You are assuming that a 20:1 ratio of legal vs illegal songs is a market problem, or an actual (as opposed to emotional) problem for artists. This is not at all clear.
There are four kinds of copying:
Copying where the copier would have bought the original without access to a copy, and does. This is neutral for the content provider and positive for the copier (or else he wouldn't copy.)
Copying where the copier would have bought the original without access to a copy, and doesn't. This is negative for the content provider and positive for the copier. The reason for not buying may be having access to the copy, or it may be that the thing copied sucks so much that no way the copier would support more of that.
Copying where the copier would not have bought the original without access to a copy, and buys it after copying. This is positive for the content provider and positive for the copier.
Copying where the copier would not have bought the original without acess to a copy, and does not buy it after copying. This is neutral for the content provider and positive for the copier.
Notice that all categories are positive for the copier, that only category 2 copying is negative for the content provider, and that copying is only net negative for the content provider if category 2 is larger than category 3. The statistics seems to indicate that category 3 is larger than category 2, and copying lead to overall increase in purchase of content.
On a personal level, I can very much relate to that - I've never bought as much music as when I used Napster actively, by a wide margin. My overall consumption of music just went up.
My stand on this is that (A) it is not at all clear that somebody should be allowed to monopolize a part of culture and not have it copied - that's a temporary thing we granted in a different world, and may no longer be for the best, and (B) it is not at all clear that copying leads to less purchases overall. On this basis, it is definately not clear that there should be laws prohibiting this "crime".
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I'm an expert on the subject. I do operating systems and kernel development, and I'm part of the community around it. The grandparent is correct. What you are calling "operating system" is called "kernel" by the overall community. "Operating system" is a somewhat fuzzy concept, but it is different from kernel.
As for whether Lisp etc is an operating system: Lisp was the OS the Lisp Machines. Java has been used as the OS for the Java buttons. I do not know of any case where emacs or.NET has been used as operating systems.
Look into influence theory and "reactance". It's sort of reverse psychology, only more formalized and correct. Basically, we have a built-in wish to break rules that are forced upon us.
Uhm, you're mixing timelines again. CAM wasn't until 1998 (or so) and replaced the old SCSI subsystem, ATAPICAM came after that again. And the ULE scheduler is important TODAY, while I'm talking about what was important in 1993-1995.
The filesystem metadata policy I see as screwing over mostly for the use on servers etc; and the point is that users *expect* their filesystem to work. They don't go into a system asking "Hmm, when I save a file here, will it be saved or will it be fucked up in some cases? I'd better check the filesystem documentation. Oh, it says nothing about metadata updates. Let's go see the source code. WHAT? UNORDERED, ASYNCHRONOUS METADATA UPDATES? It's not possible to database semantics over this!!!!"
The increased speed it gives can be a large selling point - it's just that people aren't aware of what they're being screwed over with for that speed.
As for losing data: Well, many of us filesystem and VM hackers in FreeBSD actually ran our devel boxes with async metadata back before soft updates. We knew the rough odds, and knew what would happen on a failure. Mail and database servers is what this is critical for - if we got a few fucked up files, we could generally recover from it.
As for PnP on 3c509, that's not quite PnP, and it was also implemented much much later (1997 or 1998, I think). I believe I wrote it. I didn't even remember I'd committed that code - I remembered that I'd hacked on it, I just thought I'd abandoned that patch along with all the 509s I had, as I remember it being semi-rough when I switched away from the 509s. The 509s needed a special hack for PnP, as they used a slightly different but very similar protocol to the official PnP stuff. I believe the offical PnP hardware protocol must have been based on the 509 protocol as the 509 predated the PnP protocol.
And as for 24MB RAM: You're assuming a much more high end developer than most people were at that time. Yes, these existed, but there were also a LOT of people working on lower end hardware. Especially people that just wanted to test out things, didn't know if they wanted to run Unix at all, just testing because something cool was available, and later turned into developers for various pieces around this.
If you fear that, you're probably posting too little relevant information. I say my mind at all times, having checked out available information before saying it. I get a ton of upmods, and some downmods. End result is Karma: Excellent, with no censoring of my opionions.
However, I have the pride to try to avoid forming opinions until I have made sure I am informed, and at the very least not show such dirty opinions in public.
Your question does not make sense to me. DNA strings are reproduced (ie, created) a billion times each day, just in your body. This reproduction occasionally increase data (through mutation) which is shaped into information by natural selection (culling of the bad data).
If that didn't help, and I'm not sure it does, please ask the question another way, and I'll try to give a better answer:)
Why is it appropriate to grieve? This is a serious question, BTW. The best answers I can find are "To fit in with people" (it's assumed, and you communicate that you really cared about that person and can thus really care about other people), "To kick in the "let's change things" response" (but that's not really depression), and "As a threat against yourself to make you keep the person alive".
BTW: I've been depressed and I've been filled with grief. These are really different situations; I've had periods when I was depressed and "should" have grieved, and couldn't.
And yes, you're correct - I was skipping over details to simplifiy a bit. The drugs boost serotonin in some areas by stopping reuptake, but do nothing for the overall level of available serotonin. I'm not certain what overall levels would be relevant for except synthesis of melatonin (where serotonin is a precursor.) Theoretically, I'd guess hindering reuptake would also overall dumb down neural reactions - there's less potential available for change.
All in all, I prefer to stabilize by other means (like you've done) - I've stayed away from pharmaceuticals for my own issues, going for exercise, regular sleep, and better diet as more sustainable than medication. Less side effects, too:)
I have never bought anywhere near as much music as when I copied a ton of it. I'm talking at least 10x more than any other time period, probably 50x more than now.
By removing my ability to copy (basically, making it risky and annoying enough that I don't bother), you've made me stop my habit of getting new music.
And I know that I'm not the only one that has cut drastically - I've seen similar reports from many others, and the statistics point to this being the overall trend.
Abscence of serotonin in certain areas can lead to feedback loops of various kinds; for instance, the feelings after a breakup (pining for the beloved) comes from decreased serotonin along a certain set of pathways.
The mental side of depression tend to work similarly, I believe.
As for the TREK-1 gene, as far as I understand and remember (and this isn't my field of specialty): The connections between neurons (nerve cells) are regulated as pulses of potassium (K) ions. The TREK-1 channel is a channel for transmission of K+ ions, and it is partially regulated by 5HT (serotonin). When they knock out the TREK-1 gene (the gene responsible for creating the channel) in mice, the efficiency of 5HT (serotonin) increase, and the mice become depression resistant.
TREK-1 is also said to be involved in several protective activities, including neuroprotection from polyunsaturated fat in mice, and protection against epilepsy.
Go away from that edge - it's sharp, and standing on it just hurt you;)
Contrary to popular belief, depression is to a large degree a physical thing. It is possible to treat with talk therapy, but it's more reliable to treat with a clinical diet (well over 95% reliability) or heavy exercise. It is sourced from stress, both physical and mental.
And depression generally isn't motivating. It's the exhaustion stage, where you have very little motivation left, because you've spent your reserves.
I'm trying to think of the best references to give you here - a good intro to psychology (including biopsychology) should cover this. For the original source for a lot of this, Hans Selye's research into stress would be the place to go - it's summarized in a semi-popularized form in "The Stress Of Life". That's still a fairly hard read, though. An easier read is "Why zebras don't get ulcers" (I don't remember the name of the author).
0.9x till 1.0 lasted a long time, and yeah, 0.95 and later were definitely usable for research and hobby, and definitely felt like a Unix system. That said, I have tried to run a multiuser machine with a bunch of terminals connected to share an internet connection, and while that worked well for users who tried to behave on the system, it was really not yet upto the task for such things (no way of stopping a single user from hogging the machine or even bringing it down at times for example). This was post 0.95, but I do no longer know which version exactly. There is a bit more then 'looks and feels like Unix' to actually acting like a somewhat well developed one (and how could it, it was mostly a 'scratch an itch' derived kernel that was rapidly developing maybe, but only had done so for a short time.
Ah, here we seems to end up agreeing. Maybe where we have most different perspectives is in our views of what is important for a kernel to "take"? I believe running on developer's desktops is most important. This means that low end hardware must be supported (and Linux was better than BSD there for a while), and it means that low file system latency is important. The Linux default for filesystem updates was faster than the BSD default for a long while, because Linux did the choice of running async metadata updates, which violates POSIX and can lose user data but runs faster. I had a couple of fights with Linus over this - basically, I don't see it as OK to fuck over users' data by default because it gives you better benchmarks, and that was actually Linus original primary argument ("We get such lousy benchmarks if we do it right", paraphrased). This is also one of the reasons I'm less than impressed with Linus.
Back to primary topic: Scheduler quality and VM quality isn't that important in the desktop context, and while we (BSD) beat Linux on that for a long while (with 2.6, I think Linux has finally gotten a VM system that is comparable to FreeBSDs), that didn't make a difference at that point, especially compared to Linux other advantages.
There's also one other thing that gave Linux an advantage compared to BSD: The GPL handles people fear of being "exploited". I personally see that fear as irrational and to a large degree fueled by the propaganda in the GPL - but that doesn't matter. The fear is there, and it influence people's behaviour.
If you wonder, find out... The answer is somewhat complex.
To give you at least some help: Part of the reason for the apathy of the anti-depressant crowd is that the most common anti-depressants are serotonin boosters (SSRIs), and serotonin is an inhibitory neurotransmitter. Now, certain other antidepressants (e.g, MAOIs) work by boosting other neurotransmitters, and can handle depression without apparently leading to the kind of apathy/nonchalance you're talking about.
With the usual Slashdot disclaimer: I am not a psychiatrist.
The BSD options were not reasonably available at the time Linux gained a foothold, due to licensing problems with AT&T.
This is not true. FreeBSD 2.x was readily available and had been for some time when Linus released the 1.0 kernel. Of course there were kernels before 1.0, and they were even being used and distributed (I still have a Snow CD based on Linux 0.9 kernel around for example), but fact is that the legal issues for BSD got clear before Linux had become anywhere near the usable system it is now.
Linux was active WAY before 1.0. The first release of Linux was in mid 1991, while the firt semi-usable release of the 386BSD project (predecessor to Free/NetBSD) was in mid 1992. And I remember using pre-1.0 versions of Linux for at least a year prior to 1.0, and having it feel like a full Unix system.
Anyway, I don't think either of us will change our mind on this topic, so it's probably as well to just go on with our lives:-)
In peace, Eivind.
The BSD options were not reasonably available at the time Linux gained a foothold, due to licensing problems with AT&T. In addition, I believe there were some issues with hardware support, especially IDE support AFAIR. And, not least, the BSDs were fairly complete in themselves, and didn't have any reason to coopt the GNU system - which missed mainly a kernel.
Also, the BSD projects have more or less always given people a "them" feeling, due to the way version control etc is run. It's a communication problem we have, and one that I don't see any way of solving without going to fully distributed VC and doing some other moves.
I give Linus credit for sticking to his project long enough for it to "take" - but I see this as a lesser achievement than some of the other GNU projects, and a much lesser achievement than people tend to believe it is.
Depending on perspective, there's several "Why's". You can say that OSKit replace it, and probably a few of the other experimentals, and that your question is based on a wrong implication. You would then reply that nothing else has gotten as large or complete, and that's another "Why" - Linux is good enough that people use that kernel instead of another, so the feedback loop keeps that kernel on top.
As for "If it is such a small part, why is it so important" - that's sort of like saying "Why are sparkplugs for a car so important, they're so SMALL?"
And, when they work reasonably well, they don't make much of a difference to the average consumer, who will just "Get some sparkplugs", rather than try to shop around for something else. The same with the kernel - people will generally just default to Linux, with very few even testing out anything else.
Now, my personal interest in the GNU/Linux side of this is fairly academic - I tend to avoid using either GNU tools or the Linux kernel, for a variety of reasons. I just wanted to correct the misunderstanding around how large part of the job a kernel is. A complete, production quality kernel IS a lot of work, it's just much less than the rest of the system. And a hack-level kernel (which was what Linus started with) isn't that much work at all.
The kernel is actually a minor part of an operating system. And the tools are runnable on other systems.
The FSF was working towards creating a full operating system, and Linus came and filled in a fairly small part of it, proportionally. Afterwards, all the Unix systems derived from this is called "Linux", for some strange reason - as if they were all really similar systems, instead of a collection of fairly different Unix systems that happen to share a kernel.
My assumption was correct: You're too chicken to read the references I give you, instead handwaving.
You are missing the high level view of this. That's why I'm pointing you at Dawkins as the best-written high level view I know about. Another I could recommend is Carl Zimmer's "Evolution", but Dawkins is better.
And no, you've not shown me wrong in either of those articles, which is why I've just ignored them. I was saying that you can more or less ignore mutations and the details of mutation in your understanding - YOU need to understand natural selection. And I'm saying most mutations are neutral, not that most mutations to the HOX genes are neutral, so mutations to HOX genes leading to abortions is perfectly within my world view. (If I've said something leading you to the understanding that mutations to HOX genes are usually viable, I'm sorry - I've been thinking "including junk DNA and useless indels" for most of this.)
As for the reason for significant DNA changes: Yes, no, somewhat. Mutation occurs. This is a well known fact, and demonstratable by the pure strain mice experiments I mentioned. Saying that "mutation is responsible for the significant DNA changes in the pool" is sort of correct - but attempting to do deep understanding of mutation disconnected from some understanding of pool dynamics, the timelines involved, embryology, and especially natural selection - it just gets in the way, I think.
Mutations occur, on the level of changing lengths of limbs etc, as discussed in a previous comment.
A simulation of evolution (reproduction + natural selection) over this magnitude of changes is enough to give us the complex structures we see in nature (such as eyes) fairly rapidly.
The evidence we find indicate that this is what has happened to produce species and phyla. The evidence is both morphological (large scale differences) and molecular (genetic), and these tend to agree.
And you've been writing back all this time while I've given you references that show you've misunderstood (especially the role of chromosomes vs real effects), so I feel no issue with writing back when you've misunderstood again. It's part of my project to ATTEMPT to get you to read something that fix your worldview so you stop lying to other people.
You start of with rats, you only get rats. You may get different rats, bigger rats(with limits), differently colored rats(with limits), rats with longer legs; but you will never change phyla, let alone species.
Please look up "ring species", which are living, breathing proof that your conclusion is wrong. Species can occur from a single breeding pool (which would happen if you killed off part of the pool of a ring species.)
Now, with the example that we CAN split species (it's been shown a number of other times), and the example that we DO get inheritable mutations (from the mice), as far as I can tell, your only argument at the moment is "I can't believe it!"
Argument from personal incredulity is very, very weak.
And I would be interested in discussing more advanced topics if you had understood and accepted the basics. As it is, this is just an attempt by me to point you at the relevant information so you can get your facts straight. But, you're so chicken you won't even read Dawkins. You're so stuck up in your own little world, fearing change to your beliefs that there's no way you'll come back here in a week and say "I read Climbing Mount Improbable now." You'll just chicken out, and keep lying to people by your misunderstandings.
You're misstatings the important of chromosomal mutations. Please read the link I sent you in the last post, it covers this in detail - both how chromosomal mutations occur, and how unimportant they (sort of) are.
Body plan changes are controlled by HOX genes, not chromosomal mutations. Other large changes are the result of a series of selections of small differences, where the small differences come into the genepool from mutations. Meiosis is the primary driving force. YOU ARE IGNORING GEOLOGICAL TIME.
These are points I have made to you several times. Instead of actually looking at the evidence, you're coming with (A) incorrect claims, and (B) claims that I've already refuted.
In my view, if you are doing this to somebody that does NOT know this area well, it is in violation of the commandment "Thou shalt not bear false witness". As it is, it doesn't work as a lie towards me, because I've got the knowledge to negate it.
And the simulation in question created a human-like eye - not an exact human eye, but a similar design. I do not remember exactly what the 7000 generation simulation started from; I think it was a single light-sensitive cell. The 50,000 generation simulation started from a flat light-sensitive patch with a non-transparent background (but using very conservative options for all the mutation).
As for misunderstanding: While I tend to always take responsibility for misunderstandings in what I communicate - I think I see one extra factor here. You do not seem to be searching for the truth, but instead to be picking up knowledge with the intent to argue a particular viewpoint. When you've already , you tend to interpret counterarguments as being unreasonable.
Now, if you tried to get your information from credible sources, and tried to actually understand how evolution works (instead of looking for counterarguments to it), then you might be in a position to come with serious critiques of sides of evolution. As it is, you're just showing up with fragmented information trying to support a preconceived idea. This information varies between "almost completely wrong" and "correct, but misunderstood in context." I'm sure you also have some things you understand correctly, but because you're not willing to assume truth *even when trying to understand things*, you're missing out on the context. You have to FIRST assume truth of evolution for learning, THEN try to understand how biologists claim that evolution works, and THEN look for problems - and see if there are already available resolutions to those problems. Like your chromosome problem above - it's trivially resolvable. We know how chromosomes split and merge. We also know that they're not important in the way you claim they are, e.g. from the equine family (horses, zebras, donkeys, etc.)
When you say the idea is laughtable, you're understandable from your perspective. Alas, again, this perspective is missing a point: The simulation occurs at a much higher level. We look at what kind of variation occurs, in nature, at the cellular level, from individual to individual inside a sexually reproducing species. Then we simulate this level of difference accumulating through reproduction and natural selection. You're continually missing natural selection in your arguments - and natural selection is KEY. It's ABSOLUTELY crucial. You can almost ignore mutations - they're fairly much irrelevant. It's natural selection you have to understand.
As for mutations, WE KNOW THEY OCCUR. We've seen what happens in nature. Genetically identical mice start breeding apart, with measurable differences of the kind necessary for natural selection, inside 3-4 generations. Different proportions of legs, slight overall size difference, that kind of things.
When it comes to chromozome counts, this is covered here. I feel you're fairly arrogant when you're attacking something that is generally accepted without doing a trivial Google search to see how your extremely obvious counterarguments are handled. Scientists think of these kind of problems THEMSELVES. Attacking scientific theories/hypotheses is the primary hobby (nay, job) of scientists. They're happy about it.
Just yesterday, I sent an email attacking the hypothesis of an UCLA professor for mortality rates in married vs unmarried people. This was basically shooting down the conclusions he'd drawn in a paper he'd published. The response I got from him was "Very interesting explanation! Thanks!"
And yes, evolution IS about minor changes to properties. Evolution is effectively ONLY about minor changes to properties, stacked on top of each other one after each other, for billions of years. Do you get that number? If you took the whole evolutionary timeline and put it between your outstretched arms, the whole of human history would be gone with a single brush of a nail file. Easily.
The minor, minor changes to properties is introduced by mutations.
Also, "Most mutations are neutral" is generally accepted. It is the basis for the molecular clock. I can ask my girl, of course, but she'd probably just laught at you;)
The heritable variation necessary to do natural selection over is present. We also see the kind of variation appearing quickly in nature when we start out with genetically clean (identical) mice.
In other words, I believe your arguments again are founded on a misunderstanding: You seem to assume that there has to be complex positive mutations every generation in a single line for 7000 generations. The way it really works is that mutations introduce genetic variation into the genepool, so every member vary a little bit. Mutations are mostly neutral, occasionally negative, and very occasionally positive. They may be the replacement of a single base with a different one, coding for a slightly different protein at some point in the embryologic sequence (development of the adult form). They may also be somewhat larger genetic differences (duplication of genes, for instance).
I don't know enough molecular genetics to say the frequency of different results when a single base is randomly changed through a transcription error, or what tends to happen when a piece of DNA is duplicated etc. I know some particular cases, but not the general frequencies. I know that those in the know assumes that the original mutations that natural selection works over are perfectly random, and I believe they have evidence for it, but I do not personally know that evidence. I'm going to check this out tomorrow - I've got a date with a molecular biologist that likes to talk about these kind of things.
Slashdot Mirror
It's got the perfect goods for this particular discussion.
There are four kinds of copying:
- Copying where the copier would have bought the original without access to a copy, and does. This is neutral for the content provider and positive for the copier (or else he wouldn't copy.)
- Copying where the copier would have bought the original without access to a copy, and doesn't. This is negative for the content provider and positive for the copier. The reason for not buying may be having access to the copy, or it may be that the thing copied sucks so much that no way the copier would support more of that.
- Copying where the copier would not have bought the original without access to a copy, and buys it after copying. This is positive for the content provider and positive for the copier.
- Copying where the copier would not have bought the original without acess to a copy, and does not buy it after copying. This is neutral for the content provider and positive for the copier.
Notice that all categories are positive for the copier, that only category 2 copying is negative for the content provider, and that copying is only net negative for the content provider if category 2 is larger than category 3. The statistics seems to indicate that category 3 is larger than category 2, and copying lead to overall increase in purchase of content.On a personal level, I can very much relate to that - I've never bought as much music as when I used Napster actively, by a wide margin. My overall consumption of music just went up.
My stand on this is that (A) it is not at all clear that somebody should be allowed to monopolize a part of culture and not have it copied - that's a temporary thing we granted in a different world, and may no longer be for the best, and (B) it is not at all clear that copying leads to less purchases overall. On this basis, it is definately not clear that there should be laws prohibiting this "crime".
Eivind.
Thanks for taking your responsibilities seriously. We need more people that do.
As for whether Lisp etc is an operating system: Lisp was the OS the Lisp Machines. Java has been used as the OS for the Java buttons. I do not know of any case where emacs or .NET has been used as operating systems.
Eivind.
Eivind.
The filesystem metadata policy I see as screwing over mostly for the use on servers etc; and the point is that users *expect* their filesystem to work. They don't go into a system asking "Hmm, when I save a file here, will it be saved or will it be fucked up in some cases? I'd better check the filesystem documentation. Oh, it says nothing about metadata updates. Let's go see the source code. WHAT? UNORDERED, ASYNCHRONOUS METADATA UPDATES? It's not possible to database semantics over this!!!!"
The increased speed it gives can be a large selling point - it's just that people aren't aware of what they're being screwed over with for that speed.
As for losing data: Well, many of us filesystem and VM hackers in FreeBSD actually ran our devel boxes with async metadata back before soft updates. We knew the rough odds, and knew what would happen on a failure. Mail and database servers is what this is critical for - if we got a few fucked up files, we could generally recover from it.
As for PnP on 3c509, that's not quite PnP, and it was also implemented much much later (1997 or 1998, I think). I believe I wrote it. I didn't even remember I'd committed that code - I remembered that I'd hacked on it, I just thought I'd abandoned that patch along with all the 509s I had, as I remember it being semi-rough when I switched away from the 509s. The 509s needed a special hack for PnP, as they used a slightly different but very similar protocol to the official PnP stuff. I believe the offical PnP hardware protocol must have been based on the 509 protocol as the 509 predated the PnP protocol.
And as for 24MB RAM: You're assuming a much more high end developer than most people were at that time. Yes, these existed, but there were also a LOT of people working on lower end hardware. Especially people that just wanted to test out things, didn't know if they wanted to run Unix at all, just testing because something cool was available, and later turned into developers for various pieces around this.
Eivind.
However, I have the pride to try to avoid forming opinions until I have made sure I am informed, and at the very least not show such dirty opinions in public.
Eivind.
You're bearing false witness (by omission, and hopefully from lack of knowledge.) Please stop.
If that didn't help, and I'm not sure it does, please ask the question another way, and I'll try to give a better answer :)
Eivind.
BTW: I've been depressed and I've been filled with grief. These are really different situations; I've had periods when I was depressed and "should" have grieved, and couldn't.
Eivind.
And yes, you're correct - I was skipping over details to simplifiy a bit. The drugs boost serotonin in some areas by stopping reuptake, but do nothing for the overall level of available serotonin. I'm not certain what overall levels would be relevant for except synthesis of melatonin (where serotonin is a precursor.) Theoretically, I'd guess hindering reuptake would also overall dumb down neural reactions - there's less potential available for change.
All in all, I prefer to stabilize by other means (like you've done) - I've stayed away from pharmaceuticals for my own issues, going for exercise, regular sleep, and better diet as more sustainable than medication. Less side effects, too :)
Eivind.
By removing my ability to copy (basically, making it risky and annoying enough that I don't bother), you've made me stop my habit of getting new music.
And I know that I'm not the only one that has cut drastically - I've seen similar reports from many others, and the statistics point to this being the overall trend.
Eivind.
The mental side of depression tend to work similarly, I believe.
As for the TREK-1 gene, as far as I understand and remember (and this isn't my field of specialty): The connections between neurons (nerve cells) are regulated as pulses of potassium (K) ions. The TREK-1 channel is a channel for transmission of K+ ions, and it is partially regulated by 5HT (serotonin). When they knock out the TREK-1 gene (the gene responsible for creating the channel) in mice, the efficiency of 5HT (serotonin) increase, and the mice become depression resistant.
TREK-1 is also said to be involved in several protective activities, including neuroprotection from polyunsaturated fat in mice, and protection against epilepsy.
Eivind.
Contrary to popular belief, depression is to a large degree a physical thing. It is possible to treat with talk therapy, but it's more reliable to treat with a clinical diet (well over 95% reliability) or heavy exercise. It is sourced from stress, both physical and mental.
And depression generally isn't motivating. It's the exhaustion stage, where you have very little motivation left, because you've spent your reserves.
I'm trying to think of the best references to give you here - a good intro to psychology (including biopsychology) should cover this. For the original source for a lot of this, Hans Selye's research into stress would be the place to go - it's summarized in a semi-popularized form in "The Stress Of Life". That's still a fairly hard read, though. An easier read is "Why zebras don't get ulcers" (I don't remember the name of the author).
Eivind.
Back to primary topic: Scheduler quality and VM quality isn't that important in the desktop context, and while we (BSD) beat Linux on that for a long while (with 2.6, I think Linux has finally gotten a VM system that is comparable to FreeBSDs), that didn't make a difference at that point, especially compared to Linux other advantages.
There's also one other thing that gave Linux an advantage compared to BSD: The GPL handles people fear of being "exploited". I personally see that fear as irrational and to a large degree fueled by the propaganda in the GPL - but that doesn't matter. The fear is there, and it influence people's behaviour.
Eivind.
To give you at least some help: Part of the reason for the apathy of the anti-depressant crowd is that the most common anti-depressants are serotonin boosters (SSRIs), and serotonin is an inhibitory neurotransmitter. Now, certain other antidepressants (e.g, MAOIs) work by boosting other neurotransmitters, and can handle depression without apparently leading to the kind of apathy/nonchalance you're talking about.
With the usual Slashdot disclaimer: I am not a psychiatrist.
Eivind.
Also, the BSD projects have more or less always given people a "them" feeling, due to the way version control etc is run. It's a communication problem we have, and one that I don't see any way of solving without going to fully distributed VC and doing some other moves.
I give Linus credit for sticking to his project long enough for it to "take" - but I see this as a lesser achievement than some of the other GNU projects, and a much lesser achievement than people tend to believe it is.
Eivind.
As for "If it is such a small part, why is it so important" - that's sort of like saying "Why are sparkplugs for a car so important, they're so SMALL?"
And, when they work reasonably well, they don't make much of a difference to the average consumer, who will just "Get some sparkplugs", rather than try to shop around for something else. The same with the kernel - people will generally just default to Linux, with very few even testing out anything else.
Now, my personal interest in the GNU/Linux side of this is fairly academic - I tend to avoid using either GNU tools or the Linux kernel, for a variety of reasons. I just wanted to correct the misunderstanding around how large part of the job a kernel is. A complete, production quality kernel IS a lot of work, it's just much less than the rest of the system. And a hack-level kernel (which was what Linus started with) isn't that much work at all.
Eivind.
The FSF was working towards creating a full operating system, and Linus came and filled in a fairly small part of it, proportionally. Afterwards, all the Unix systems derived from this is called "Linux", for some strange reason - as if they were all really similar systems, instead of a collection of fairly different Unix systems that happen to share a kernel.
Eivind.
You are missing the high level view of this. That's why I'm pointing you at Dawkins as the best-written high level view I know about. Another I could recommend is Carl Zimmer's "Evolution", but Dawkins is better.
And no, you've not shown me wrong in either of those articles, which is why I've just ignored them. I was saying that you can more or less ignore mutations and the details of mutation in your understanding - YOU need to understand natural selection. And I'm saying most mutations are neutral, not that most mutations to the HOX genes are neutral, so mutations to HOX genes leading to abortions is perfectly within my world view. (If I've said something leading you to the understanding that mutations to HOX genes are usually viable, I'm sorry - I've been thinking "including junk DNA and useless indels" for most of this.)
As for the reason for significant DNA changes: Yes, no, somewhat. Mutation occurs. This is a well known fact, and demonstratable by the pure strain mice experiments I mentioned. Saying that "mutation is responsible for the significant DNA changes in the pool" is sort of correct - but attempting to do deep understanding of mutation disconnected from some understanding of pool dynamics, the timelines involved, embryology, and especially natural selection - it just gets in the way, I think.
Mutations occur, on the level of changing lengths of limbs etc, as discussed in a previous comment.
A simulation of evolution (reproduction + natural selection) over this magnitude of changes is enough to give us the complex structures we see in nature (such as eyes) fairly rapidly.
The evidence we find indicate that this is what has happened to produce species and phyla. The evidence is both morphological (large scale differences) and molecular (genetic), and these tend to agree.
And you've been writing back all this time while I've given you references that show you've misunderstood (especially the role of chromosomes vs real effects), so I feel no issue with writing back when you've misunderstood again. It's part of my project to ATTEMPT to get you to read something that fix your worldview so you stop lying to other people.
Eivind.
Now, with the example that we CAN split species (it's been shown a number of other times), and the example that we DO get inheritable mutations (from the mice), as far as I can tell, your only argument at the moment is "I can't believe it!"
Argument from personal incredulity is very, very weak.
And I would be interested in discussing more advanced topics if you had understood and accepted the basics. As it is, this is just an attempt by me to point you at the relevant information so you can get your facts straight. But, you're so chicken you won't even read Dawkins. You're so stuck up in your own little world, fearing change to your beliefs that there's no way you'll come back here in a week and say "I read Climbing Mount Improbable now." You'll just chicken out, and keep lying to people by your misunderstandings.
Eivind.
Body plan changes are controlled by HOX genes, not chromosomal mutations. Other large changes are the result of a series of selections of small differences, where the small differences come into the genepool from mutations. Meiosis is the primary driving force. YOU ARE IGNORING GEOLOGICAL TIME.
These are points I have made to you several times. Instead of actually looking at the evidence, you're coming with (A) incorrect claims, and (B) claims that I've already refuted.
In my view, if you are doing this to somebody that does NOT know this area well, it is in violation of the commandment "Thou shalt not bear false witness". As it is, it doesn't work as a lie towards me, because I've got the knowledge to negate it.
And the simulation in question created a human-like eye - not an exact human eye, but a similar design. I do not remember exactly what the 7000 generation simulation started from; I think it was a single light-sensitive cell. The 50,000 generation simulation started from a flat light-sensitive patch with a non-transparent background (but using very conservative options for all the mutation).
As for misunderstanding: While I tend to always take responsibility for misunderstandings in what I communicate - I think I see one extra factor here. You do not seem to be searching for the truth, but instead to be picking up knowledge with the intent to argue a particular viewpoint. When you've already , you tend to interpret counterarguments as being unreasonable.
Now, if you tried to get your information from credible sources, and tried to actually understand how evolution works (instead of looking for counterarguments to it), then you might be in a position to come with serious critiques of sides of evolution. As it is, you're just showing up with fragmented information trying to support a preconceived idea. This information varies between "almost completely wrong" and "correct, but misunderstood in context." I'm sure you also have some things you understand correctly, but because you're not willing to assume truth *even when trying to understand things*, you're missing out on the context. You have to FIRST assume truth of evolution for learning, THEN try to understand how biologists claim that evolution works, and THEN look for problems - and see if there are already available resolutions to those problems. Like your chromosome problem above - it's trivially resolvable. We know how chromosomes split and merge. We also know that they're not important in the way you claim they are, e.g. from the equine family (horses, zebras, donkeys, etc.)
Eivind.
When you say the idea is laughtable, you're understandable from your perspective. Alas, again, this perspective is missing a point: The simulation occurs at a much higher level. We look at what kind of variation occurs, in nature, at the cellular level, from individual to individual inside a sexually reproducing species. Then we simulate this level of difference accumulating through reproduction and natural selection. You're continually missing natural selection in your arguments - and natural selection is KEY. It's ABSOLUTELY crucial. You can almost ignore mutations - they're fairly much irrelevant. It's natural selection you have to understand.
As for mutations, WE KNOW THEY OCCUR. We've seen what happens in nature. Genetically identical mice start breeding apart, with measurable differences of the kind necessary for natural selection, inside 3-4 generations. Different proportions of legs, slight overall size difference, that kind of things.
When it comes to chromozome counts, this is covered here. I feel you're fairly arrogant when you're attacking something that is generally accepted without doing a trivial Google search to see how your extremely obvious counterarguments are handled. Scientists think of these kind of problems THEMSELVES. Attacking scientific theories/hypotheses is the primary hobby (nay, job) of scientists. They're happy about it.
Just yesterday, I sent an email attacking the hypothesis of an UCLA professor for mortality rates in married vs unmarried people. This was basically shooting down the conclusions he'd drawn in a paper he'd published. The response I got from him was "Very interesting explanation! Thanks!"
And yes, evolution IS about minor changes to properties. Evolution is effectively ONLY about minor changes to properties, stacked on top of each other one after each other, for billions of years. Do you get that number? If you took the whole evolutionary timeline and put it between your outstretched arms, the whole of human history would be gone with a single brush of a nail file. Easily.
The minor, minor changes to properties is introduced by mutations.
Also, "Most mutations are neutral" is generally accepted. It is the basis for the molecular clock. I can ask my girl, of course, but she'd probably just laught at you ;)
Eivind.
In other words, I believe your arguments again are founded on a misunderstanding: You seem to assume that there has to be complex positive mutations every generation in a single line for 7000 generations. The way it really works is that mutations introduce genetic variation into the genepool, so every member vary a little bit. Mutations are mostly neutral, occasionally negative, and very occasionally positive. They may be the replacement of a single base with a different one, coding for a slightly different protein at some point in the embryologic sequence (development of the adult form). They may also be somewhat larger genetic differences (duplication of genes, for instance).
I don't know enough molecular genetics to say the frequency of different results when a single base is randomly changed through a transcription error, or what tends to happen when a piece of DNA is duplicated etc. I know some particular cases, but not the general frequencies. I know that those in the know assumes that the original mutations that natural selection works over are perfectly random, and I believe they have evidence for it, but I do not personally know that evidence. I'm going to check this out tomorrow - I've got a date with a molecular biologist that likes to talk about these kind of things.
Eivind.