Josh M

We think of computer calculations as being infinite because we're reaching into the trillions of units of capacity, but here's what happens when you try to calculate all the moves in a chess game: White 1 = 20 possibilities Black 1 = 20 possibilities White 2 = ~23^2 = 529 possibilities Black 2 = ~23^2 = 529 possibilities White 3 = 529 * 25 = 13,150 possibilities . . . In many of these possibilities, bishops & rooks are freed up seven to ten moves in, and average possibilities at a given move jump to 27 or 30, so by the time you reach the average game length of 30 moves you're looking at 2 colors * ~ 27 average moves ^ 30 gamelength = 1.75 * 10^43 possibilities to calculate. That's a really conservative estimate, and we're way beyond billions and trillions at this point. I really do need to develop a whole different method of analysis just for pawns. Their distance from the end of the board, their proximity to each other, and the type of pieces protecting & threatening them matter a lot more than the number of squares to which they can move. Not all positions or squares are of equal value by any means, and this metric does double-count squares. For example, a white knight on f3 has access to d4 in the center, and g1 way in the back. This metric regards both these options as equal, which most chess players would regard as erroneous. If there's a white rook on h1, g1 is counted twice because both the rook and the knight can move to it. If there's a white pawn on d4, the knight's access to d4 doesn't even show up on this metric, since pieces cannot move to squares occupied by their own color. On the flip side, part of the reason squares like d4 are so powerful is simply because they have access to other squares, so measuring position by counting options already places more value on central squares. On an empty board, a bishop can access 13 squares from d4, and only seven from g1. A knight can access 8 squares from d4, and only 2 from d1. Additionally, it could be argued that pieces weaken themselves by protecting other pieces. Take the aforementioned white knight on f3. Its access to the white pawn on d4 strengthens the chance that d4 will remain under white control, but if the knight's square is threatened by a pawn or bishop, d4 is not an escape route. In such a case, the weak position on g1 is more useful, simply because it is vacant. So far I've avoided a focus on piece values. They're proportional to piece mobility, but don't adjust to the complications of the game. If we look at the mobility of each piece on b3 of an empty board, it's Queen = 23, Rook = 14, Bishop = 9, Knight = 6, pawn = 1. Knights reach their most valuable point on a gridlocked board, and it reflects in their mobility stabilizing at 5-8 while other pieces get stuck. Queens are most valuable as endgame players, and it reflects in their mobility score surpassing 20 as pieces disappear. If we compare their mobility scores to their point values (Queen = 9, Rook = 5, Bishop = 3, Knight = 3, Pawn = 1), it's clear points are merely an attempt to average the mobility of pieces with no considerations of the stage of the game or the usage of each piece. I have looked up a few things about chess engines; I know many rely on internally stored master games, relying on the historical human intuition to clarify that squares like d4 are more valuable than squares like g7. Though I'm particularly interested in dissecting the theoretical reasons why such distinctions would be so relevant, I'm really interested in obtaining access to such a database, and would appreciate any materials you can reference which discuss the methodology of chess engines.

Ah yes, touche. I really should build a "basic blunder detector" that would raise a red flag in positions like move 19. This mobility score is very broad, sweeping, and abstract.

This game already happened. I'm not trying to win it or figure out how I could have won it; I'm trying to develop metrics that aid in machine learning and game theory.

Granted c5 on move 19 was a mistake; black Qd8 on move 25 would have just led to white Qxf7#, checkmating me one move faster.

I'm building a statistical package for positional analysis in R. One of the metrics that has proven useful at predicting the outcomes of my games is "piece mobility." For example, here's a chess game I lost: https://www.chess.com/echess/game?id=111224894 Here's its mobility chart: https://docs.google.com/spreadsheets/d/1xnlpOszUF9uPowNvYPSGTHx27OAYp3sT5o1vrdJPDco/edit?usp=sharing And the attached image is the game's mobility broken into types of pieces. White won the game, but first it clearly won a war of options. Its mean & median total mobility was 38.30 and 39.5 respectively, compared with black's mean & median of 30.46 and 31.00. As a disclaimer, I do not use the software package I'm writing to boost scores on chess.com. Chess is my pet project for learning data science. As Popper stated, "Science may be described as the art of systematic over-simplification." I'm just trying to simplify the game of chess. I've used this square-counting technique while playing chess, no program, just eye-balling it, and it feels pretty potent. However when I've shared it with other chess.com players, I've been told it's a truly moronic concept. I'm curious what I'm missing from chess theory, or what my critics are missing, and I'm looking for ideas for additional scalar measurements to predict or influence the outcome of a game.

Why does SFN not have forums for economics, sociology, psychology, anthropology, or other social sciences?

What's the debate topic? Are you comparing scientific theories about the origin of the universe, or is it a creationist vs. evolution argument?

The Zombie-Ant parasite doesn't infect herbivores. It's one of many species of the Ophicordyceps fungus, each of which kills an insect, grows from the insect, releases spores into the air, and kills other insects of the same species.

"And the reference intext: was it (Jones, 2006) or (Boeing Research, 2006)? Do your fellow groupmembers also interprete the apa in the same way?" It's not a matter of interpretation, and it's the name and year whether it's a book, academic article, news article, website, etc. Suppose Rodriguez, Wasserman and Kotlowitz also work for Boeing and published in 2006. Rodriguez might disagree with Jones and then you'd reference Boeing Research, 2006 disagreeing with itself. You reference an author to represent an idea, and anyone who disagrees with that idea can challenge them, so that author takes on a risk-reward relationship between embarrassment and credibility. Boeing Research might sponsor Jones' research or write his paycheck, but would not list itself as the author without putting it through some procedure defining official approval, and then the name Jones would be on a long list of names, or not even present. >>"It can be difficult to find the needed information. So who exactly wrote this nameless article on that website? Is this a co-author I should mention? In what *&^%*^%* year has this article been written?" That's probably the entire reason your professors require that format - it's probably not worth citing. Citing without an author name partially undermines the purpose of peer-review. The existence of a name for every new idea is part of how scientists get a feel for which researchers are reliably objective or sporadically brilliant. The risk of being the author to an idea is much of what makes researchers and reporters think before they publish. "So why not make things easier and turn it around: not the person who uses the source has to write down the reference in a perfect way, but the author of the source has to!" I could imagine a rule where authors listed their own articles in their "works cited" page, either as the first or last citation, or even alphabetically placed but with an asterisk or something. Citing them in other journals would require reformatting anyway though. Many Journal sites already have a "cite this text" link that opens up MLA and APA formatting for the articles, which I like as a peripheral feature. More should do that, and I expect eventually it will be standard.

Nice to meet you, Matt, I'm also new. I don't know the mechanism of how heat or light destroys a vitamin, but I have what I'd like to believe is a simple but mechanically dynamic understanding of the two forms of damage on the skin, which I hope and suspect can be applied to your understanding to derive at least a probable answer. For both heat and light, the damage to the skin is defined by A ) the intensity of the energy (as opposed to the form of energy, even though intensity on a microscopic scale is defined partially by the form of the energy inflicted), B ) the biological defense against the energy (the body sweats more readily in response to heat than to light, produces melatonin only in response to light, and the most vulnerable cells produce the most melatonin, etc...), and C ) the location of the energy (i.e., light rays have the potential to selectively damage portions of the cell, which differs from the more evenly distributed damage of heat waves). Vitamins have no biological defense (correct me if I'm wrong, but I'm fairly confident on this one), and they're not stratified enough for the energy distribution difference between light and heat to be significant (again, correct me if I'm wrong), which leads me to challenge the original premise that any difference between the damage of heat and of light exists. So, I guess our next step (unless I'm wrong or missing something) is for you to elaborate on this part right here: By the way, this is a fun topic, and I appreciate it!

I'm curious about the definition of "mindless killing machine" (I haven't seen the film in question), because the aggression of rabid animals is often both mindless and lethal.

Would it still be physiology if it could be reduced to this level of simplicity?

I certainly didn't pick up on that. His point is actually worded as a demonstration of the need for a clear differentiating factor between appropriate and inappropriate forms of parenting. Just reading the posts so far, I'd say our only differentiating factor is "sexual" versus "nonsexual," which gives every argument on this thread a sense of pointlessness, for we have yet to define our own aversion to the topic.

Lol. It's freakin' awesome that you know that.

I could see that test proving something if the body replaced cells by shedding them and re-growing them, but since they split into daughter cells for a variable number of generations, it seems the "original" cells could easily be disposed of within seven years and show no significant change in carbon-14 content. If they control for that, I'm very interested to see how they did it.

A ) I think the dog would try the water before dying (I think Maslow, at least, would agree with me here) B ) I think it'd get over its fear as soon after drinking it once or twice (I think Pavlov would agree) C ) If "reacting to reflection" is a common element only in apes and humans, I would expect them to be rather late in the evolution process. Neurologically, most of what characterizes apes and humans is found in portions of the brain that dogs don't even have. But, as has been said, guessing at evolution can be a misleading form of logic. I just Googled 'self awareness definition' it came up with "conscious knowledge of one's own character, feelings, motives, and desires." It's a flexible definition, so before we conclude it's a dumb test, does anyone have the actual paper? They might have a more specific definition. Also, I'd be curious to know whether other research papers have suggested a regional or anatomical correlation in the brain between self awareness and the mirror test.

More aptly put, "only under weak circumstances."

Haha makes three of us.

It doesn't just slowly, steadily decompress throughout the night and compress throughout the day. An instantaneous effect from just standing up versus lying down is demonstrated empirically in 5:07 to 11:14 of this video. You can read it on the transcript provided, starting with the phrase, "My grandmother used to tell me" and ending with the phrase, "otherwise, it is meaningless." http://ocw.mit.edu/c...ures/lecture-1/

Thing is.... I was taught that "secretion" is a function of stratified squamous epithelium, stratified cuboidal epithelium and stratified columnar epithelium, all of which have more than a single layer of cells. If you look at how kidneys work, you'll notice they don't shove everything through a sheet-like filter, they run it through ducts. Maybe if they had to shove it through the filter, they'd break the single layer of cuboidal epithelium that absorbs and secretes the materials they deal with. But instead they just run it through, and if they miss something, they catch it the next time it comes around. That's how and why they must work so steadily and slowly (actually there are a few dozen reasons, but that'll come together later). That's how blood vessels work too. Everything they secrete and absorb runs through mesothelium, a single layer of squamous epithelium, which sounds impossible until you consider that this single layer lines the entire surface area of the blood vessels, which, as you'll recall, has close access to every cell in the body. I think the one common element you'll find while studying simple epithelium is that it's never (okay, there's probably an exception somewhere, but it's undoubtably remote) used for secretory or absorptive tasks that require sudden results. It's too delicate. You won't find it secreting hormones or anything - it does slow, steady work, like lubricating serous membranes to reduce friction from muscle movement (in the case of mesothelium). I would also keep in mind (as immortal demonstrated) that although simple epithelium is, in itself, only a single layer of cells, there's usually several layers of something else on each side of it.

A trainer explained this to me once, but I don't know how much of his explanation was a guess. Here's the condensed version though: Working out causes swelling, which impedes blood flow. Skin contact with cold surfaces (i.e., water) decreases swelling, which increases blood flow. As mentioned, a decrease in blood flow can preserve internal body heat, which eventually becomes a priority in a cold environment. The idea is that for the few minutes they spend in the bathtub, the physiology of an intense athlete has precisely the opposite priority.

Calories from an egg (see links below): 72 Protein (6.3g x 4 Cal) = 19.2 Cal = 27% Carbohydrate (0.36g x 4 Cal) = 1.44 Cal = 2% Lipid (4.8g x 9 Cal) = 43.2 Cal = 60% Content of an egg in grams: http://www.eggnutrit...0Egg%202010.pdf Calories per gram of edible biomolecules: http://www.nutristra...on/calories.htm I'm a college student, and I do experiments like this too. This one gives you ketone breath. The problem with ketone breath is that it sneaks up on you. You feel great, you think great, you act great, you smell horrible, and you don't even know it. You don't wanna be within a mile of a date while you've got ketone breath. You get it from not getting enough carbohydrates. This doesn't threaten your survival or even give you a feeling of starvation, because your liver converts part your diet of protein and lipids to glucose. When your liver does this, the pH of your blood drops, and that's where the ketone breath comes in. Obviously, since it comes from your blood content, brushing your teeth won't fix it for more than thirty seconds. "Nutrition experts suggest dietary calories be 50 - 60% from carbohydrates, 30% or less from fats, and 12 - 15% from proteins." Tortora, Gerald J. and S.R. Grabowski. 2004. Introduction to the Human Body: the Essentials of Anatomy and Physiology. Wiley Inc., 111 River Street, Hoboken, NJ. Page 526. Oatmeal is the cheapest carbohydrates per dollar I've found. I recommend looking into it. And yes, I hung out with friends several times before my mom finally told me I had ketone breath

Relationship between insulin degrading enzyme and Alzheimer's: http://www.sciencema...5500/2302.short Lowered glucose metabolism in Alzheimer's: http://www.pnas.org/...7/11/6037.short I'm wondering whether Alzheimer's is associated with insulin deficiency, and if so, why its treatments don't include insulin injection.

I'm an undergraduate freshman at a community college. I have a recently attained fascination with the studies that pop up when I do Google Scholar searches on the vocabulary from my anatomy and physiology class.