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Everything posted by Dagl1

  1. An hemocytometer, microscope, tally counter in hand, oh and trypan blue if I really need it (depends a bit on your cells, and how important the counting is, no reason to not use it other than that you have to find where your labmates have hidden it). We also have some fancier machine, but it isn't calibrated for my cell types so haven't used it. Do you want to know the brand of some automated counters like that, or this question is just about how to count your cells?
  2. Hi there, I have been recently been thinking about the determinant chromosomal positions we see for each chromosome within a given cell type, many of the chromosome pairs are quite far away inside the nucleus, and these positions seem to not be moving that much at all (that is, we can consistently find the same/similar topology in a given cell type). Now that is all good and nice, but it breaks my expectation of homology directed repair (HDR) a bit. In HDR, a double-stranded break on one chromosome is fixed through the recruitment of the other chromosome, and while I am aware that HDR is
  3. An overexpression screen? You have a WT yeast, in which you knockout an essential gene, now this has become a lethal phenotype, if during this time you now add start overexpression of a random gene, and your yeast survives, then you have rescued said phenotype. One way to do this is to make a overexpression library, get your plate/plates with knockouts and just add the library. Then pick the clones that survive and genotype them (or if you added barcodes to your plasmid library, identify by barcodes). If the essential gene knockout leads to a lethal phenotype only under certain condit
  4. Could you not just design some primers for your specific genes, do PCR amplification and check on an agarose gel if the sizes are larger/smaller than expected? I am not entirely sure if that is the most feasible method, but at least I would assume you could see deletions, and duplications if they happened in the same region (of course if a duplication happened to be present in another chromosomal region, I would expect these to not be visible as the primers wouldn't lead to PCR amplification of 1 long transcript but just 2 equal sized ones, which I suppose you won't detect. Otherwis
  5. I quoted only the relevant responses I want to discuss: 1. You say that each profile has its own specific pattern, and then you talk about gene expression and silencing, but that doesn't really answer my question: How did you determine what the boundaries are of 1 profile versus the next, if 2 people have the exact same gene expression except for 1 gene, are they the same profile? If so, at how much deviation do we find ourselves in another profile? How did you determine these boundaries? Have you considered alternatives? 2. So your profiles always match a trait, it never is wrong?
  6. How are epigenetic profiles defined, how are they measured or determined, where are there boundaries? What does this list tell us? Is the frequency at which epigenetic profiles and these features match higher than what would be expected from regular distributions? How often do these profiles and features match and how often do they not? Are there differences for particular features or profiles? What is the total sample size of the evidence? How are these features defined, why these features and not other ones? At the moment, I don't really see any evidence yet, nor explanat
  7. This is a discussion forum, so people here would like to discuss things. You have stated you made some discoveries (and briefly and pretty vaguely described those discoveries), but what is there to discuss. I am interested in epigenetics, I would love to see and discuss your research, but then you need to post some of it. If you have so much evidence, what about sharing some of it HERE. Otherwise what is the point of this thread, without evidence there is nothing for us to discuss, so it seems like you are just (for a lack of a better term) gloating about discoveries made. Basically gi
  8. The specific type of lipid may signal that a cell is undergoing apoptosis. Under normal conditions specific lipids are moved to either the outside or the inside of the cell, during apoptosis (and maybe other cell death inductions) a scrambling protein is activated. You may be interesting in those enzymes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613456/ for the more general mechanism https://pubmed.ncbi.nlm.nih.gov/28844836/ additional links that I just browsed through: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307283/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4
  9. A few questions and maybe some suggestions (that you need to verify and check, or use as step off points). I am not a statistician, but I do have experience with statistics. Hopefully I don't say anything just blatantly wrong;/ So you have k keywords, and their averages on a single day. Do you put k keywords into a single variable KEYWORD or do you want to measure whether there is a difference for every k keyword? If you want to do k comparisons, please apply some type of multiple comparison correction as your p value (assuming 0.05 is used as cut-off) only means the type of for a type 1
  10. Although you asked Markus, isn't there a lot of material on this? https://en.wikipedia.org/wiki/Heritability_of_autism Of course maybe you are just asking if there are other people in his family, regardless of how much it is inherited?
  11. I unfortunately am not of any help, but am curious to see how this advances and hope some people can hep you out! Well written account of what is up, although I do think you may need to elaborate more on what type of help you exactly want. The resources on various topics you ask for may be too broad (but you never know!). It would probably also help if you explain in more detail what you have done so far regarding the TensorFlow implementation and where you can't see a good way of doing it. Otherwise it may feel to some members that you are asking them to walk you through from start to finish
  12. Note: While writing this, and putting my thoughts on paper, I changed my mind, I am keeping my reasoning because the questions I want to ask still follow from them. Well I do personally hope that we may have a bunch of people there at that point 😛, because what if these aliens try really hard to use microexpressions or are mimicking the general human expressions in order to convey meaning. Anyway that is kind of off topic and more a joke than anything else. Thank you Markus for sharing this, whenever you explain things about how your brain and that of other people on the autistic sp
  13. I suppose 'plenty' is not a right word, but just so I do understand correctly (and understand the other people's responses as well): The sol system sun (our sun), contains radioactive isotopes, its not a first generation star, so supernovea have happened already. There is fission in stars, regardless if that contributes (or not) significantly to anything within the sun? When you say 'basically' no fission, do we mean: no fission, or fission happens but is basically irrelevant? I am asking because MigL says the following (so I assume that we just mean there is little fission compared to al
  14. You inherit them from your father and mother, maybe some combinations make very similar phenotypes, maybe just like with eye color, there can be some genes that are dominant or co-dominant. We inherit DNA (and maybe some epigenetic stuff), DNA leads to protein production, and all the proteins together will determine the phenotype (together with the environment). It is really difficult to predict emerging properties, especially when so many genes interact with each other. Thus by just inheriting the right combination, you may get phenotypes that are very similar.
  15. Ehh? He didn't say anything very controversial I think, so ye I think those other criticisms are valid? Like I don't think I have ever heard of anyone describing light as anything other than always being at c? The big bang thing seems pretty much how I have heard and seen it explained, the whole of space time expanding, no consuming anything. Am I missing anything? I was just interested in his statement about fission in stars?
  16. Oh, I thought there was. But maybe I am being a little pedantic, and you may mean there fission doesn't contribute to much in the star? It seems strange to me if there is no fission in stars , there are plenty of radioactive isotopes and it feels logical (I say feel because I don't know) to think that a place full of particles moving at high speed around and towards fissionable elements would also lead to fission?)
  17. Isn't this the same question? We don't know (or at least I don't) which parts of autism are reprogammable at age 10, we can only speculate about it. If the gut micriobiome can affect it THAT MUCH, then you could of course argue that even if you change the DNA of the whole head (or even the gut) you may not be changing the gut microbiome, therefore actually having less effect. But again, at this point is really speculative and I think the question is answered by (bold added by me for clarification)
  18. Pretty sure if you would that in an embryo, and you knew what to tweak then most likely. If you do it in an adult or a 10 year old, maybe, it depends on how much of those things are reversible, but maybe.
  19. Thank you! I would be careful with saying things like: The schizophrenia article is about a model for schizophrenia, which requires the loss of a single allele of SETD1A. The risk of getting schizophrenia increases from SETD1A mutations, but that doesn't mean that by fixing this mouse model we can also fix scihizophrenia, especially if someone has a SETD1A unrelated type of schizoprhenia? The paper regarding autism talks about how autism related symptons will be lessened in mice by correcting SHANK3, but also that SHANK3 is really rare (aprox 2% of autistic people have mutat
  20. They have? Links please, I am interested. I would say that memory formation potential and hormone related stuff will become different the most, other stuff almost by definition as well but I don't know how much of the initial neuron paths/connections will be able to change, that feels kind of structural. I don't think you will suddenly get Neil, but there will certainly be things that change in how it works in that person, and then many years later those differences and different behaviours will manifest more (I imagine that from the moment that you change this person's genes, him and wha
  21. Probably some bone structures will be set, but I suppose (ignoring the full on immune response this would probably elicit) skin colour and any other thing that is dependent on regenerating/remodelling tissue, will at least change a bit. Significant is more a measure of how sure we are, I think could definitely notice the difference, but how extreme those differences would be are hard to predict.
  22. Yes, it seems this is a possibility in black are my comments: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5696326/ Communication between the systemic immune system and the brain and its consequence on microglia is a critical poorly understood component of the inflammatory response to systemic disease (78). Systemic infections activate neural and humoral pathways that communicate with the brain and initiate a coordinated set of metabolic and behavioral changes (79). However, these adaptive responses may become maladaptive when microglia have been “primed” by an ongoing pathology and re
  23. I don't know of evidence that there is a single gene or set of genes responsible for having 'wide eyes'. So whether 'wide eyes' are dominant, I don't know and don't think we know, but wide eyes are probably at least partially going to be hereditary, like most body features I think.
  24. Not entirely sure if exactly what you are asking, but potentially relevant: DNA positioned relatively close to the nuclear lamina also undergoes inhibited gene regulation, but you could of course argue that that still is chromatin remodeling (eventually histones, cohesins, and other proteins will still be involved in the actual gene regulation). I feel lately more and more research is also looking into phase separation as an part of gene regulation, that is generally difficult to sequence as well: Lamina-associated Domains: https://www.biorxiv.org/content/10.1101/464081v1.full
  25. @Capiert Could you do the calculations people ask you to? If you want to convince people here that your ideas are valid, show it with numerical examples. Show the formulas you use and the numbers you put in. Words are great, but eventually you will need to show math, and I really think this is that moment (or it was a few posts ago already). You make many claims, so why not just do the simple thing, use your own formulas/ideas to calculate some stuff, showing what you do and why. It shouldn't be hard. Oh and, if your answer is different from that of standard physics, please don't y
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