Dagl1

A quick explanation; Genes are just the code or blueprint that cells use to make proteins, which are in all essentially little machines that can do almost anything. There is gene for a protein that helps with a specific chemical reaction, there are proteins that work as little pumps, there are proteins that look at how much energy is available in the cell and if needed they can then increase energy production if there isn't enough. Dystrophin is a structural protein, it acts as the beams or pillar within a building to give muscle cells their strength (and other things but this is a good analogy). Dystrophin is only present on the X chromosome and thus will either come from the mother or have happened spontaneously. Unfortunately, because males only have 1 X chromosome, there is not such a thing as autosomal recessive for them. They either have a mutation in dystrophin gene, or they don't. However there are several types of mutations; some will reduce the amount of dystrophin, others make it less functional (think instead of having steel beams, they are now a little shorter and made of a weaker metal). Some of these are not as bad as others, please take a look at this section of the following article (also check out Becker's Muscular Dystrophy). https://www.hindawi.com/journals/bmri/2009/325210/ BMD = Becker's muscular dystrophy In DMD patients, immunohistoanalysis shows total absence of dystrophin; whereas BMD patients have 10% to 40% of the normal amount or produce a partly functional dystrophin protein with an altered size [12]. During healthy conception, 23 chromosomes will come from the father and 23 from the mother, 22 of these pairs will contain the same genes (although the exact protein may be slightly different (think of, pump with 500 bolts and 1 motor vs pump with 488 bolts and 2 motors)). The last pair is either X X (so both from the father and the mother, in which case it is a girl) or X Y, where the Y is given by the father. While all the other chromosomes allow for 2 variants of each protein (and thereby autosomal recessive mutations can exist) this is not the case for a mutation on chromosome X when the child (boy) only has 1 X chromosome. If you are a carrier of one of these mutated proteins, then there it most likely is autosomal recessive for you, but unfortunately not for him. I hope that gives a bit more clarity, I can imagine this is a worrying time and having a bit more knowledge about the subject may help with further understanding as well. -Dagl

Spontaneous mutation can of course happen, however this will be independent of the fathers chromosomes. If, as the mother you are carrying a DMD-causing error, there is a chance you will have light symptoms, however this is rare and may be even difficult to notice without exact testing. I am not entirely sure what you mean with "Can we assume that the X chromosome in the child is exactly as it should be in the mother?" Hope it turns out that your son doesn't have DMD! -Dagl

I am not entirely sure what you are looking for, do you want to find the sequences of specific organisms? https://science.sciencemag.org/content/277/5331/1453 shows the length of the E. Coli genome: 4,639,221 basepairs NCBI contains the sequences of many organisms: https://www.ncbi.nlm.nih.gov/nuccore/U00096 Encode is database containing elements of DNA, which should help you with the characteristics of the DNA https://www.encodeproject.org/ If I may ask, what do you mean by "decoding the DNA"? -Dagl

So maybe i'm a bit biased here but this seems to be: Observations > trying out some ideas (based on both observations and possibly a bit intuition) > idea contained undiscovered but predicted elements > elements are discovered > idea seems to hold true This is science no? I am not saying people shouldn't speculate, or everything has to be based on evidence, but as far as I understand, the OP's idea is based on... well.. not a lot, nor does it predict things that can be tested. -Dagl

Could you elaborate? From my (possibly limited) knowledge, the periodic table is based on arranging the elements in particular groupings based on common or similar characteristics? If this was somewhat was the case, isn't that just science? Apologies if I misunderstand you, not trying to strawman;p

So first off, either science can answer it or it can't. But if science (so... evidence) cannot right now answer it, then you believing your idea makes no sense, as we just said that science (evidence) can't answer it. Sure maybe it turns out that what you believe is correct, but since right now there is no evidence to support your idea, you believing it is equally valid as believing ANY other random thought. Do you see what I am trying to say; either there is a logical (evidence based) reason why you think it is that way, thus it is something science can support. Or science can't/doesn't support it right now, and thus you shouldn't be believing it as there is reason to believe it. -Dagl

So what I understand is that you want to share your ideas and theories but in the thread in question, you seem to ignore (or more accurately evade) questions such as; what evidence is there for your conjecture, what evidence would point to the contrary, how do we test it. You say that you don't want to start an argument AND you ask people to let you first post all of your ideas (no one has been stopping you, have they?) before people criticize them. Two problems; first off, that is exactly like making this your personal blog.... secondly, why should people hear out your entire ideas (which seem very very long winded and without effective or clear summary) when they have problems with certain parts. It is very possible to counter or criticize certain parts of your argument without hearing all of it. If you would be doing some math or physics equations, and before you have posted the ENTIRE thing, someone points out that you are saying 2+2 = 5, then that is completely fair isn't it? -Dagl

It's like you just ignore the real reasons why people have a problem with the equations and ideas you posted here. Yet you keep saying it is just because you no formal training or use the wrong terminology. If that makes you feel better, you do you, but it just seems so not useful for you. Why not pop the bubble you are living in, use your 160 IQ and go learn some basic physics, in what way would this hurt you? It will only make you more knowledgeable and probably gives you a lot clearer ideas... -Dagl

Well Phi... I mean the dude does have an IQ of 160... so... I mean, if you had an IQ of 160 (no offence if you do, but I am just going to assume that you don't;p) then I would of course believe that 12 is a prime number, I must have seen it all wrong, just like ALL those other people.... /s

I.... I wanted to say that I think Strange and some other responses were a bit harsh and could have been worded better, but you... just ignored half of what people said here and boil it down to "you criticize me because I don't fit your mold". Dude (or madam), please get a reality check, you have less than complete knowledge of basic physics. Why don't you go and show HOW this is possible seeing as you are saying things which are contrary to so many different theories, hypotheses and general ideas of how stuff works. How is it that there is sooo much evidence for such things. Get rid of the idea that you have some brilliant insight and at least get some basic knowledge. I honestly wanted to help you and encourage you to learn and then potentially speculate, but if you don't even do the basics of producing new ideas or looking critically at your own thoughts, it may be better for you to just live inside your own bubble, believe what you want to believe and go publish your idea. Just realize that when it is real science (not just a forum), you will be scrutinized endlessly more, possibly by people more in depth into this field than those on this forum (I don't know what Swanson and Studiot do for instance). It doesn't seem like you need this forum.... -Dagl

@Bez I think that both Beecee's earlier post and Phi's post are worth rereading; Having ideas and thinking about science is great, but without enough knowledge it becomes difficult to truly understand a subject AND to explain it clearly. However clearly you see your ideas in your head, you should take criticism of your ideas and use it to further develop your ideas. If you find out you were completely wrong (as explained by people), it may be a good idea to find more information before speculating and asserting. What you see/saw so clearly was wrong and thus proves that your mind isn't infallible. But this isn't a problem on its own, many people have many wrong ideas before they have the right one. I feel like you aren't taking people's comments into account and are doubling down on your idea. To you, the dogmatism and rigidness of science may be a hurdle, but in truth it is also the only way to move forward at a steady pace. I don't think that a real formal education is necessary, but basic knowledge on a subject is. You need to have enough knowledge to know when you go AGAINST the established scientific theories or most accepted hypotheses and should first show why your theory is more right than the established ones. If we have 2 ideas, and one (1) is supported by A to Z, and you have an idea (2) that is mutually exclusive with or is contrary to idea 1, then it is not enough to just provide evidence AA. You need to show that A-Z ALSO supports your idea AND that AA doesn't happen in idea 1. This is of course only, when A-Z and AA are all real evidence and not assumptions, assertions or new ideas. I think a good way to start is; be able to explain, in detail, the theories and hypotheses that are relevant to your idea (so do research into it, Khan academy, Coursera or formal education). Verify if your explanations are correct and if that is all true, formulate your idea (now in the scientific terminology that you have learned) and show why the previous hypothesis isn't sufficient. It is NOT enough to just say "idea x is JUST an hypothesis, so is mine", that's just not how it works. From my limited time on this forum, I think a lot of people may come off as harsh or impatient, but most are trying to help and it would most likely be very helpful for you to take their comments into account. -Dagl

Interesting, but shouldn't that mean that suppressing the immune system would alleviate T1 diabetes (or well, I suppose we can't assume that the damaged cells will repair themselves and I don't know if these cells are actively being renewed)? I suppose immune suppression does have some beneficial effects, but I also realize that the cons may not outweigh the gain. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405831/ Dagl I think the root of the problem (B/T cells) are a bit more difficult to target/modify, and as the trigger of their autoimmune activity doesn't seem to be known, we cannot stop it from happening again if we could fix it. As I mentioned in my first reply, there is of course the possibility of modifying the beta cells in such a way that the immune system may not target them or combine it with general immunosuppressive medication. -Dagl

That is not what I read; this article discusses cells which have been MADE to become pluripotent. So mouse cells are, typically, grown in a state that is similar to what you would find if you examined preimplantation blastocysts. While the human cells are typically cultured in conditions which lead them to be similar to postimplantation epiblasts. This doesn't mean they are obtained from any of these cells, just that they resemble them. While I am unsure if postimplantation epiblasts cannot become all germ layers as you suggest (could you provide a link or quote/citation?), just 4 lines down the article discusses: " There have been several attempts to generate human naïve pluripotent stem cells (nPSCs) over recent years. Most often when putative human naïve cells are generated in vitro they are analysed using criteria that are known to distinguish mouse naïve cells from primed cells. Such criteria include responses to extrinsic and intrinsic signalling pathways, the biophysical, biochemical and metabolic status of the cells, and the overall epigenetic and transcriptomic cell identity. However, recent advances in our understanding of the human embryo also allow direct comparisons to the naïve compartment in vivo. Recently, cells exhibiting human naïve epiblast molecular features have been described [3••,4••,5••]. Over the course of this review we shall examine how closely these match the state of both mouse naïve ESCs and what is known of the human blastocyst. ". So yes it seems to be important, but did you A not read the article or B do you mean something else? -Dagl

Can you provide evidence that T1 diabetes is the result of autoimmune activity, as far as I know (but I am not very up to date in this field) we currently have no clear causal relationship, only several risk factors and some hypotheses? If it is the case, one possibility would be to use immunosuppresive drugs in combination with this treatment, or find out if it is possible to use pluripotent stem cells of another person (potentially modified to not alert the immune system of foreign tissue). Dagl

Oh yes I meant the people DOING the trials; Yes I agree the idea that this is general bad thing to do, even if YOU yourself don't join such a trial is bizarre....

While I of course can't talk for those people, I believe this occurs, in part, because people want to be in control of what they get and/or may deem 1 to be better than the other (even just based on browsing the internet) and thus may not want the 50% chance that they get the treatment that is in their opinion worse. Dagl

Firstly, there are more things than just dendrite number, length and synaptic delays which are part of memory formation (see LTP/LTD). You need to go and look into the basics before you make conclusions; the idea that "because synapses are build dynamically it must not be affected by RNA" is wrong. Synapses can and are definitely affected by and partly the result of RNA. I don't understand what you mean by point 2. Again, I think you need to make no conclusions, don't speculate and instead start with studying how most of this stuff works. Read the articles I mentioned, read a lot more and then maybe it is time to speculate. -Dagl

Ahh I see now; that article refers to a study in which they took RNA from a trained sea snail and put that in a naive sea snail, which then showed a similar behavior. My question, though, is: why do you think that it is the dendrites and not other parts that are modified by this addition of RNA. There are more parts to neuronal signal transmission than just the synapse. The other question was meant in a similar manner: why does it HAVE to be DNA (note; epigenetics is not confined to just DNA) or even epigenetics. Can't it be that the proteins or their mRNA are already in place (and primed) to (re)build those dendritic spines after they are cut. The reason for me asking these questions in this manner is because in both cases there are other options which are ignored. If you can think of a different mechanism then you cannot conclude that it HAS to be 1 mechanism. Regarding epigenetics, other examples are: histone modifications and mRNA modifications. Kind regards, Dagl

So why do they not reach the sun? is there some hard boundary around them? If I would have a spaceship, and move closer to them, will at some point I suddenly be noticing their gravitational fields? So you have this new formula, but you don't want to publish it, you don't want to further science and our understanding of the universe, because.... it hasn't passed the test of time (what does this mean?)? If you publish, other people can scrutinize it and see if it is right or not, and even use it if it is useful. But instead you tell some people on an internet forum that you found such a formula but don't want to publish it? -Dagl

Why do the dendrites HAVE to be modified if a sea snails behavior changes? Can you link this particular article? Why does DNA HAVE to hold a record of the dendrites, when they can regenerate; there are other possibilities that aren't the DNA right? Regarding reading up on it, I think it is a lot more helpful for you to first find some reviews of axonal and neuronal growth, the cell signalling components and intracellular pathways involved. I think general information is a lot more helpful for you than very in depth (experimental) articles. The following paste is from my own notes, they the first ones date back 3 or 4 years, when I personally got very interested in the molecular mechanisms of memory, they may be interesting for you (although definitely not all of them, as not all are about neuroscience, either way this may be helpful!). This is an interesting article which shows the basis of LTP quite well. (Kandel, 2012) The molecular biology of memory: cAMP, PKA, CRE, CREB-1, CREB-2, and CPEB http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514210/ This shows the differences of LTP in different neurons, quite interesting but specific. (Hu et al, 2015) cJun and CREB2 in the Postsynaptic Neuron Contribute to Persistent Long-Term Faciitation at a Behaviorally Relevant Synapse, http://www.jneurosci.org/content/35/1/386.full A quite specific article but made by our own university! (Prickaerts et al, 2014) Improved Long-Term Memory via Enhancing cGMP-PKG Signaling Requires cAMP-PKA Signaling http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207334/ An introduction into metabrotropic gutamate receptors. (Gerber et al, 2007) Metabotropic glutamate receptors: intracellular signaling pathways http://www.sciencedirect.com/science/article/pii/S1471489206001706 An introduction into NMDAR and AMPA involvement in LTP/LTD (Lüscher et al, 2012) NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367554/ The rules of spine learning, 15 rules on how spines change. (Kasai et al, 2010) Learning rules and persistence of dendritic spines http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2010.07344.x/full A very good introduction into histone post translational modifications (Bannister et al, 2011) Regulation of chromatin by histone modifications http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193420/ An indepth article surrounding transcription and the 3D genome (Rajarajan et al, 2016) Spatial genome organization and cognition http://www.nature.com/nrn/journal/v17/n11/pdf/nrn.2016.124.pdf

Sorry for the nitpicking, I just feel that for Fredreload it may be important to be as clear as possible;p I'm pretty sure you know what you are talking about, but I could already see how things are going to fuel more speculation.

What would this signal do, where does it lead to and... what type of neuron are you talking about? @Strange@CharonY While the growth is partly based on signalling and is dynamic, genes of course do play a role, and differences in genes/proteins that are involved in neuronal growth (axonal and dendritic) will possibly result in an increase or decrease of the number/length/branching pattern(?), don't you agree? Also fredreload, why not just read up on neuronal development? Instead of coming up with speculations that you then want to have verified, isn't it a lot easier to just read up on this stuff? -Dagl

Hmm I think you make some assumptions/jumps that I wouldn't (doesn't mean they are wrong, although I personally wouldn't be so sure); Just because we keep our consciousness after sleeping, doesn't have to mean that it is located within the brain stem. What if it it is more like a computer which gets rebooted, or in our case, the neurons in the cortex go into "cleaning mode" (look into the glymphatic system if you are interested)? I honestly think that you would do very good by FIRST learning the more indepth details, then using your quite speculative mind on the more... current questions? As a scientist I feel like you make too many conclusions, but you seem very interested in this stuff, which is why I would recommend you to first learn the foundations, then speculate. Most people in science are quite... rigid (mostly due to how science works), but currently for you there are too many unknowns. If you want, I can help you through several layers of (neuro)science, but it does require you to read a lot and not assume but just read for a bit, if you are interested, please send me a PM. -Dagl

I suppose you mean non-brain neurons (motor neurons for example)? I personally doubt that axons in the brain, on average, will be longer in males than in females. But I think that is also what you meant right? It may be a good idea to get some better fundamentals on both genetics and neural science. Regarding the question of synaptic delays, if we go super deep then maybe the distance from neuron to neuron can slightly alter traveling speed, or maybe some proteins require more or less time to be active, but this would be probably even unnoticeable within experiments that would be designed to look for these alterations. Now if you are talking about things like, the time it takes for a signal to go from your brain to your feet, this is mostly dependent on the amount of myeline around axons. If you are interested in more depth information, "The fundamentals of Neural Science, by Kandel" is an amazing book to learn about how neurons work. -Dagl

Nah I don't think in most cases being super strict (nice how it works in my favour now isn't it;p ) is necessary, but maybe it is personal opinion but I think a lot of leeway is given to those who do not believe science (physics). I am still interested if you agree or have another reason for why this seems to happen mostly to the physics department. I definitely agree with the idea that everyone puts their ideas in right (appropriate) section. I want to make sure that you all don;t misunderstand me; I like this this forum, and I really apppreciate how helpful some of the people are, but I also agree with the OP that there is a lot of... BS here. And while I am mostly for discussion, I think there are limits. -Dagl