differences did arise with older adults and clinical populations implementing both offline 5 and 10 Hz rTMS protocols that had enhancing effects on episodic memory.

I suppose you just transfect your cells with a T7 RNA polymerase expression plasmid (my apologies if it turns out that this doesn't work, I didn't look up any difficulties). I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171830/ You may want to use some of their methods.

Ahhh I see, that makes more sense. In that case it may be interesting to just look up what floxing is used for in general and why you would want to target a specific gene. For a school project you could also look into exon skipping (in, for example Duchenne) and see if floxing could be used there. Good luck!

Could you clarify what you mean by cellular assemblies? And could you explain the relevance of the hippocampus? I could be wrong, but it seems you have just grasped the surface of brain signalling/memory formation and you may have some overly simplified ideas. Synaptic plasticity seems to be, at least for a big part, responsible for adaption. Basically (this is highly oversimplified, see resources at the end), every thought or idea is (probably) represented by 1 or more (no reason there cannot be redundancy) networks of many neurons. Each neuron has many many connections (synapses) and these can all be adjusted (more or less likely to fire at a given signal, or a stronger/weaker signal when firing). When you memorise something, you consistently activate the group of neurons that represent that concept. More specifically, you activate THOSE synapses, not other synapses (as much). This leads to strengthening of those connections, making it easier to fire that specific pattern (concept) the next time. The Principles of Neural Science by Kandel is an amazing text book to go through. If you want some more specific articles: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514210/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367554/ https://onlinelibrary.wiley.com/doi/full/10.1111/j.1460-9568.2010.07344.x If you can't access some, remember that sci-hub is a thing. There is some evidence for signals to loop around inside the hippcomapus a few times, but I can't find the reference (nor can I find it in my notes). Hope this helps. Another paper discussing synaptic plasticity and counterarguments: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6212519/ Another one by Kandel (just like the book and first article): https://www.cell.com/cell/fulltext/S0092-8674(14)00290-6

It might help if you explained a little more. Floxing is a method to turn off or inactivate a specific DNA region (or well, move it etc, but most commonly it is used for knock out experiments I think), so you should target whatever thing you want to research? If you already have a chosen loci but want specific information on what places are best, maybe someone can help you (I wouldn't know). But at the moment your question seems to be very low on details. Of course if you want to know what exon is best to remove for knockout, you can look at some functions. I would also recommend to check if there are any genes on the opposite strand or any known regulatory elements, as I would personally try to knockout the exon that has the least amount of other effects (as far as we can predict it based on already existing information). -Dagl

Ye could definitely be the case, I am not very familiar with the details.

Never heard of it, and didn't read the following articles but; I searched for 'exercise induced fatigue nervous system' on scholar, which gave the following (I think relevant) link as first hit: Possible mechanisms of central nervous system fatigue during exercise: https://journals.lww.com/acsm-msse/Fulltext/1997/01000/Possible_mechanisms_of_central_nervous_system.8.aspx By clicking on the 'cited by' button and then setting it to some recent date (2016 but choose whatever), we can then search for newer relevant articles that still refer back to this. That brings up the following research (I have not read the abstracts, but the names seem relevant (nor did I check the validity of the journals/papers)). https://www.sciencedirect.com/science/article/abs/pii/S0149763417308527 http://www.scielo.br/scielo.php?pid=S0100-879X2017001200301&script=sci_arttext https://www.tandfonline.com/doi/abs/10.1080/17461391.2017.1296890 This paper (2019 case study of some athlete) describes in the introduction something about lower cerebral oxygenation that you could also look at: https://www.thieme-connect.com/products/ejournals/html/10.1055/a-0836-9011 This should help you start (if it is about the right type of 'CNS fatigue'); Oh if you find some interesting information, mind summarising it?:)

Sorry, but I think you are completely misunderstanding what my question is. Apoptosis does not play a role here and there is no reason for it to occur. I don't really understand what you are saying either way, but my question is just if there are any known proteins that have a ligand-binding domain inside the cell and their effector proteins outside...

How can you have the same DNA, and have differing numbers of chromosomes? Centromeres are DNA, telomeres have DNA portions right? But even disregarding those two regions, spatial proximity within in the 3D genome regulates (some part of) gene transcription etc. With more/less chromosomes, their proximity may not be the same, therefore there is no reason to believe (in my opinion) they would be phenotypically the same when they contain all the genomic/epigenetic, seperated into a different number of chromosomes (ignoring the chromosome-specific DNA regions). Replication is by definition a different process when there are more chromosomes present. As cells are dynamic systems, small changes in starting conditions may lead to significantly different outcomes.

Thanks for the comment! I don't really understand the relevance of (r)RNA in this case. Apoptosis is controlled cell death, but the thing I am wondering about is: are there any receptors which receive signals from the inside of the cell and mediates some sort of effect to the outside of the cell (while remaining stuck in the membrane). Basically, are there any (for example ) GPCR's which have their ligand binding domain inside the cell, and their G-proteins present outside the plasma membrane. I don't know of any such receptor, however I also don't see much reason why there wouldn't exist a few like that. -Dagl Edit, to answer your question about how errors can occur (I would think they could occur, I didn't read any research showing cells putting receptors backwards, but since some (most?) receptors have to be assembled, there could be errors. It would of course be naive that every assembly process allows for a 'backwards' receptor, but I don't think it would be too strange to see some misassembly leading to a backwards receptors (basically it wouldn't surprise me if it existed). I may be unaware of some RNA>protein assembly signalling, but otherwise I doubt that it is primarily rRNA 'signalling' (? not really sure what that is;p). Anyway, while it would be fascinating to see if there are any wrongly placed 'backwards' receptors, I am more interested in knowing if there are any naturally functioning receptor that mediate signalling from inside to outside with a ligand-binding domain on the intracellular part of the membrane.

If there genomes are the same, then their chromosomes and genes must be the same. It is important to note that within a species there can be many variations between the actual sequences. If you would have an exact copy of the genome, you would have an exact copy of that species. Do note that two identical genomes can have different phenotypes, based on environmental/epigenetic stimuli and because of inherent stochastic behaviour. I think, but I am not sure, that variation within organisms with identical genomes and cultured (or naturally growing in) in similar environments will be approximately normally distributed. As Strange mentioned, if you find identical genomes, it may be that the two 'species' are actually just one and were misclassified. One motivation for why identical genomes should have identical gene number and chromosomes is that each chromosome has some DNA regions which help with the overal form/structure of the chromosome (and are important in replication). These regions are called the centromere and telomeres. Having a chromosome less would mean that when we compare the total genomic sequences, there should be 1 centrosome and two telomere regions missing. Since these are DNA sequences, their genomes CANNOT be the same. Of course, within identical species there will be natural variation of telomere size, but I think that if we would consider every variation, then there would never be an 'identical' genome, so I guess it depends a bit on how strict you are with using 'identical'.

I was watching a video about someone who judged AI-created maps for a competition. These maps are quite large and he spent multiple days to review all participants. My question: What method of judging is most impartial? First reviewing every map, followed by short revisits (possibly helped by notes) and then scoring the maps. Or reviewing and scoring each map , one after the other (like how a lot of Olympic sports are scored). Or some other method, of course. I understand that there is no research about minecraft map judges, but I was wondering if there is any research into specific ways that lead to more impartiality/fairness (if you can even measure/determine that?)? And if there is such research, should it be put into guidelines for scoring / is it already? I suppose it also depends on how familiar the judge is with the topic. In sports, almost everything has been seen before, just the quality is different. But for the minecraft AI judge, he had no idea what the AI's were capable of at all, so for him judging/scoring at the end must be (I think) more optimal. But I don't know if that still applies if someone is familiar with the content at hand. Any wisdom, thoughts or references to relevant articles are appreciated! -Dagl

It may be a really good idea, if you straight up disregard news articles, interviews with scientists and other stuff that could be confusing. You also seem to like Katie Mack a lot, and maybe her research/ideas are very interesting, but wouldn't it be a good idea to first brush up your basic physics. Start with the basics, explain things here, in detail, with specifics and references to where you found the information (exactly) and first verify if you understand the basics. It is very important that you are specific, because only by being specific can we talk about the same things, especially in science. If you ask a question about anything, let's say metastability, maybe explain it. So we are all on the same page. Try to put care and thought in your explanation, as it will aid you in learning. I don't have much physics background and I would love to know what it is, just explain it for people that aren't as knowledgeable. If you can explain the concept and people here agree with your explanations, you move onto the next part, and the next. Until your question logically follows (or what regularly happens, you see that you have wrong assumptions and that is why you were confused about it in the first place).

When you claim something it may be helpful to put the piece of text which you interpret, because it seems that that is a major issue here. So if you say 'the supervoid is now at under 0 kev', can you please show where you found it (so the reference) and the specific text? The same thing for these collapse statements, please provide the piece of text which makes you think these things, then people can help you in understanding those specific pieces better and help.

Ahh I see, thanks. However I do wonder, wouldn't first sequencing the genetic code give you predicted proteins (of course not perfect if there's splicing, but I have no idea about fungi). Then it should be easier to identify the proteins in MS (as you said that this can not too great)?

qPCR is involved in RNA quantification. It is not used to extract enzymes. @CharonY How unreliable is sequencing a new species? And how does it become more reliable, just by more people confirming the same sequence? I thought that with good enough sequencing you would be able to identify at least coding regions (of course, repeats probably remain a problem), am I overestimating sequencing ability (I suppose it could also just be how a matter of how financially (un)viable adequate sequencing is in this case)?

@Bmpbmp1975 I think an important thing for you to realise is that A. Scientists, even experts in their respective fields, can be wrong. Don't take their word for gospel. Even if they had brilliant insights at other times. B. Science functions by repeated measurements, improving measurements and verifying measurements in different ways. The methodology will be different or we have looked at a different part of space, or there are flawed assumptions. We have several hypotheses for most things but new evidence will change our way of looking at each individual 'problem'. We continuously find new things and discard old things. There MAY be changes of the constants, but since this would be quite unusual, we should also look at other explanations. And one always need a lot of evidence. I think you will find this video interesting (below), specifically 9:50 -15:00. C. Science-explanations and the actual science can be different and difficult to interpret (not always good to just believe whichever metaphor or analogy people use). D. Some articles are flawed. Maybe they made mistakes or lied. -Dagl Edit:

Hi there, Are there any transmembrane receptors (metabotropic or ionotropic) which have their ligand-binding domain located inside the membrane, and (if metabotropic) has G-proteins, kinases or other signalling proteins on the extracellular side? I guess that it is possible for cells to 'misplace' their receptors and put them backwards or reversed inside the membrane. But are there any proteins which function regularly by having intracellular ligands bind and then mediating a signal to outside the membrane? Thanks in advance, Dagl

Do you mean that eating an equal amount of calories of fat or carbs will lead to different fat levels, all things being equal? Over the long term, if the same amount of calories are eaten (or well, one should find out the efficiency by which the person absorbs carbs and fat and then normalise using that) and the same amount of energy is used up, one would be exactly equally as fat right? Preferably this is not tested in full-fat or full-carb diets, but where only some % of the total calorie intake is changed so that it still remains a sort of balanced diet (carb vs fat wise). If everything stays equal and their basal metabolism doesn't increase, and they absorb the same amount of calories, then it shouldn't matter what the calories come from. And in the end fat is stored calories, the amount of fat should remain the same over the long term Edit: I did just realise that of course, there may be some differences in the efficiency of breakdown of fat and carbs, additionally, I believe (but could be wrong, can't find my notes on fat metabolism at the moment) that storing carbs in the form of fat is a net energy loss (as it requires some energy to 'convert' the carbs to fat), so that could also affect the long term fat quantities (when comparing fat vs carbs in diet). @CharonY Do you know if slowing down or quickening of basal metabolism is possible when absorbing a higher percentage of fats than carbs or vice versa (while everything else remains equal)? -Dagl