Noyau (2)

…the noyau, an animal society held together by mutual animosity rather than co-operation

Robert Ardrey, The Territorial Imperative.

[to work around page bug]

2,182 thoughts on “Noyau (2)

  1. stcordova: DNA_jock should change his handle to DNA_joke. I wiped the floor with his tongue over the chromatin discussion and the regulatory mechanisms that control SRY expression.

    His willful incomprenhension is pathetic.

    Btw, I got A’s in my graduate classes at the NIH. Even though I’m in a part-time graduate program, classes at the NIH count as credits for doctoral students at Johns Hopkins in cellular biology and other disciplines. One class I happened to take this semester was on Chromatin Modification, and it just happened to be relevant to the flap over the New Yorker article.

    I suspected some of the professional biologists here were shaky in their conception of the cutting edge in molecular biology.

    The fact I made the grade confirms to me the suspicions that some of my detractors like DNA_joke aren’t as sharp as they represent themselves to be.

    Hi, Sal.
    I am happy for you that you are getting good grades in grad school, but I am not particularly impressed. Two reasons: 1) I’ve taught similar classes, so I am aware of grade inflation. 2) Your writing here, and your inability to express yourself clearly and coherently, suggest that you are, at best, deeply confused.
    It’s nice that you think that you “wiped the floor with [my] tongue over the chromatin discussion”, but when you say stuff like that, you are making my point for me: you are clueless.

    More DNA_joke stupidity, he says SRY is unambiguously at the top of the regulatory hierarchy and then points out 16 other transcription factors regulate the chromatin that regulates the SRY. How stupid does this get. If 16 factors regulate chromatin that regulate SRY expression, then SRY isn’t unambiguously at the top of the regulatory hierarchy as he first claimed.

    You fail to comprehend. Here you are re-phrasing what I wrote, mischaracterizing it in order to try to score rhetorical points. Real scientists avoid this behavior.
    I haven’t said ANYTHING about SRY & chromatin, except to note that your characterization of Nishino 2014 as showing that “it is a fact that SRY is regulated by chromatin” is wrong. I have said, all along, that the TIMING of SRY expression involves 16 other transcription factors (see, no mention of chromatin).
    Then your hopeless logic fail. Just because X is required for SRY or MAT expression, does not in any way detract from the fact that they sit atop a regulatory hierarchy. You cold just as well claim that because MAT expression requires ATP, CTP, GTP and UTP and a temperature between 23 and 36 C, it therefore does not sit atop a hierarchy.

    Control of timing then implies it is controlled and therefore not ultimately at the top of the hierarchy.

    Still wrong, Sal.

    If SRY is influenced by 16 other transcription factors through chromatin modification, it’s regulatory context is not strictly hierarchical. It would have the same sort of complexity as might be found in the diagram below that involves other genes

    “through chromatin modification” ? When you keep making this shit up, you keep making my point for me.

    Between the misrepresentation and the sloppy writing (and thinking) there isn’t much point in continuing a conversation with you. I had been assuming that your writing was merely a display of D-K stupidity, but now I think that you are fundamentally dishonest. And D-K stupid.
    I pity the poor teachers who are holding their noses while giving you your grades.
    Been there, done that.

  2. Here to praise Gregory (who seems to have whooshed in and then left again) for FINALLY making a comment which did not deserve immediate guano-ing.

    Way to go, Gregory! I knew you could do it if you really tried. I knew your slavering paranoia and anti-Semitic anti-KN ranting was – at least – partly within your own control, and you could keep it down if you wanted.

    Too bad, Gregory, that you had to stain your effort with a gratuitous slam against atheists. But you gotta start with baby steps in improvement, I guess. Keep trying – you’ll become a decent human being yet!

  3. stcordova: So how much computer science, electrical engineering, math, physics and biology have you acquired to make you competent in these discussions.

    I was breast fed. Makes all the difference.

  4. Here’s another research paper you ignored.

    http://www.ncbi.nlm.nih.gov/pubmed/11743352
    DNA methylation regulates the expression of Y chromosome specific genes in prostate cancer.

    Dasari VK1, Deng D, Perinchery G, Yeh CC, Dahiya R.

    After demethylation SRY gene expression was restored

    To our knowledge we report the first study showing that expression of the Y chromosome specific genes DAZ, SRY, RBMY1A, RBMY1H, RBMII, BPY1, PRY and TSPY is regulated by DNA methylation in prostate cancer.

    Take that, man, you’re way behind the curve in terms of available literature.

    , no mention of chromatin

    Nishino paper mentions DNA methylation, DNA is a chromatin modification, and another researcher interpreted the methylation changes as follows:

    Epigenetics of sex determination and gonadogenesis by Francesc Piferrer*

    Sry is controlled epigenetically by a mechanism involving DNA methylation(Nishino et al., 2004).

    http://onlinelibrary.wiley.com/doi/10.1002/dvdy.23924/full#dvdy23924-bib-0064

    Oh I get it, you refuse to acknowledge DNA methylation is a chromatin modification that allows chromatin to control gene expression. Too funny.

    But since you seem bent on arguing chromatin doesn’t regulate genes, get a load of this:

    http://www.nature.com/scitable/ebooks/Chromatin-in-eukaryotic-regulation-16549786

    http://www.amazon.com/Chromatin-Gene-Regulation-Mechanisms-Epigenetics/dp/0865427437

    Chromatin is a fundamental component in the network of controls that regulates gene expression. Many human diseases have been linked to disruption of these control processes by genetic or environmental factors, and unravelling the mechanisms by which they operate is one of the most exciting and rapidly developing areas of modern biology. Chromatin is central both to the rapid changes in gene transcription by which cells respond to changes in their environment and also to the maintenance of gene expression patterns from one cell generation to the next. This book will be an invaluable guide to undergraduate and postgraduate students in the biological sciences and all those with an interest in the medical implications of aberrant gene expression.

    So you still want to argue Chromatin doesn’t regulate gene expression? Laughable.

  5. Oh dear Sal, do at least try to read for comprehension.
    At no point have I claimed that Sry is NOT regulated by methylation, or by histone modifications, or by that wonderfully fuzzy concept “chromatin”. My “see, no mention of chromatin” was pointing out to you that YOU had mischaracterized what I had written, putting words in my mouth. Read slowly now: the only comment I made regarding SRY and chromatin was to point out that your concluding based on Nishino that it is a “fact that SRY is regulated by chromatin” was wrong, and I offered to disabuse you of that error. That offer still stands. Would you like to describe in your own words the methods Nishino used? Quoting what some other random scientist concluded from the paper is , err, underwhelming.
    When you quoted Darasi 2002 as saying “After demethylation SRY gene expression was restored”, what technique did Dasari use to measure the demethylation?
    Also, if (as you appear to be claiming) differential methylation is responsible for the differences in expression observed by Dasari, why didn’t SRY show up in Wang et al. 2005, given that both studies looked at LNCaP and PC3?
    You seem to have a fundamental blind-spot regarding the nature of evidence.
    In case you still don’t get it, I am not claiming that SRY is not regulated by methylation, I am poking holes in the “evidence” that you have offered to date, and thus testing whether you are competent to defend your use of this evidence.

    You were getting an “Incomplete”, until that howler about hepatocellular carcinoma in yeast. Now it’s a “F”.

  6. Addendum:
    Multiple times dear Sal has claimed that “[Francesc Piferrer] has interpreted the methylation changes as follows:”

    Sry is controlled epigenetically by a mechanism involving DNA methylation(Nishino et al., 2004).

    But what Dr. Piferrer actually wrote was more nuanced.

    However, at 11.5 dpc this region was specifically hypomethylated in the gonad, while it remained hypermethylated in tissues where Sry was not expressed, suggesting that Sry is controlled epigenetically by a mechanism involving DNA methylation (Nishino et al., 2004). Hypomethylation of gene promoters is typically associated with genes becoming transcriptionally active and hence the observed changes in the Sry are somewhat to be expected. Nevertheless, the study of changes in DNA methylation in the promoter region of the other two dozen or so of genes currently related to sex determination and differentiation deserves further study.

    That’s dishonest, Sal.
    Of course, using the same logic we can take Wang et al 2005 as “suggesting that Sry is NOT controlled epigenetically by a mechanism involving DNA methylation.”
    So you might want to explore that the researchers actually did. Or not. Your choice.

  7. At no point have I claimed that Sry is NOT regulated by methylation, or by histone modifications, or by that wonderfully fuzzy concept “chromatin”.

    So are you admitting SRY is regulated by DNA methylation, therefore SRY is regulated by something else. Hahaha!

  8. stcordova: So are you admitting SRY is regulated by DNA methylation, therefore regulated by something else. Hahaha!

    Yet another logic fail from Sal.
    I know this may be difficult for you to comprehend, but I am not making any claim or admission one way or the other.

  9. I am not making any claim or admission one way or the other.

    Even after pointing out two papers that show DNA methylation regulating SRY.

    To our knowledge we report the first study showing that expression of the Y chromosome specific genes DAZ, SRY, RBMY1A, RBMY1H, RBMII, BPY1, PRY and TSPY is regulated by DNA methylation in prostate cancer.

    For the reader’s benefit, since there is a long list of genes, I’ll put an ellipsis in the above to help get the point across:

    …we report the first study showing that expression of …SRY is regulated by DNA methylation…

    There you have it both in this study and backed up by the Nishino study and my interpretation confirmed by Francesc Piferrer.

    The DNA methylation state regulates SRY expression.

    The problem with you DNA_jock is you can’t admit you made a mistake. I can since I don’t have to save face like you do.

    Thanks for the free-of-charge tutoring on yeast MAT not being the same as human MAT. I thought the two having the same name made them homologous as is usually the convention for gene names.

    But even with you pointing that out, I should your claim that MAT unambiguously at the top of the regulatory hierarchy can be only true by omitting the fact MAT is regulated by other things like the HO endonuclease.

    From Wiki:

    Yeast mating type promoter structure

    The process of mating type switching is a gene conversion event initiated by the HO gene. The HO gene is a tightly regulated haploid-specific gene that is only activated in haploid cells during the G1 phase of the cell cycle. The protein encoded by the HO gene is a DNA endonuclease, which physically cleaves DNA, but only at the MAT locus (due to the DNA sequence specificity of the HO endonuclease).

    Once HO cuts the DNA at MAT, exonucleases are attracted to the cut DNA ends and begin to degrade the DNA on both sides of the cut site. This DNA degradation by exonucleases eliminates the DNA which encoded the MAT allele; however, the resulting gap in the DNA is repaired by copying in the genetic information present at either HML or HMR, filling in a new allele of either the MATa or MATα gene. Thus, the silenced alleles of MATa and MATα present at HML and HMR serve as a source of genetic information to repair the HO-induced DNA damage at the active MAT locus.

    But HO is regulated also by MAT domains.

    http://europepmc.org/articles/PMC545453

    There is a loop apparently. As I said, hard to characterize things with a strict hierarchy.

  10. stcordova: For the reader’s benefit, since there is a long list of genes, I’ll put an ellipsis in the above to help get the point across:

    Heh.

  11. Wow, just wow!
    I pointed out to you that HO “regulates” MAT. And that MAT expression requires ATP, CTP, GTP and UTP.
    None of these facts, all of which I pointed out to you, detract from the fact that MAT sits atop a regulatory hierarchy.
    DO try to keep up.
    How are the alleles of MAT found at HML and HMR kept silent? (Careful, it’s a trap!)
    So are you admitting that, in heterothallic yeast, MAT sits atop a regulatory hierarchy. Hahaha!

  12. Scenario where professor DNA_jock teaches.

    Student:

    Professor DNA_jock, is it true DNA methylation regulates the SRY gene? I read this paper that says:

    …we report the first study showing that expression of …SRY is regulated by DNA methylation…

    Do you believe that’s true?

    Professor DNA_jock pauses and considers how his response will affect his saving face at TSZ:

    Professor DNA_jock:

    I am not making any claim or admission one way or the other.

  13. stcordova: Scenario where professor DNA_jock teaches.

    Sal, you are the person making claims. When you write a paper at university and you are challenged on some of the points it makes, will you insist the challenger presents their version of events? If not, why not?

  14. Actually, my response would be:

    That’s a good question, young man. What did the investigators do? What does this actually show? What alternative explanations for their results can you think of? Are there other papers that might seem to contradict the authors’ conclusion? What did THOSE investigators do? What might be going on here? How would you distinguish cause from effect? How can you reconcile these apparently contradictory results?

    Why on earth would Professor Jock make a claim one way or the other? This isn’t middle school, where students are spoon-fed the answers. Grow up and think for yourself, ferchrissakes!

    You may or may not notice that Prof. Jock’s first question here was part of my original response to you regarding Nishino — ‘what techniques did the researchers use’…Of course, Sal concluded that it was a fact that SRY was regulated by “chromatin” — sloppy ambiguous language that any professor should beat out of his student. I notice that the hypothetical student here avoided that particular mistake.
    That’s progress, I guess.

  15. MAT expression requires ATP, CTP, GTP and UTP.
    None of these facts, all of which I pointed out to you, detract from the fact that MAT sits atop a regulatory hierarchy.

    Oh I get it, your point was that if you omit the fact MAT is controlled by things like chromatin and other genes (and the proteins they code for), one can argue MAT sits atop one regulatory hierarchy even though it’s not the atop the other regulatory hierarchies.

    If one is free to omit or include what sits at the controlling top, then a hierarchy is in the eyes of the beholder. Then what’s the point of arguing. You have no right then to declare someone else’s view of the order of control is unequivocally wrong.

    If someone wants to argue epigenetic memory is stored and therefore gene expression is regulated by chromatin modifications (as in Turner’s book), that’s not really wrong is it?

    But that doesn’t really help your insinuation that transcription factors have absolute priority in the scheme of things, maybe in a regulatory network topology, it is inappropriate to say one class of molecules takes absolute priority over all others.

    But you said:

    I am not making any claim or admission one way or the other.

    So is there ambiguity then over what controls MAT and therefore some ambiguity as to which hierarchy we should take as defining what ultimately rules epigenetic inheritance (somatic and/or transgenerational).

    But if chromatin can be modified by non-Transcription Factors, it sort of weakens the claim Transcription Factors are solely in control. By the way, for the benefit of the readers is 10-HDA a transcription factor or not? 🙂

  16. Why on earth would Professor Jock make a claim one way or the other?

    Because DNA_jock claims SRY is unambiguously at the top of a regulatory hierarchy.

    But If the hierarchy where SRY is placed at the top is only because other things possibly regulating SRY are omitted in the conception of the hierarchy, it only shows the hierarchical model is somewhat in the eyes of the beholder.

    The paper suggests that the claims “SRY is at the top of a regulatory hierarchy” is only due to the omission consider molecules and systems that possibly regulate SRY.

  17. stcordova: Oh I get it, your point was that if you omit the fact MAT is controlled by things like chromatin and other genes (and the proteins they code for), one can argue MAT sits atop one regulatory hierarchy even though it’s not the atop the other regulatory hierarchies.

    Well that took a lot longer than it should have. Phew.
    Still with the howlers though. MAT is not controlled by “things like chromatin”, although I will grant you that it needs pol-II (i.e. “other genes”, LOL) for its expression. So?
    Or are you looking to discuss the HDAC-mediated silencing of HML and HMR?
    (It’s a trap!)
    TGTKOG

  18. stcordova,

    I worked with Jon Widom. I knew Jon Widom. Jon Widom was a friend of mine. You, Sal, are no Jon Widom.
    </Lloyd Bentsen mode>

    That’s the 30nm fiber, duckie. Calling it merely “chromatin” is more overly vague and fuzzy language.

  19. That’s the 30nm fiber, duckie. Calling it merely “chromatin” is more overly vague and fuzzy language.

    That’s a 30nm fiber of Chromatin. 30nm fiber is one of the ways Chromatin is organized in vitro, but it is still chromatin. Your comment is as stupid as saying when a string coils into an x-sized conformation it is no longer a string.

    From wiki article on Chromatin:

    In general terms, there are three levels of chromatin organization:

    1.DNA wraps around histone proteins forming nucleosomes; the “beads on a string” structure (euchromatin).
    2.Multiple histones wrap into a 30 nm fibre consisting of nucleosome arrays in their most compact form (heterochromatin). (Definitively established to exist in vitro, the 30-nanometer fibre was not seen in recent X-ray studies of human mitotic chromosomes.[3])
    3.Higher-level DNA packaging of the 30 nm fibre into the metaphase chromosome (during mitosis and meiosis).

  20. From wiki:

    https://en.wikipedia.org/wiki/Chromatin

    Chromatin is a complex of macromolecules found in cells, consisting of DNA, protein, and RNA. The primary functions of chromatin are 1) to package DNA into a smaller volume to fit in the cell, 2) to reinforce the DNA macromolecule to allow mitosis, 3) to prevent DNA damage, and 4) to control gene expression and DNA replication.

    Apparently DNA_jock was having problems when I stated the gene expression of SRY was controlled by chromatin, but there you have it in wiki that gene expression is controlled by chromatin, and I cited 3 peer-reviewed papers that specifically said the SRY gene was regulated by chromatin — specifically DNA methylations which are a chromatin mark.

    As far as DNA_Jock’s comment:

    that wonderfully fuzzy concept “chromatin”.

    A Nobel Prize was awarded for elucidating some of the structure of chromatin:

    http://www.nobelprize.org/nobel_prizes/chemistry/laureates/1982/press.html

    The DNA-protein complex of cell nuclei, chromatin, is condensed to chromosomes during cell division. In a given cell only a part of the genetic message in DNA is transcribed, a fact which must also be related to structural changes in the chromatin. Knowledge of chromatin structure is consequently of great importance for an understanding of the control functions of the cell.

    So even on the Nobel Prize website, the word “chromatin” is used. It’s not that fuzzy a concept, what may be fuzzy are the list of all the components of chromatin at any given time, but that is true of living things in general.

  21. Sal:

    That’s a 30nm fiber of Chromatin.

    Yes, yes it is.

    30nm fiber is one of the ways Chromatin is organized in vitro, but it is still chromatin.

    That’s right! Very good that you chose to add the caveat “in vitro”. That’s being specific.

    Your comment is as stupid as saying when a string coils into an x-sized conformation it is no longer a string.

    But that is NOT what I wrote, now, is it? Again with the mis-representation.
    I wrote

    Calling it merely “chromatin” is more overly vague and fuzzy language.
    [emphasis added]

    See the difference? No? Okay, My comment is as stupid as saying when a wire is coiled into an spring, calling it merely a “wire” is overly vague and fuzzy language. Yes, Sal, it’s still a wire, I never said it was not, but you really, really need to work on the specificity of your use of language. The fuzzy terms “epigenetic” and “chromatin” are both frequent sources of confusion and misunderstanding for you. You would be well advised to avoid their use. Be more specific, and you might thereby reduce your tendency for equivocation. Sadly, I suspect that you find your equivocations beneficial, not detrimental. Your failure to distinguish between mitotic “inheritance” and “inheritance” across generations has been particularly long-running, and self-serving.
    Anyhoo, do you have any interest in actually discussing how Nishino tested the effect of methylation, or how Darasi measured demethylation? Or how you would reconcile Darasi with Wang et al. 2005, given that both studies looked at LNCaP and PC3? Y’know, discussing the actual science?
    I thought not.
    As you put it yourself:

    FWIW, in debates where one side is losing, they sometimes start making up things in their mind and believe what they want to believe — self-delusion.

    Yeah.

  22. Calling it merely “chromatin” is more overly vague and fuzzy language.

    I never called the photo “merely” chromatin. You’re attributing something to me that I didn’t say.

    Your failure to distinguish between mitotic “inheritance” and “inheritance” across generations has been particularly long-running, and self-serving.

    Baloney, I made a distinction here for example in just a few posts above:

    epigenetic inheritance (somatic and/or transgenerational)

  23. Oh Sal, you called the 30nm fibre “chromatin”, without any qualification. I pointed out that that was overly vague use of language. You accused me of claiming that the 30nm fibre was NOT chromatin.
    Your misrepresentations are quite transparent.
    Likewise, only Sal could distinguish between somatic and transgenerational inheritance by lumping them together.
    LMAO

  24. Oh Sal, you called the 30nm fibre “chromatin”, without any qualification.

    It’s still chromatin.

    If I showed a picture of a man and said “that’s a picture of a human”, I don’t have to put a qualifier saying he’s 6 feet tall, it’s still a picture of a human.

    The photos is an example of chromatin that happens to be in a 30nm conformation, but it’s still chromatin. The point of the photo was to falsify your argument that chromatin is a fuzzy concept. That photo refutes your claim pretty easily. The fact it is in the 30nm conformation is not relevant to the fact it is still chromatin and that chromatin is not a fuzzy concept since it evidently can be seen in a photograph (vs. some conceptual diagram).

    Likewise, only Sal could distinguish between somatic and transgenerational inheritance by lumping them together.
    LMAO

    I was listing the two forms of epigenetic inheritance, not lumping them together as the same thing. You’re just laughing at your ability to misread.

    There are two forms of epigenetic inheritance:

    1. somatic
    2. transgenerational

    Note wiki lists them the same way in the article on epigenetics:
    https://en.wikipedia.org/wiki/Epigenetics

    Somatic epigenetic inheritance, particularly through DNA and histone covalent modifications and nucleosome repositioning, is very important in the development of multicellular eukaryotic organisms

    and

    Main article: Transgenerational epigenetic inheritance

    Epigenetics can affect evolution when epigenetic changes are heritable

    So wiki lists:
    1. somatic epigenetic inheritance
    2. transgenerational epigenetic inheritance

    Compares well with what I said:

    epigenetic inheritance (somatic and/or transgenerational)

    You’re just laughing at your misreadings, not what I actually said.

  25. Holy shit, Sal, do you ever read what you write?

    stcordova: The point of the photo was to falsify your argument that chromatin is a fuzzy concept. That photo refutes your claim pretty easily. The fact it is in the 30nm conformation is not relevant to the fact it is still chromatin and that chromatin is not a fuzzy concept since it evidently can be seen in a photograph (vs. some conceptual diagram).

    So, if I were to claim that “British man” is a fuzzy concept, you could “refute my claim” merely by posting a photograph (not a painting, an effing photograph) of Oscar Wilde!
    Wow! Sal-logic(tm) is even more fun than I originally suspected.

  26. Since DNA_jock is having some trouble understanding this phrase

    epigenetic inheritance (somatic and/or transgenerational)

    let me render the phrase in an alternate way along with some bolding to help him better comprehend:

    somatic epigenetic inheritance and/or transgenerational generational epigenetic inheritance

    The wiki article on epigenetics uses the phrases:
    1. somatic epigenetic inheritance
    2. transgenerational epigenetic inheritance

    DNA_jock is eager to misread a simple statement since he can’t bring himself to admit that he was wrong to accuse me of not making a distinction between the two types of epigenetic inheritance. He’ll find ways to delude himself that I actually never made that distinction at TSZ in this thread or others.

  27. Correct me if I’m wrong , Sal, but I have asked a number of times whether you are asserting that any of the changes you are worked up about survive more than a few generations.

  28. Richardthughes: I’ll take the same bet Joe F offered you.

    His bet was that intelligence offers better results than ignorance. You agree with Joe that intelligence offers better results than ignorance. You want me to bet what, exactly? You want me to wager that ignorance offers better results than intelligence?

    What odds do you offer?

  29. Mung,

    The bet was very simple Mung. You keep changing things. You wanted a test . You got one. Now you’re moving the goalposts. Pathetic.

  30. Richardthughes: The bet was very simple Mung. You keep changing things. You wanted a test . You got one. Now you’re moving the goalposts. Pathetic.

    I’m willing to put up $10,000.00 dollars. What odds do you offer?

  31. So, Mung, remind me what you are whining about regarding that trivial learning example that IDists are so obsessed with refuting called WEASEL?

    If you cared to restate your position and then state your bet you might actually win some money. As it is it just seems like you’ve whined about something you don’t understand then when called on it you create a “bet” that you’ve no genuine intent of taking regarding something you’ve invented yourself based on a mangling of something someone else said.

    So either you can refute WEASEL as is or you can’t. Either cumulative selection is demonstrated or it is not. Either you have honor or you do not (you don’t).

  32. OMagain, to Mung:

    So either you can refute WEASEL as is or you can’t.

    He can’t. And it bugs the crap out of him.

  33. keiths:
    OMagain, to Mung:

    He can’t.And it bugs the crap out of him.

    Here’s a typical example of what is so counterproductive from Keiths.

  34. @ Keiths

    That you pepper your comments with snark and insult means people avoid dialogue with you. It also loses TSZ members. I’m sad about that.

  35. “He can’t. And it bugs the crap out of him” is pretty mild, Alan, not to mention truthful. (It refer’s to Mung’s failed attacks on Weasel.) How many people here haven’t exceeded that rather tame level of snark?

    In any case, I thought you were going to answer my question about the interaction with Neil:

    Alan:

    He was mistaken in attempting to discuss perception with you.

    keiths:

    Why was it a mistake? I’ve quoted his claims in his own words and responded to them, carefully explaining where I agree with him and where I disagree, and why. That’s how it’s supposed to work.

    Other than the fact that he wasn’t prepared to defend his position, why was it a mistake for him to discuss perception with me?

  36. What I think is funny is that, while I’ve regularly disagreed with keiths about this or that, my own most recent dust up with him involves some (ridiculous) thing that we AGREE on–Elon Musk’s hot tub estimation that it’s highly likely that we’re in a simulation. I just said I’d “put” something differently than Keiths did. And keiths told me I was wrong about that. The headline of the interview is

    There’s a ‘one in billions’ chance our reality is not a simulation

    I said I’d call that a billions-to-one shot. Keiths felt it important to correct me on how I’d put that.

    Anyhow, while he’s thinking about his crucial OP, I want to mention that it could be that some people display what might be called a “fear of being wrong” when they assiduously refuse to answer questions about or objections to their own views, utilizing a preferred MO of “Always Attack.” (Could call that “Double A” but it’s already been used in Season 2 of Silicon Valley). So I’m hoping keiths’ promised OP treatise on internet psychological failings that people besides him have will get into those aspects as well.

    I note with sorrow, however, that Keiths has a history of promising posts that he doesn’t deliver. (Of course, how COULD he give us all that he might? We may wish it, but….do we DESERVE it?) And since this one is such a big topic, and one that keiths has considered so carefully, I know that he may be forced to focus on just one of his own virtues instead of covering the vast waterfront of them, which would probably require at least weekly entries on his own blog for a couple of years.

  37. keiths:
    “He can’t. And it bugs the crap out of him” is pretty mild, Alan, not to mention truthful. (It refer’s to Mung’s failed attacks on Weasel.) How many people here haven’t exceeded that rather tame level of snark?

    In any case, I thought you were going to answer my question about the interaction with Neil:

    Alan:

    keiths:

    My prediction that this would be a mistake was not mistaken. :sad face:

  38. Alan,

    You wrote:

    He [Neil] was mistaken in attempting to discuss perception with you.

    I asked:

    Why was it a mistake? I’ve quoted his claims in his own words and responded to them, carefully explaining where I agree with him and where I disagree, and why. That’s how it’s supposed to work.

    Other than the fact that he wasn’t prepared to defend his position, why was it a mistake for him to discuss perception with me?

    You replied:

    To tell you what I think without restraint, I need to move to Noyau.

    And I said:

    OK. See you there.

    Well, here we are, and now you don’t want to answer the question.

    There must have been something about my exchange with Neil that prompted you to write this:

    He [Neil] was mistaken in attempting to discuss perception with you.

    What was it? Quote, please.

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