Are there international differences on how people react when they are guilty of something?

It sounds like you're describing cultural differences in the fundamental attribution error, which, according to Wikipedia, is:

  People's tendency to place an undue emphasis on internal characteristics to explain someone else's behavior in a given situation, rather than considering external factors. It does not explain interpretations of one's own behavior, where situational factors are more easily recognized and can thus be taken into consideration.

Here's an excerpt from the cultural differences section (emphasis added):

  There are many cultural differences which arise when attempting to explain this error [(Lagdridge & Butt, 2004)]. Previous research has shown that cultural differences exist in the susceptibility of making fundamental attribution error: people from individualistic cultures are more prone to the error while people from collectivistic cultures are less prone [(Miller, 1984)].

  It has been found that there is a differential attention to social factors between independent peoples and interdependent peoples in both social and nonsocial contexts. Takahiko Masuda and his colleagues (2004) in their cartoon figure presentation experiment showed that Japanese people's judgments on the target character's facial expression are more influenced by surrounding faces than those of the Americans, whereas Masuda and Nisbett (2001) concluded from their underwater scenes animated cartoon experiment that Americans are also more likely than Japanese participants to mark references to focal objects (i.e. fish) instead of contexts (i.e. rocks and plants). These discrepancies in the salience of different factors to people from different cultures suggest that Asians tend to attribute behavior to situation while Westerners attribute the same behavior to the actor. Consistently, Morris & Peng (1994) found from their fish behavior attribution experiment that more American than Chinese participants perceive the behavior (e.g. an individual fish swimming in front of a group of fish) as internally rather than externally caused.

  One explanation for this difference in attribution lies in the way in which people of different cultural orientation perceive themselves in the environment. Particularly, Markus and Kitayama (1991) mentioned how (individualistic) Westerners tend to see themselves as independent agents and therefore focus more on individual objects rather than contextual details.

To apply this information to your specific comparison between England and Brazil, consider the following:

Brazilian culture is fairly moderate in terms of individualism vs. collectivism.

Tu, Lin, & Chang (2011) found India more individualistic, China more collectivistic, and Russia roughly equivalent to Brazilian culture in terms of individualism/collectivism.

English culture is highly individualistic (Way & Lieberman, 2010).

See the second figure depicting cultural differences in individualism/collectivism in this answer
Way and Lieberman found English culture more individualistic than Russian and Indian culture.
However, Way and Lieberman found Indian culture less individualistic than Russian culture.

Therefore the contrast between American and Chinese culture – which is a contrast between extremes of individualism and collectivism, respectively – applies to a lesser extent when contrasting England and Brazil. This contrast points in the direction your friend observed: individualistic cultures (including English) attribute successes and failures to personal factors (including effort) more often than collectivistic cultures, which tend to attribute such outcomes to situational factors (including "luck"). Brazilian culture isn't especially collectivistic, but it is probably less strongly individualistic than English culture.

It's very cool that your friend could pick up on these cultural differences in attributional tendencies among Olympics commentators! Hopefully that wasn't due to confirmation bias!

References

- Lagdridge, D., & Butt, T. (2004). The fundamental attribution error: A phenomenological critique. British Journal of Social Psychology, 43(3), 357–369.
- Markus, H. R., & Kitayama, S. (1991). Culture and the self: Implications for cognition, emotion, and motivation. Psychological Review, 98(2), 224–253. Retrieved from the International Association for Chinese Management Research.
- Masuda, T., Ellsworth, P. C., Mesquita, B., Leu, J., & van de Veerdonk, E. (2004). A face in the crowd or a crowd in the face: Japanese and American perceptions of others’ emotions. (Unpublished manuscript). Hokkaido University.
- Masuda, T., & Nisbett, R. E. (2001). Attending holistically versus analytically: Comparing the context sensitivity of Japanese and Americans. Journal of Personality and Social Psychology, 81(5), 922–934.
- Miller, J. G. (1984). Culture and the development of everyday social explanation. Journal of Personality and Social Psychology, 46(5), 961–978. Retrieved from http://www.personal.psu.edu/users/n/x/nxy906/COMPS/indivdualismandcollectivism/culture%20lit/to%20print/Miller1984culturalexplanation.pdf.
- Morris, M. W., & Peng, K. (1994). Culture and cause: American and Chinese attributions for social and physical events. Journal of Personality and Social psychology, 67(6), 949–971. Retrieved from http://www.southalabama.edu/psychology/gordon/EmotionCulture%281994%29MorrisPeng.pdf.
- Tu, Y. T., Lin, S. Y., & Chang, Y. Y. (2011). A cross-cultural comparison by individualism/collectivism among Brazil, Russia, India and China. International Business Research, 4(2), 175–182. Retrieved from http://www.ccsenet.org/journal/index.php/ibr/article/viewFile/10019/7136.
- Way, B. M., & Lieberman, M. D. (2010). Is there a genetic contribution to cultural differences? Collectivism, individualism and genetic markers of social sensitivity. Social Cognitive and Affective Neuroscience, 5(2–3), 203–211. Retrieved from http://www.replicatedtypo.com/science/genetic-components-and-cultural-differences-the-social-sensitivity-hypothesis/1620/.


It is not. At least not always: In this famous experiment Tulving and Thomson show that under certain circumstances recall can be better than recognition.

It seems that the reason why recognition is usually more accurate than recall, is the context. Usually, the context in the recognition test is very similar to the conditions in the learning phase - the subject sees a list of words. In the free recall test, the context is different - the subject is not given any external stimulus.

Tulving and Thomson changed that in their experiment: the context of learning was more similar to the recall test, which resulted in higher performance in the recall.

This indicates that the encoding in memory has some context specificity. Items that were encoded using a visual stimulus will be easier to recognize or recall if the same or similar stimulus is presented during the test.

Note: I interpreted the word 'easier' in the question as 'more accurate' because typically accuracy is measured, and not the 'ease' of the recall/recognition, which could be defined in many different ways.

  Tulving, E., & Thomson, D. M. (1973). Encoding specificity and retrieval processes in episodic memory. Psychological review, 80(5), 352-373. PDF


Is there evidence or indication that highly sensitive people (HSP) can feel elektromagnetic waves?

As of 2009 apparently not.

In Rubin's 2009 paper, he looked at studies analyzing symptoms and investigating triggers in more than 1,000 people who reported having electromagnetic hypersensitivity.
He concluded in the paper that "repeated experiments have been unable to replicate this phenomenon under controlled conditions."
It may be that Wi-Fi isn't the culprit, but that something else is to blame for people's symptoms, Rubin said. A number of health and environmental conditions, different for each individual, could be responsible.
Another factor at play could be the "nocebo effect," in which a person's belief that exposure to EMF triggers symptoms actually causes the real symptoms to appear, even if no exposure occur has occurred, he added.
Regardless of whether Wi-Fi "allergies" are real, the suffering certainly is, Rubin said.

And I think I tracked down the actual paper that is talking about; it's been reasonably summarized by the press.
I honestly expected researchers to stop bothering after that, but I found some 2017 experiments, which were also negative:

In the double-blind trials, no significant difference in symptom severity or exposure detection was found for any of the participants between the two conditions. Belief of exposure strongly predicted symptom severity score for all participants.

In the latter experiments, they really went out of their way to remove possible non-response causes, including testing people in their usual places where they reported the problems (using portable equipment), taking into account the history of their complaints, i.e. using equipment that was as close as possible to the sources the subjects claimed to be sensitive to, counterbalancing for time of day and time on task etc.


What kinds of information can (and cannot) be extracted from connectome?

First at all, the connectome must be interpreted like a static picture of the brain. So anything related with plasticity and dynamical processes will be lost in this map. There are connectome at macroscopic areas using fNMR but I'm going to focus in the cellular level.

We can define three types:

Dense Connectome - It is the classical idea of connectome that consist in mapping all the neuronal connections of the whole nervous system or a part of it.
Functional Connectome - It is focus only in the connections that play any role in a process (i.e. perception of a color, motor action,...)
Saturated Connectome - It is the most wide definition. It is the mappping of all the cells and organelles in the nervous system.

Before answer your questions I need to advise that all of this is limited by the technology. The most extended technique is the electron microscopy (EM) because we obtain a nice resolution for mapping, the problem is that is very hard automatize the annotation step (Characterize different cells and processes). The last year a new technique was released called Clarity this can be used in the connectome but it's too early to see results. In response to your questions:

Yes, with techniques like Clarity we can use markers for the different neurotransmitters. I'm not completely sure if we can characterize the vesicle type with EM, but we can define the pre and post synapses and know the strength (via the amount of vesicles).
Do you mean the amount of ions in the synaptic terminal and in the extracellular space? I think that it could be realize with markers but it is out of the connectome purpose. (Maybe in the Saturated connectome)
Yes. (Answer 1)

In my opinion the most interesting part of the connectome is the mathematical analysis of the network topology.

Check the authors bibliography in the 3 connectome kinds for more info.


Can a biological entity be thought as a simple algorithm? Case-study with the concept of randomness

Yes, you can think of biological entities as algorithms, but that doesn't give you any explanatory power.

Unfortunately, most people have little to no understanding of algorithms, and how little actually constraint is imposed on something when you say it is "algorithmic". In particular, there is no restrictions on algorithms that require them to be deterministic. When theoretical computer scientists talk about pseudorandom number generators, they are talking at a much higher level of rigour than any biologist, psychologist, or neurologist ever uses. From their point of view, unless the biological entities you are thinking about are trying to defeat each other's cryptosystems, all random or stochastic events in biology can be viewed as pseudorandom with absolutely no consequence for biological theory. In fact, Keegan's answer that we can think of stochastic events as deterministic events with a mechanism that is outside of our model scope would be equivalent to the worry of pseudorandom versus true-random numbers.

Even if you subscribe to the (silly) Penrose-Hameroff stance that quantum effects in microtubles have a macroscopic effect at the level of consciousness that leads to "true randomness" then that still wouldn't place you outside of algorithmic thinking. You would just have to think in terms of quantum algorithms, which is more difficult mathematically, but a well studied field of computer science. Finally, cstheory extends the notion of algorithms beyond the typical confines of randomness as studied by statistics and most scientists, and looks at rigorous models of non-determinism.

In fact, there are people (for example, I advocate algorithmic philosophy as an extension of standard analytic philosophy) that believe that any communicable theory is inherently algorithmic and ammendable to analysis of cstheorists. Hence, not thinking of something as algorithmic would be impossible.

That being said, is that useful? In general, no. Algorithms are incredibly difficult to study. In the case of the computing machines, we make it easier by separating the algorithm underlying the physics of the hardware from an abstraction that we call the software. This often leads non-cstheorists (as you can see in Keagan's answer) to thinking that the idea of algorithms applies only at this "software abstraction" level. Of course, this is not the case. However, this distinction can be a useful metaphor at times, and much of cognitive science is based on the idea that the mind is software that is at least in principle capable of being implemented by different hardware. This is the philosophical stance of multiple realizability.

Neuroscientists hold this stance much less often, and - as suggested in Keagan's answer - view the mind and brain as non-seperable and best analyzed at the same level. This does not make the process non-algorithmic, it just takes away any handles we have at easily isolating properties of this algorithm.

If we continue this idea further, and just consider an algorithmic black box then we return to the ideas of behaviorism that are now considered passe in the cognitive sciences, but still popular in many parts of biology. In this setting, the black-box algorithm is a correct but completely useless notion. We have mathematical theorems that tell us that if we try to treat algorithms at this level of abstraction then we can never (in general) conclude anything. In this case, we have to be more restrictive than just "algorithmic" or "computable". This can get us to fun cstheory questions like "What is the complexity class most closely associated with what the human mind can accomplish quickly?"


Are there professional cognitive science test subjects?

There are a few people who have been very extensively experimented on because they have unusual brain lesions (which is kind of like the opposite of a skill). The most famous is Henry Molaison (HM), who developed a rare case of episodic anterograde amnesia following surgery for severe epilepsy. He spent the entire latter part of his life in a care institute and was a continuous subject of various learning experiments and imaging studies. Another patient with very specific memory-related lesions is KC, who has been the subject of at least 20 case studies.

A couple of other studies that might be of interest are West et al. (2008), who recruited experienced video game players in order to find people with strong skills at rapid visual scanning, and research by Eleanor Maguire and colleagues that examined structural changes in the brains of new London taxi drivers as they acquired their fantastically detailed spatial map of the city's streets.

  West, G. L., Stevens, S. A., Pun, C., & Pratt, J. (2008). Visuospatial
  experience modulates attentional capture: Evidence from action video
  game players. Journal of Vision, 8(16).

  Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D.,
  Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000).
  Navigation-related structural change in the hippocampi of taxi
  drivers. Proceedings of the National Academy of Sciences, 97(8),
  4398-4403.


Relationship between oculometry/pupillometry and disorders of consciousness

I have listed several articles below for your reference:

(Search terms: "oculometry pupillometry disorders of consciousness" in Google Scholar, nothing special):

Grandchamp et al, 2014, DOI: 10.3389/fpsyg.2014.00031 - A primary research article related to consciousness (mind wandering) where the authors investigated various pupillometric responses, among other measures. Good journal.

(Search terms: "pupillometry consciousness" in Google scholar):

Laeng et al., 2012, DOI 10.1177/1745691611427305 - Nice looking review on pupillometry and consciousness that should be a good source of additional references;

Smallwood et al., 2011, DOI: 10.1371/journal.pone.0018298 - A primary research article on attention and perception in Plos One. It is open source, but not my favorite journal


Does having wrong answers available while studying distract the mind from the correct answer?

Which is the best way to learn the correct answer?

There is no correct or best way to learn if phrased that way, let me elaborate:

In the first case you are really learning 2 things:

A series of statements : a),b),c), d).
4 relationships : a)= false, b) = false, c) = true , d) = false.

In the second case you are only learning a single relationship:

statement X ( c in the previous case) = true

This might sound counter intuitive, but the first case will prepare you better (even though it takes longer to practice), Why ? Because it simply matches better the recall task,which can be read as: out of this 4 cases which 3 are false and which one is true. ( a discriminating strategy can even be formulated by grouping the wrong ones via some similarity)

The opposite learning strategy is expected to fare poorly since instead of being helpful, the additional wrong choices work as recall distracters, they will each elicit the same response ( technically the correct one will also have an extra priming effect, but in order to outweigh the distracters, it would need to be consolidated over time), that is you would be expected to write it down word by word.

So your choice comes down to either learn to discriminate or learn to recall perfectly, in general we fare poorly on the second task for short to medium term memories and only after repeated (or emotional) and complementary exposure can we master perfect recall ( mnemonic devices can also be used).

Sources:

The Oxford Handbook of Memory(Tulving,Craik) (expertise, familiarity, distracters,etc,etc)
Cognitive Science (Gazzaniga) General discrimination in memory.


Do characters in a dream have their own separate thoughts or identity?

EDIT:  To address the changed question:

Similar to how mental visualization stimulates the same neurons/blood flow that actually seeing something does, I suspect that brain scans will show similar processing occuring during the dream interaction as occur during real interactions.

The difference is that the brain is creating the entire subjective experience.

The crazy thought is that there isn't a difference though: subjective experience is ALWAYS completely constructed by the brain, though it's constructed through nerve impulses from external inputs such as electromagnetic waves (sight) or physical waves (sound).  During sleep, the body is paralyzed to prevent us from acting out our dreams (which WILL happen if the paralysis is lifted), which implies that sensory data is still coming in (or being generated) and we are simply mis-perceiving it and then trying to catch up.

This was my answer to @alan2here's original question.  It mostly still applies, though is also a mixture of philosophy, psychology, and cognitive neurophilosophy (EDIT: i.e. uncited, lol)
Take this as you will:

First off, this is definitely a philosophy question, but I'll try to stay within the bounds of Cog Sci. No promises though...

From my understanding, the mind does not create consciousness. While this is a very thorny issue, and one I'm not super familiar with, I believe a generally accepted view is that consciousness is a (by-)product of the sheer complexity of the human brain coupled with governing systems and feedback loops (and a hell of a lot more of course!).

Furthermore, the perceived barrier between the self and separate beings is just that: perception. Differences in physical properties aside, there are no real barriers between anything. Air is just as much a molecule as plastic, and behaves in a remarkably similar manner. The difference is semantics (not unimportant to subjective beings, but objectively the difference is inconsequential). We just can't see it, and we're conditioned to ignore it, so we see a vast gulf of nothingness where there is actually incredible hidden complexity. Also, the notion of self is a misguided one that we're given through culture. As many Eastern philosophies will tell you, the self is a lie! (just like cake).

To address the actualy question though (kinda), I think you unintentionally answered it yourself with this phrase: sentient seeming entities. The 'people' in your dreams are amalgamations of 'people'-like semantic attributes your brain has constructed from your experiences. These seem like real people and can act like real people, but that's because you've met and experienced real people. If you have never met real people, it's very doubtful that any people-like dream constructs will be created (unless generated from mirror reflections).

Lastly, I have to add this caveat: dreams and dream science is still an incredibly unexplored black box. We still don't have a clear idea about why dreams occur and until then, this question is literally unanswerable. In fact, everything I've said may turn out to be false, but we don't really know. That's why this falls under philosophy.

However, I'll leave you with this: assuming that the human mind is an individual entity (and cannot connect with other people through undiscovered mental (physical, likely subatomic and certain microscopic) means), then the people in your dreams do not exist anywhere else nor to anyone else. Therefore: does it matter? It's a completely subjective experience, so only you can decide how to perceive it.


Sense of time: Evaluation and correlation with psychological traits and states

People who are entitled tend to have a slower perception of time. In any given situation, a person can feel some level of entitlement. If a person is waiting in line for 10 minutes to check out groceries, he would experience that 10 minutes as passing by very slowly. On the other hand, if that same person was waiting 10 minutes to meet the President, he would experience the 10 minutes as passing by quickly.

So time perception can be manipulated in any given situation. It depends on the level of entitlement you are feeling in that environment. Perhaps entitlement could artificially be manipulated to create different perceptions of time (e.g. by thinking quickly and variably).

Source

Time Crawls When You're Not Having Fun: Feeling Entitled Makes Dull Tasks Drag On. Edward H. O'Brien, Phyllis A. Anastasio and Brad J. Bushman, Pers Soc Psychol Bull published online 12 May 2011, DOI: 10.1177/0146167211408922


Steven J. Luck's "An Introduction to the Event-Related Potential Technique" is a great beginner's book on EEG. It's basic but not too simple, and it goes into the structure of the signals as well as into issues on experimental design.


Is it common for OCD sufferers to experience schizophrenic episodes

As someone who has had OCD since the age of 12, I can assure that this sounds very much like an OCD symptom. It is likely that you walked into the store "like a zombie", and at the time, did not consider your personal appearance, assuming only that the store owner was acting strange. However, if you had been aware of the way you were acting, you would have likely picked up on this instantly and dismissed it. Unless we are salient to our own features, we are unaware of how others are perceiving us. Your ability to gauge your salience was likely decreased due to just waking up from your nap.

As an OCD sufferer, I've definitely had bouts where I was concerned I was developing schizophrenia, only to realize later that I was hyper-aware of every little "sign" that pointed in that direction. If this is an ongoing worry of yours, confirmation bias will likely amplify the most ambiguous of symptoms related to losing your mind.

Let's get a little further into schizophrenia, however. The Diagnostic and Statistical Manual - IV (yes, the old one, though the symptoms have not changed much) states:

  Characteristic symptoms:

  Two or more of the following, each present for much of the time during a one->month period (or less, if symptoms remitted with treatment).

  Delusions
  Hallucinations
  Disorganized speech, which is a manifestation of formal thought disorder
  Grossly disorganized behavior (e.g. dressing inappropriately, crying
  frequently) or catatonic behavior

  Negative symptoms:

  Blunted affect (lack or decline in emotional response)
  Alogia (lack or decline in speech)
  Avolition (lack or decline in motivation)
  Imapaired communication (due to hearing voices)
  Social or occupational dysfunction: one or more major areas of functioning, work, interpersonal relations, self-care, are markedly below the level achieved prior to the onset.

  Significant duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if symptoms remitted with treatment).

  If signs of disturbance are present for more than a month but less than six months, the diagnosis of schizophreniform disorder is applied. Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, and various conditions may be classed as psychotic disorder not otherwise specified.

First and foremost hallucinations and delusions are NOT something that you are able to identify. Schizophrenia leaves the sufferer out of touch with reality. The sufferer believes in their hallucinations and delusions with every fibre of their body, they don't simply think that they are hallucination or becoming deluded. That being said, no, you are not developing schizophrenia. If you were, you wouldn't know it, and once you found out that you had it, you'd be the last one to know.

Note "positive" and "negative" symptoms, are not "good" and "bad". Think of a positive symptom as an addition to one's life (the addition of delusions), and a negative symptom as something that's being taken away from one's life (motivation). If you read further down the DSM criteria, you will see that "one-off" events like this do not substantiate a diagnosis of schizophrenia. However, a brief psychotic episode is still possible, possible, but extremely highly unlikely based on the fact that you have a great amount of insight (self-knowledge) of what was going on with you in the store.


Is there evidence that "people in Eastern societies are more in touch with their communities while Western societies value uniqueness more"?

While I can't, and won't make any comment on the accusations of racism (I think the comments below your question answer that quite well), the Western/Analytic vs. Eastern/Holistic dichotomy is pretty well established and supported by studies in cognitive and social psychological literatures.
This may be a little different to what you had in mind, as your question is more about social notions like 'valuing independence' versus 'coexisting in harmony', which are harder to empirically demonstrate (I'm not a social psychologist).  What I'm referring to here is more like 'logic, rules, and working details out step by step' versus 'taking everything into account, and seeing the bigger picture'.
However, the idea is a bit more complicated than what I'm able to explain in a few sentences.  Nisbett et al's (2001) review (free preprint copy here) is the Rolls-Royce of reviews when it comes to this, and that paper will address most of the questions you might have (note the racial diversity of the authors).
You can also find more work by the same authors here.
References
(just the one)
Nisbett, R. E., Peng, K., Choi, I., & Norenzayan, A. (2001). Culture and systems of thought: holistic versus analytic cognition. Psychological review, 108(2), 291.


Why do people blame others rather than take responsibility?

The Abilene Paradox is one of the situations in which individuals may blame others for their actions because that is how they perceived the situation. Consider this anecdote (video):

On a hot afternoon visiting in Coleman, Texas, the family is
comfortably playing dominoes on a porch, until the father-in-law
suggests that they take a trip to Abilene [53 miles north] for dinner.
The wife says, "Sounds like a great idea." The husband, despite having
reservations because the drive is long and hot, thinks that his
preferences must be out-of-step with the group and says, "Sounds good
to me. I just hope your mother wants to go." The mother-in-law then
says, "Of course I want to go. I haven't been to Abilene in a long
time." The drive is hot, dusty, and long. When they arrive at the
cafeteria, the food is as bad as the drive.
They arrive back home four hours later, exhausted. One of them dishonestly says, "It was a great
trip, wasn't it?" The mother-in-law says that, actually, she would
rather have stayed home, but went along since the other three were so
enthusiastic. The husband says, "I wasn't delighted to be doing what
we were doing. I only went to satisfy the rest of you." The wife says,
"I just went along to keep you happy. I would have had to be crazy to
want to go out in the heat like that." The father-in-law then says
that he only suggested it because he thought the others might be
bored. The group sits back, perplexed that they together decided to
take a trip which none of them wanted. They each would have preferred
to sit comfortably, but did not admit to it when they still had time
to enjoy the afternoon.

Nobody wanted to go, yet the group decision was contrary to everyone's personal opinion since every individual perceived that another individual had taken a decision, arguing against which would simply result in discord.
When the decision turns out to be bad, then everybody simply states what they initially believed which was that another individual of the group had clearly wanted to go, and they had simply consented to the decision. This of course, is one scenario, in which individuals may blame another (specific) person for a group decision.
The benefits of this can be explained in many ways. One of the ways to analyze the benefit is by using cognitive dissonance theory. In simple terms, when our behavior (or thinking) does not match up with our belief, it results in mental stress due to the incongruity of the situation. To counter or save ourselves from that incongruity, we either adjust our belief or alter our behavior(thinking). In this case, the act of taking the trip was against our belief, and hence taking responsibility (agreeing that the decision was yours) for the action would be incongruous. Therefore, we blame another individual for the group decision, as that is easier to process (congruent) and less mentally stressful.


Are any kinds of behavior proved to correlate with testosterone levels?

"There was a significantly higher level of plasma testosterone in the
  aggressive group as compared with the nonaggressive group or with the
  other two groups combined. The socially dominant group also had a
  significantly higher level of testosterone than the nonaggressive
  group."
  http://journals.lww.com/psychosomaticmedicine/Abstract/1974/11000/Plasma_Testosterone__Correlation_with_Aggressive.2.aspx

-

  "Analysis of archival data from 4,462 U.S. military veterans supported
  the first hypothesis: Testosterone was correlated with a variety of
  antisocial behaviors among all individuals."
  http://pss.sagepub.com/content/1/3/209.short

-

  "Plasma testosterone levels did not differ in fighting and nonfighting
  individuals. Although there were significant correlations between
  psychologic tests, the test scales did not correlate either with
  plasma testosterone or with fighting behavior. The 10 prisoners with
  histories of more violent and aggressive crimes in adolescence had a
  significantly higher level of testosterone than the 11 prisoners
  without such a history. An hypothesis is presented that within a
  population that is predisposed by virtue of social factors to develop
  antisocial behaviors, levels of testosterone may be an important
  additional factor in placing individuals at risk to commit more
  aggressive crimes in adolescence."
  http://journals.lww.com/psychosomaticmedicine/Abstract/1972/07000/Assessment_of_Aggressive_Behavior_and_Plasma.6.aspx

-

  "Statistically significant changes in MMPI–2 scale scores were found
  at 3-month follow-up after initiating testosterone treatment relative
  to baseline for transgender men compared with female controls (female
  template): reductions in Hypochondria (p < .05), Depression (p < .05),
  Hysteria (p < .05), and Paranoia (p < .01); and increases in
  Masculinity–Femininity scores (p < .01)."
  http://psycnet.apa.org/psycinfo/2014-32641-001/

-

  Baron-Cohen and his colleagues recently found that giving testosterone
  to women decreases their ability to empathize, particularly among
  women whose bodies show evidence that they were exposed to higher
  levels of testosterone in utero. And previous research has linked high
  levels of testosterone in the womb to autistic traits. (Interestingly,
  in-utero exposure to testosterone can be estimated by looking at the
  ratio between the length of the ring finger and index finger.)
  http://healthland.time.com/2011/05/18/study-why-some-transgendered-people-have-higher-levels-of-autistic-traits/

-

Contrary to what many believe:

  No direct associations were found between testosterone and solitary or
  dyadic sexual desire.
  http://www.eje-online.org/content/165/2/331.full.pdf

Some transgender people say they have changes parts of their personality, but I've found no studies to prove this.

  "Chris Edwards, a trans advertising executive, says that
  post-transition, he was given greater levels of responsibility—but he
  thinks it’s because the testosterone he took changed his behavior. He
  became less timid and more outspoken—and was seen, at work, as more of
  a leader. Indeed, some suggest that transmen might experience these
  workplace benefits partly because, post-transition, they are happier
  and more comfortable, and that this confidence leads to greater
  workplace success. But if that’s the case, one would expect that
  transwomen, armed with this same newfound confidence, would see
  benefits. The opposite seems to be true. "
  http://www.newrepublic.com/article/119239/transgender-people-can-explain-why-women-dont-advance-work

-

  "Now that we’re roughly two years into the process there has been a
  dramatic change in personality. This was expected, I knew there would
  be highs and lows because the process takes a huge toll. However now
  she just treats everyone like garbage. The whole world absolutely has
  to revolve around her. No one can be right unless it happens to be
  from her prospective. She exemplifies all of the negative stereotypes
  of both transgender people and women. The personality change went from
  laid back punk rocker to being what I can only sum up as a stuck up
  diva."
  https://answers.yahoo.com/question/index?qid=20100430043917AAYcyD8

Note that stories like the one above may have several possible causes, including identity changes (suddenly seeing oneself as a different gender), depression (generally bad mood) or placebo.


Which human instincts do gamification systems appeal to?

In general, I believe gamification taps into 2 main human behaviours. Competition & Pride (in that order)

Competition should drive more engagement and Pride should help breed loyalty (b/c their stature is linked on your projects stature)

1. Competition

contests (top editor of week)
leaderboards
featured users

2. Pride

badges
achievements
unlocked features

Various systems balance these differently, and of course it's also very subjective but I believe that when people first sign up, it's about competition, and after they compete (and win trophies) it's about Pride.

Update: OCT-25-2013

The above 2 drivers really refer to those users who indeed buy-in and engage with your gamifications - But if you run a public website where buy-in rate could be considerably low you may have many users simply exploring. Below are some considerations to keep these users involved in your gamifications and hopefully convert them to competitive patrons.

3. Exploration (Look Before Leap Users)

public profiles (customizations, badges)
public leaderboards
faq / knowledge-base for details on rewards


So why might people post seemingly excessive concerns regarding the danger in their neighbourhood?

@what has a great point in wanting to know the the social context. Sounds to me simply like fear, but to know the origin of the fear we need more context. A lot more.

My hypothesis is that something is giving the perception of danger to some people, either real or perceived, and they spread the mentality; some are more susceptible to it than others.

It can also be an effort to try to keep people away, like not wanting new people moving in. In a xenophobia (also a flavor of fear) fashion:

  An excessive and irrational fear of anything foreign. This fear is most often of foreign people, places or objects. People who are xenophobic may display fear or even anger toward others who are foreign.

Knowing how these people got this perception of fear is the blurry part. In a very safe neighborhood, these claims sound slightly paranoid. People can mix some story told from family or friends, plus some media, add a bit of cultural backing, mix up with a particularly fearful personality and bang, chaos ensured.

Given an incomplete scenario, like the tales above, our cognitive bias will fill out some details which we are missing, or we have trouble understanding, and we might have bad tendencies in what to fill. Negativity bias is a good example:

  The negativity bias refers to the notion that, even when of equal intensity, things of a more negative nature (e.g. unpleasant thoughts, emotions, or social interactions; harmful/traumatic events) have a greater effect on one's psychological state and processes than do neutral or positive things.

Suppose a crime happened in our very peaceful neighborhood some time ago. Not everyone is used to it. It is new, dangerous and provides a feeling of unsafeness:

I'm vulnerable at home
It represents danger to my possessions
It represents danger to my family
There will be invasions to the safeness of my property.
I don't know what it will bring, but it won't be good

This is an article from UK, but features some context-agnostic points when it comes to the fear of crimes:

  Many crimes have emotional effects on
  victims that include upset, fear and anger. They can also result in psychological
  problems where the crime involves the victim coming face to face with the
  offender, particularly when violence or the threat of violence occurs

  ...

  Robbery and its effects on victims may also
  affect the feelings and behaviour of non-victims, some of whom may be able to
  appreciate its effects at first hand.

  ...

  Street robbery is predominantly an urban phenomenon, with most robberies
  taking place in streets near the victims' home and close to transport access points
  (Barker et al., 1993; Mirlees-Black et al., 1996). Though not a seasonal crime,
  more attacks occur when it is dark, with violence used in approximately 44% of
  incidents (Barker et al., 1993) and weapons involved in about a third (Mayhew
  et al., 1992). Young people represent a substantial proportion of the victims of
  street robbery (e.g. Barker et al., 1993) and, though only slightly, males are more
  at risk (Mayhew et al., 1992)

This article, also from the UK, presents studies on risk perception in the fear of crime:

  Instead perhaps
  the strongest evidence relates to
  the importance of public concerns about neighbourhood disorder,
  social cohesion and collective efficacy (Ferra
  ro, 1995; Perkins & Taylor, 1996; Jackson, 2004;
  Wyant, 2008). The idea here is that the incidenc
  e and risk of crime has become coupled in the
  public mind with issues of social stability, mo
  ral consensus and the colle
  ctive informal control
  processes which underpin neighbourhood order (Ba
  nnister, 1993; Walklate, 1998; Girling, Loader,
  & Sparks, 2000; Jackson, 2006).

Forgive the below-average english.


Does a short nap improve learning efficiency?

Naps may help if you are so sleepy that you can't focus in learning/training anymore. More importantly however, even a short sleep gives start for the memory consolidation process. So all the things you learned before the nap, get better shielded against the new conflicting or overlapping information in future. Especially in procedural learning (e.g. fingers on guitar chords), which is slow, gets important boost by a training -> consolidation -> training -> consolidation loop. Deep sleep (slow wave sleep at night) is more important, but already nap with light sleep phases (state II with k-complexes) will help.

You can search research papers for "memory consolidation" and "sleep".


How does emotional pain cause as much suffering as physical pain?

Some research that I have dug up:

According to the article "Emotional and Physical Pain Activate Similar Brain Regions" (Fogel, 2012), the anterior insula and the anterior cingulate cortex are activated for both physical and emotional pain.  Also, physical pain can lead to emotional pain as it would in the reverse direction (emotional --> physical).

This conclusion is further discussed in the articles "Does Rejection Hurt? An fMRI
Study of Social Exclusion" (Eisenberger et al. 2007) and "Social rejection shares somatosensory representations with physical pain" (Kross et al. 2011). Even though both articles use the insidious form of bullying: social exclusion as an example, the same conclusion could be reached for proportionally greater pain of both types.

What I alluded to in my comment is true, I have fallen from a decent height, both emotionally and physically in 2 separate incidences - reflecting on what I remember of the pain I felt when I landed, it was about the same.


Why do people feel the need to make changes to a solution presented by another person?

This sounds to me very much (but not exactly) like a phenomenon Dan Ariely has done some research on, which he terms 'the IKEA effect'.
Of course, he will describe it better than me, specifically in Norton and Ariely (2012), Ariely et al (2008), and this TED talk.

Basically, what he's found is that people value things (furniture, lego models, plans) more when they themselves have contributed their own labour in creating them.

In Ariely et al (2008), they found that:

People are more willing to do dull, monotonous paperwork for less money if their name goes on the top of the sheet, and less willing if the paper was shredded after they had finished.
The same effect is found if you pay people to put together Lego models: people do more for less money if you don't take apart the models afterwards.

Norton and Ariely (2012) took a different approach, but showed largely the same thing:

People believe that the IKEA furniture which they themselves assembled was worth more than anyone else's furniture (measured by how much they would pay to keep it)
The same effect was found for origami animals.
..and for Lego models, but not if you take the model apart after you build it (because it's no longer the thing which you created).
...and not getting to finish assembling the furniture reduces this bias.

Hopefully, the link between this research and your question should be clear: by making changes to a solution, that solution becomes in some way 'ours', and because of that, we overestimate it's intrinsic value.

References

Michael I. Norton, Dan Ariely, and Daniel Mochon (2012), “The IKEA effect: When labor leads to love.” Journal of Consumer Psychology. Vol. 22: 453-460.

Dan Ariely, Emir Kamenica and Drazen Prelec (2008), “Man’s Search for Meaning: The Case of Legos.” Journal of Economic Behavior and Organization. Vol. 67: 671-677.


Why do very different people attract each other?

Concepts like love and attraction are not only poorly defined, but in this context are too complex to discuss meaningfully, if a scientific answer is what you are after. It is also hard to quantify 'different' when it comes to people - there are just too many variables to compare.

But, there is actually some principles and models that could be part of a more complete answer.

Total Free Energy

Both the TOTAL1 model (an extension of the famous TOTE2 model), or the free energy principle3, assert the following:

  Us humans constantly form predictions that serve as expected state, and then compare them to the actual state of the world/body (via senses).

This applies to both micro levels (say, communication between neuron layers) and micro level (consciousness).

It then goes:

  When the predicted state matches the actual state, nothing to do. When there is incongruity, we must either change our predications (models/goals) or the world (by acting).

In this view, the brain is largely a differential processor - rather than processing stimuli all the way bottom-up, it generates top-down predictions and only left with validating them against stimuli.

This is a hugely efficient optimisation strategy for the sake of metabolic economy.

It also goes to explain:

Why we stop perceiving mechanical clocks after spending some time in a room.
Why new objects (shoes, houses) excite when new but hence after peter out.
Why relationships tend to cool-off over time (and in turn why some people cheat on their partner).

In extremely general terms - that that doesn't change doesn't excite.

Now back to Friston:

  For survival sake, all living things strive to minimise surprises by forming and updating a model of their environment.

Things get interesting when survival is no longer a concern...

Diversity

Taking into account the said above, picking someone who's different from you in many aspects means your mental models are challenged more often, which could yield excitement.

I think a good example is dating someone of different nationality, say a Westerner dating an Easterner. Differences can go both way (good and bad), but it is exciting nevertheless.

1 Wang, C. and Mukhopadhyay, A., 2012. The Dynamics of Goal Revision: A Cybernetic Multiperiod Test- Operate-Test-Adjust-Loop (TOTAL) Model of Self-Regulation. Journal of Consumer Research, 38(5), pp. 815-832.

2 Miller, G.A., Galanter, E. and Pribram, K.H., 1986. Plans and the Structure of Behavior. Adams Bannister Cox.

3 Friston, K., 2010. The free-energy principle: a unified brain theory?. Nature reviews neuroscience, 11(2), p.127.


Measuring postsynaptic potential vs action potential at axon hillock?

Measuring voltage at a synapse gives you a measure of the input to a cell.
Measuring voltage at the axon hillock (for a typical neuron, practically the soma can substitute as well) gives you a measure of the output of a cell: how near it is to threshold and/or if it has reached threshold and produced a spike.
Measuring voltage at intermediate sites in the dendritic tree can be a measure of spatial integration, which can be quite complex.
All of these measuring sites can be of interest, though there is a lot of variance in how difficult each will be.


What are the observable differences between "pure" antisocial personality disorder and psychopathy?

Antisocial personality disorder (APD) and psychopathy are not distinct entities, but highly overlapping constructs. APD is the diagnosis currently supported by the latest iterations of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), and psychopathy is rarely used in clinical contexts today, though the terms are often used interchangeably.
The criteria of APD are centered around antisocial behaviors such as norm violating behavior, impulsivity, aggressiveness, and a lack of remorse. Psychopathy lacks a specific set of criteria, but for instance the often used Hare Psychopathy Checklist (PCL-R)include aspects such as impulsivity, aggressivity, and a greater focus than APD on the lack of empathy and Machiavellianism, that is manipulativeness and callousness.


The Hodgkin and Huxley model of neuronal firing is based on non-linear differential equations. A significant portion of research on sensation and perception is based on such models.


How do we know bipolar is one illness rather than two comorbid illnesses?

Short answer: Bipolar disorder is probably not composed of two comorbid illnesses, but it may be on a continuum that includes some depressive disorders.

This is a good question, though it does convey some confusion associated with this diagnosis that should be cleared up.

Bipolar symptoms:

The first confusion I think is the idea that "depression", "mania", and "bipolar" are disorders.  Depression and mania are not disorders - they are symptoms.  And bipolar is a "spectrum" disorder - a collection or continuum of similar diagnoses, that all feature at least one manic or hypomanic episode, and in most cases at least one depressive episode.

It is true that depression without mania is one of the key symptoms of a variety of depressive mood disorders (such as major depressive disorder, sometimes referred to as "unipolar" because of the lack of manic episodes), so it may be confused with a disorder.  However, this is not the case for mania, so diagnostically bipolar disorder would not be confused with a comorbidity of 2 disorders - depression and mania - because mania is not a disorder.

Mania rarely presents without other symptoms:

  Although bipolar disorder is by far the most common cause of mania, it
  is a key component of other psychiatric conditions (e.g.,
  schizoaffective disorder, bipolar type; cyclothymia) and may occur
  secondary to neurologic or general medical conditions, or as a result
  of substance abuse.

Presumably, a standalone manic episode may be sufficient for a diagnosis of bipolar I disorder or a "not otherwise specified" (NOS) diagnosis, depending on the severity and other symptoms involved.  So diagnostically, "mania" as a standalone disorder is actually a sub-type of bipolar.

Bipolar unitarity:

The second confusion I think is the idea that a bipolar diagnosis in some way precludes the symptoms of depression and mania from having separate causes.

Historically, bipolar disorder was not seen as 2 separate illnesses because (1) it was believed that mania and depression were mutually exclusive in time - as 2 extremes (poles) of a single mood continuum, and (2) mania rarely presents without depression.  The assumption of mutual exclusivity of mania and depression was called into question by the occurrence of mixed-state episodes - a condition that features symptoms of both mania and depression simultaneously.

Ultimately, many psychiatric diagnostic criteria are encumbered by some historical precedence, common clinical presentations, how patients perceive their symptoms, and also some political influence, as diagnoses are associated with healthcare subsidization, stigma and prejudice, and explanatory power for the patient.  So diagnostic criteria should not generally be confused with an understanding of common cause.

The cause of bipolar spectrum disorders is not well understood, and the question of whether unipolar and bipolar disorders are distinct, or part of a single continuum, remains a hotly debated topic.  The very common co-occurrence of depressive episodes whenever manic episodes are present suggests that they may be related in some way.  On the other hand, depression disorders and bipolar disorders are treated with different medications, suggesting that they may be distinct disorders - depression is typically treated with anti-depressants, while bipolar depression may be more effectively treated with mood stabilizers.  The disorders have some predictors (genetic, environmental, comorbidities) in common, and some different.  It's also entirely possible that both disorders incorrectly encompass several unrelated sub-types.


The relationship between semantic memory and concepts/procedures

You are right, procedural memory is defined as implicit. Semantic memory on the other hand is part of explicit memory. It includes declarative knowlegde (knowledge of facts or ideas) that can be made conscious. As far as I know there is no particular relationship between the two but they will definitely interact during cognitive processes. For example, experts often possess declarative knowledge thas has been proceduralized, which means that the declarative knowlege is incorporated in automatic procedures without making strong demands on working memory.

It is believed that concepts ("a concept is a mental representation used to group similar events, ideas, objects, or people into a category", see Woolfolk, Educational Psychology) are part of semantic memory and thus explicit memory. The term for "memory of procedures to execute" comes closes to two things that are part actually procedural memory:

Scripts: actions sequences or plans of action stored in memory. For example, we have scripts for ordering food at a certain type of restaurant.
Productions (or condition-action rules): if A happens than B happens. If good behavior occurs than reinforce that behavior if you want it to occur again. Or if you want to ski faster than you automatically lean back.

In order for the procedure to become more easy to execute or even automatic for you as an individual, you need to proceduralize your declarative knowledge. So explicit knowledge has to become implicit. These skills are often referred to automated basic skills. For this to happen you will need to practice the skill a lot in a realistic context. However, not all skills can be come expert. Some skills such as driving can be automatic but you will still need to monitor the traffic consciously while driving, in other words you cannot do this automatically. Such a conscious procedure is called domain-specific strategy. After reading your example, I think the skill your are referring to can become automatic, however you need to practice each individual procedure (how and when to do a certain statistical test) for it to become automated.

I know this might not entirely answer your question but I think the information is usefull nevertheless.

Reference used: Educational Psychology by A. Woolfolk, Chapter 8.


What is the leading alternative to the "stages" model of grieving?

According to "Theories of Grief and Bereavement" by Boerner et al. (2015) the leading theories are:

The Four Component Model from Bonanno and Kaltman

Context in which loss occurs
Subject meanings associated with loss
Changes in representation of the lost loved ones over time
Presence of coping and emotion processes

The Dual Process Model from Stroebe and Schut

Loss-oriented coping
Restoration-oriented coping

The article also notes that further work needs to be done in terms of:

Effects of inter-personal relations
Influences of cultural background
Biological aspects


A quick Google search reveals a list of computer-based cognitive testing software. Apparently,

Cogstate computerized cognitive tests

  have been used in hundreds of clinical trials––guiding decision-making for safety and efficacy across many indications and all phases of development.

CANTAB Connect Research

  is the world’s most validated, precise and reliable research software providing sensitive digital measures of cognitive function for all areas of brain research. Delivering leading neuroscience through our secure cloud platform, CANTAB Connect Research is an efficient and easy-to-use system providing insights into behaviours, underlying brain circuits and neurochemical systems and measurement of digital cognitive biomarkers.


Aesthetic pleasure hormone or neurotransmitter

μ-opioid receptors (MOR) have been demonstrated to be involved in our perception of beautiful faces (https://www.medicaldaily.com/seeing-pretty-faces-rewards-brain-perceiving-beauty-all-chemical-reaction-269074).
Here’s one study that demonstrates an uptick in dopamine upon listening to music: https://www.bbc.com/news/health-12135590


How is "being in a flow" explained cognitively?

There is a six-step breakdown of 'the flow' or 'zone' from it's creator Mihály Csíkszentmihályi

  Intense and focused concentration on the present moment
  Merging of action and awareness
  A loss of reflective self-consciousness
  A sense of personal control or agency over the situation or activity
  A distortion of temporal experience
  Experience of the activity as intrinsically rewarding, also referred to as autotelic experience

Which can be found from his website

There's also a photo available that denotes when flow would be considered achieved. (Upper Right)

For even easier understanding, an example of the six steps in order from my personal life,

When implementing or working on a new project in Excel/VBA (Work I'm very comfortable with) I usually start with music to block out distractions and assist in focusing.
As my process moves on I'm no longer able to hear the music, though it's still on. My brain is queuing next lines of code to test and my fingers are an output.
I'm less focused on mistakes, mishaps, meetings, or just general things on my plate. My only issue is my task-at-hand
I am the author and implementation. The code is mine. It's finished when I am.
In deep focus, a day that started at 9am and feels like may be 10am is actually closer to 1pm... and I should eat.
Every proper step IS rewarding, I'm challenging myself with a problem and completing work.


An Adaptive LIF is just one approximation of a biological learning rule. It is not a model for how biology actually works.

The most-studied biological learning rule is long-term potentiation in the hippocampus, though similar processes occur elsewhere including neocortex. "LTP" can come in shorter or longer forms, but the longest forms of LTP are potentially permanent. The processes for maintaining this permanence are referred to as maintenance and consolidation. Some of the longer lasting forms of LTP have been shown to last weeks to years (for example, see Abraham et al., 2002).

At that point, any 'adaptation' is just as well thought of as additional plasticity, because living neurons are constantly getting input and adjusting synaptic weights. Depression is just as important in biological circuits as is potentiation, and depressed circuits can atrophy completely, effectively being permanently lost.

All nervous connectivity is due to some sort of plasticity at some point in development, and some of those connections will persist throughout the lifetime of the organism. However, synapse weights are constantly being updated in a living system. It isn't really appropriate to think of any certain weight as being permanent, while also not appropriate to think of any arbitrary synapse as possessing an adaptation time constant.

References

Abraham, W. C., Logan, B., Greenwood, J. M., & Dragunow, M. (2002). Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. Journal of Neuroscience, 22(21), 9626-9634.

Collingridge, G. L., Peineau, S., Howland, J. G., & Wang, Y. T. (2010). Long-term depression in the CNS. Nature reviews neuroscience, 11(7), 459.

Malenka, R. C., & Nicoll, R. A. (1999). Long-term potentiation--a decade of progress?. Science, 285(5435), 1870-1874.

Lynch, M. A. (2004). Long-term potentiation and memory. Physiological reviews, 84(1), 87-136.


Not entirely sure what specific stats you'd be interested in, but Wikipedia has plenty on prevalences of specific mental disorders. For anxiety disorders, which include obsessive compulsive disorder:

  A review that pooled surveys in different countries up to 2004 found overall average prevalence estimates for any anxiety disorder of 10.6% (in the 12 months prior to assessment) and 16.6% (in lifetime prior to assessment), but that rates for individual disorders varied widely. Women had generally higher prevalence rates than men, but the magnitude of the difference varied [(Somers, Goldner, Waraich, & Hsu, 2006); emphasis added].

However, Wikipedia's section on epidemiology of anxiety disorders page gives different numbers:

  Globally as of 2010 approximately 273 million (4.5% of the population) had an anxiety disorder [(Vos et al., 2013)]. It is more common in females (5.2%) than males (2.8%). In Europe, Africa and Asia, lifetime rates of anxiety disorders are between 9 and 16%, and yearly rates are between 4 and 7% [(Simpson, Neria,  & Lewis-Fernández, 2010)]. In the United States, the lifetime prevalence of anxiety disorders is about 29% [(Kessler et al., 2005)] and between 11 and 18% of adults have the condition in a given year. [Emphasis added.]

For OCD specifically:

  OCD occurs in between 1 to 3% of children and adults [(Sarvet, 2013)]. It occurs equally in both sexes...A 2000 study by the World Health Organization found some variety in prevalence and incidence of OCD around the world, with figures in Latin America, Africa, and Europe at two to three times those in Asia and Oceania [(Ayuso-Mateos, 2000); emphasis added].

Here's a cool figure of "age-standardized disability-adjusted life year rates from OCD by country (per 100,000 inhabitants)" uploaded to Wikipedia by Lokal_Profil (darker $>$ lighter; click for the scale):

"Bad thinking, cognitive distortion, and other strong, dysfunctional personality traits" is a little too vague to work with much further, but here's Wikipedia's info on prevalence of personality disorders in general:

  Studies of the prevalence of personality disorders (PDs) have been fewer and smaller-scale, but a broader Norwegian survey found a similar overall prevalence of almost 1 in 7 (13.4%), based on meeting personality criteria over the prior five-year period. Rates for specific disorders ranged from 0.8% to 2.8%, with rates differing across countries, and by gender, educational level and other factors [(Torgersen, Kringlen, & Cramer, 2001)]. A US survey that incidentally screened for personality disorder found an overall rate of 14.79% [(Grant et al., 2004); emphasis added].

Finally, neuroticism is a continuous dimension of individual differences with an approximately normal distribution. As such it is largely defined in terms of degree relative to population norms, and it doesn't make much sense to say "most people are childish and neurotic." (That is, I imagine we'd want to define "childish" in a similar way if we wanted to make any objective statements about population levels.) I'm unaware of any ratio-scaled measures of neuroticism (and find it hard to imagine any that wouldn't be very controversial), so as an interval-scaled construct at best, there is no meaningful "zero neuroticism". Hence, depending on what it means to you, you could either say:

"Everyone's a little bit neurotic (at least)!" or,
"$\approx49.\bar{9}\%$ of the population is neurotic, and the same proportion are not."

Statement 1 would be Giacobbe's best defense, but that's not saying much – nor does the statement as I've phrased it, though it's an improvement. A better interpretation of his statement (at least, as you've phrased it) would probably be as the subjective opinion, "I find most people to be childish and neurotic [compared to myself, or compared to how I would expect them to act due to other factors, which I'm probably ignoring]."

References

- Ayuso-Mateos, J. L. (2000). Global burden of obsessive-compulsive disorder in the year 2000. World Health Organization. Global program on evidence of health policy, global burden of disease. Retrieved from http://www.who.int/healthinfo/statistics/bod_obsessivecompulsive.pdf.
- Grant, B. F., Hasin, D. S., Stinson, F. S., Dawson, D. A., Chou, S. P., Ruan, W., & Pickering, R. P. (2004). Prevalence, correlates, and disability of personality disorders in the United States: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Clinical Psychiatry, 65(7), 948–958.
- Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 593–602. Retrieved from http://www.ph.ucla.edu/epi/faculty/detels/PH150/Kessler_DSMIV_AGP2009.pdf.
- Sarvet, B. (2013). Childhood obsessive-compulsive disorder. Pediatrics in Review, 34(1), 19–28.
- Simpson, H. B., Neria, Y., & Lewis-Fernández, R. (Eds., 2010). Anxiety disorders: Theory, research and clinical perspectives. Cambridge University Press.
- Somers, J. M., Goldner, E. M., Waraich, P., & Hsu, L. (2006). Prevalence and incidence studies of anxiety disorders: A systematic review of the literature. Canadian Journal of Psychiatry, 51(2), 100–113. Retrieved from http://ww1.cpa-apc.org/Publications/Archives/CJP/2006/february/sommers-RP.asp.
- Torgersen, S., Kringlen, E., & Cramer, V. (2001). The prevalence of personality disorders in a community sample. Archives of General Psychiatry, 58(6), 590–596.
- Vos, T., Flaxman, A. D., Naghavi, M., Lozano, R., Michaud, C., Ezzati, M., ... & Brooker, S. (2013). Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. The Lancet, 380(9859), 2163–2196.


How do I handle contradicting study results?

Short answer
Many individual papers report non-reproducible findings. I would advise you to look for review papers and meta-analysis studies to get the bigger picture. If not available, you can consider to set up a literature study yourself.

Background
Nature puts it down neatly (emphasis mine):

  Science moves forward by corroboration – when researchers verify others’ results. Science advances faster when people waste less time pursuing false leads. No research paper can ever be considered to be the final word, but there are too many that do not stand up to further study

Recently it has appeared that the results of a great many studies cannot be reproduced, leading to what is referred to now as the "Replication crisis".

Many factors may contribute, chief among those are according to Nature:

  the increased levels of scrutiny, complexity of experiments and statistics, and pressures on researchers.

More reliable resources than individual primary research reports are the so-called meta-studies, i.e., review studies that collects as much information there is and where the authors attempt to synthesize the bigger picture to extract solid conclusions from them, as well as confounding factors explaining why some studies may have drawn less correct conclusions.


Do we perceive contrast colour patterns easily because of adaptation?

Short answer
Contrast is hardwired in the visual system and can be explained by retinal and brain connectivities without the need for adaptive processes. My answer pertains to adaptation at the neurophysiological level. In other words, short-term neural adaptation in the retina or the visual cortex are not necessary components for color-contrast coding in the visual system.

Background
According to the model of Hering, color contrast in trichromatic species (such as most humans) is basically established between three sets of opponent systems: yellow-blue, red-green and the achromatic channel (dark-bright), and depicted in Fig. 1. The opponent system is established in the brain by cells in the visual cortex responding to both colors of a pair, but one color (e.g. blue) excites and the other (yellow) inhibits the cell, or vice versa. These systems are basically established by funneling the color information of opponent colors from the primary sensory neurons (the photoreceptive rods and cones) to color sensitive cells in the visual cortex (Gouras, 2009). In effect, we cannot perceive a yellowish blue, or a reddish green, because these colors are opponent colors in a pair.

Fig. 1. Hering model of color opponency. source: Mark Green

Because of this, the primary color-pairs yellow-blue and red-green yield excellent contrast, because in the brain the opponent response of cells will cause the edge to be sharply defined. Likewise, the achromatic channel yields high-contrast acuity. Mixed colors will impinge on this system not in an ON/OFF way, but in a gradient. For example, in your example, the blue chalk will be visualized through the yellow-blue opponent channel. On a black background, color contrast will be established against the achromatic channel. The highest possible contrast would be delivered with the blue chalk on a yellow background such that the blue-yellow opponent system could be used (e.g. blue chalk on a yellow 'white' board :-). However, blue chalk on a blackboard had to be contrasted using the yellow-blue against the achromatic channel, which are phsyiologically not opponent systems and therefore yield less sharp contrast.

Another reason is foveal tritanopia: the fovea has the highest resolution for perceiving fine detail. There are no short wave cones (blue cones) in the very center, the area of maximum resolution (Williams et al., 1981), so presumably it is impossible to see blue with the area of the retina with the highest contrast acuity.

Note that while the aforementioned Hering model does not depend on adaptation, many illusions do depend on adaptive processes in the color system, most notably after-images.

References
- Gouras, Color Vision. In: Webvision. The Organization of the Retina and Visual System (2009)
- Williams et al., Vis Res (1981) 21(9): 1341–56


It has to do with the excitatory affect alcohol has on almost all neurotransmitters and their receptors, including serotonin, dopamine, and GABA.

Very, very broadly:
Serotonin: Generally makes one seek a human connection.
Dopamine: Motivation to do things that are stimulating, like conversation.
Gaba: Surpresses anxiety.

GHB will do this even more - but it may do it to way too much of an extent.  (Mostly Gaba, but increases tyrosine hydroxylase as well which = more dopamine.)
MDMA obviously (it causes your serotonin receptors to instead of soaking up the neurotransmitter pump them out).
Amphetamines to an extent.  (Similar to the last two)


The emotions may include: duplicitousness, slipperiness, artfulness, craftiness, deviousness, wiliness, cunningness, deceitfulness, slyness, sneakiness, crookedness, vanity, haughtiness, pretentiousness, affectation, conceitedness, smugness, superciliousness, bumptiousness, condescension, obstreperousness, grandiosity, hubris.


Is decision making/theory/analysis applicable to game design?

This question seems to arise out of a slight terminological confusion. Empirical studies of human decision-making in particular are not covered by decision theory. Decision theory is the mathematical study of strategies for optimal decision-making between options involving different risks or expectations of gain or loss depending on the outcome. These sometimes overlap, such as in economics, but one need not use decision theory to study decision making.

Decision theory could conceivably have some uses in game design, such as identifying dominant strategies (strategies that are always optimal, regardless of what any other player does), but decision theory takes the game rules as a given. Hence, while it can help formalize the mechanics of a set of rules once they are designed, it doesn't have a way to actually generate rules. Decision theory is not so much helpful in designing game rules as in evaluating them.

You may be interested in what's called mechanism design theory, or reverse game theory. In contrast to decision theory, mechanism design theory is designed to work 'forwards' rather than 'backwards.' Instead of taking the rules of the game (or mechanism) as a given, mechanism design theory takes the goal as a given and finds a suitable mechanism. This seems to more closely fit what the question is looking for.


I don't know anything about those with lower than average.. BUT
Emotional Intelligence can be learned.

Read on:
http://www.lifehack.org/articles/communication/7-practical-ways-improve-your-emotional-intelligence.html

http://www.wikihow.com/Develop-Emotional-Intelligence

This will not be a process of a few hour, nor a few days.. It will take you a few weeks or months to grasp and, maybe, a few years to have something robust.
You have only positive "things" to gain if you go this route


What is the independent variable in this memory experiment?

It seems this experiment is trying to test two different things:

If participants falsely recognize (respond "yes") to more similar
sounding unstudied words than unrelated unstudied words it is taken as
evidence that they encoded the sound of the words they studied.

For this part of the experiment, the independent variable is the type of word on the recognition test, specifically whether the words on the recognition test sound similar to the studied words or not. In this case, the dependent variable is the likelihood of recognizing the words, with the hypothesis being that participants will be more likely to recognize words that sound similar to the studied words than words that are unrelated to the studied words.

Comparing "yes" responses between unstudied words that sound similar
to remember instructed study words and those that sound similar to
forget instructed study words can reveal whether the process of
remembering or forgetting is more likely to lead to the encoding of
sound.

For this part of the experiment, the independent variable is the memory-instruction (and whether words on the test sound like remember-instructed or forget-instructed words, since these variables go hand-in-hand). In this case, the dependent variable is still the likelihood of recognizing the words, with the hypothesis (probably) being that participants will be more likely to recognize words that sound similar to remember-instructed words than words that sound similar to forget-instructed words.
Edit: I just realized you designed the experiment. I would recommend choosing a single hypothesis because there seem to be two hypotheses and corresponding independent variables which makes things kind of confusing.


Is there a mindfulness meditation technique that tends to produce gamma rhythms in the brain (and not just the alpha frequencies that are typical)?

It looks like increased gamma activity is pronounced simply for long-term meditation practitioners.

  Long-term Vipassana meditators sat in meditation vs. a control rest
  (mind-wandering) state for 21 min in a counterbalanced design with
  spontaneous EEG recorded. Meditation state dynamics were measured with
  spectral decomposition of the last 6 min of the eyes-closed silent
  meditation compared to control state. Meditation was associated with a
  decrease in frontal delta (1–4 Hz) power, especially pronounced in
  those participants not reporting drowsiness during meditation.
  Relative increase in frontal theta (4–8 Hz) power was observed during
  meditation, as well as significantly increased parieto-occipital gamma
  (35–45 Hz) power, but no other state effects were found for the theta
  (4–8 Hz), alpha (8–12 Hz), or beta (12–25 Hz) bands. Alpha power was
  sensitive to condition order, and more experienced meditators
  exhibited no tendency toward enhanced alpha during meditation relative
  to the control task. All participants tended to exhibit decreased
  alpha in association with reported drowsiness. Cross-experimental
  session occipital gamma power was the greatest in meditators with a
  daily practice of 10+ years, and the meditation-related gamma power
  increase was similarly the strongest in such advanced practitioners.
  The findings suggest that long-term Vipassana meditation contributes
  to increased occipital gamma power related to long-term meditational
  expertise and enhanced sensory awareness.

Also,

  Early studies of meditators implicated alpha (8–12 Hz) power increases
  as both a state and trait effect of Yogic, Zen, and Transcendental
  Meditation practice. Later studies have failed to replicate the early
  findings of increased alpha in advanced practitioners but have
  reported increased alpha coherence, especially in assays of TM
  practitioners (Gaylord et al. 1989; Travis 1991; Travis and Pearson
  1999; Travis et al. 2002), theta (4–8 Hz) power, especially in the
  assays of concentrative/focused attention practitioners (Aftanas and
  Golocheikine 2001; Baijal and Srinivasan 2009; Hebert and Lehmann
  1977; Pan et al. 1994), or gamma effects (Lehmann et al. 2001; Lutz et
  al. 2004).

Cahn, B. Rael, Arnaud Delorme, and John Polich. "Occipital gamma activation during Vipassana meditation." Cognitive processing 11.1 (2010): 39-56. doi: 10.1007/s10339-009-0352-1

Whether one can accelerate the gamma power with a particular meditation training technique is another question, however.

Activities likely to trigger gamma power

Even if particular subtypes of mindfuless meditation techniques promoting gamma power in novices may not be known yet, we can conjecture the characteristics thereof based on other activities that trigger gamma activity in the prefrontal cortex. From the comments, Angela Richardson writes

  Noise, flashing lights, movement and high-contrast or striped patterns
  can all increase gamma activity. In some people the resulting increase
  in gamma activity is so large that it causes seizures or migraines. If
  you want a meditation exercise to increase your gamma power then
  imagine loud music, strobe lights and brightly coloured rapidly moving
  shapes and patterns.

However, the corresponding gamma waves are primarily observed in the visual cortex. See

Adjamian, Peyman, et al. "Induced visual illusions and gamma oscillations in human primary visual cortex." European Journal of Neuroscience 20.2 (2004): 587-592. https://doi.org/10.1111/j.1460-9568.2004.03495.x

Azizi et al. note that gamma waves also get activated during an n-back exercise, which requires active focus and working memory utilization:

  during cross-modal sensory processing (perception that combines 2
  different senses such as sound and sight). Also, it is shown during
  short-term memory matching of recognized objects, sounds, or tactile
  sensations

Roohi-Azizi, Mahtab, et al. "Changes of the brain’s bioelectrical activity in cognition, consciousness, and some mental disorders." Medical journal of the Islamic Republic of Iran 31 (2017): 53. https://doi.org/10.14196/mjiri.31.53

A common theme in the gamma activity literature seems to be a mental state that is awake and alert, with a deep and selective focus/attention. It has also been observed in the phenomenon of "getting it right" and feature extraction, as Phillip Gilley demonstrates in this beautiful visualization:

https://www.youtube.com/watch?v=OCpYdSN_kts

A mental state that sufficiently mirrors these characteristics during meditation may possibly lead to the desired gamma activity.


What is the information storage capacity of the human brain?

Disclaimer: Quantifying the capacity of the human brain is quiet complex as you might imagine. And although in cognitive neuroscience we often compare the brain to computers this is not an exact comparison, in many ways the brain is far more complicated and encodes information in a very different way than the comparison of CPU processors and hard-drives. The short answer is that we have understandings about capacity under specific situations regarding STM, but LTM capacity is mostly based on estimates.
TL;DR: Estimates vary from 10^13 to 10^18 bytes (10 terabytes - 1 exabyte), and even this range should probably be taken with a grain of salt.
The long version:
Memory in the brain is often split by cognitive psychologists into several different modules, such as the memory storage model suggested by atkinson and shiffrin; attention->short-term(STM)->long-term(LTM).
Fig 1.

This model is largely inaccurate as the brain encodes information relative the type of information received, for instance auditory inputs will be processed by neural areas associated with auditory processing first. In addition attentional processing, unlike in this model, relies heavy in precognitive processing e.g. if you are hungry you will attend more to food. That being said we still use STM and LTM to distinguish between memory that is in use and memory that is stored.
Short-term memory capacity
The rather brilliant researchers Baddley and Hitch developed what is perhaps the most compelling models for short-term memory processing. The working memory model (see Fig. 1) accounts for differences in information types and how it is held within the processing centres of the brain.
Fig 2.

A meta-analysis of 400 studies has displayed good support for the three main modules of cognitive memory. Generally speaking the central executive can be considered as the processor, while while the episodic buffer, phonological loop and visit-spatial sketchpad may be the modular RAM which holds information for processing.
According to Baddley the phonological loop can hold about 2 seconds of auditory information, this would be a list of unrelated words with a task designed to restrict rehearsal and encoding of information. However if the information was related, say "Our lecturer told us to read chapter 3 of working memory" we could hold more of the information as its related and may be chunked together. 'Chunking' is a feature of memory that complies similar information together. The capacity recorded generally depends on numerous factors, such as the task type, time between learning and recall, and the significance of the information. In addition we can also add age and context (internal and external) as factors influencing memory recall. Overall we can't identify the exact capacity of working memory due to the complexity of information processing, what we can say is that working memory deals with small amounts of information spit across different modules, and relates this to LTM. Although that small amount of information is probably a lot more than your average super computer can process as this post indicates.
Long-term capacity
As with STM, LTM is modular in anyways. However the total capacity is somewhat related too neurons, with 86-100 million neurons and 1000 glia cells thats means the human brain has a large capacity for storing information. However as previously mentioned these neurons relate to particular types of information. With regard to processing capacity the human brain is estimated to be [10 to the power of 17] 11 flops per sec, according to the blue brain project. Another recent estimate puts the processing capacity of the brain at 10^28 Flops.
Fig 3. A comparison of recent predictions of neural processing capacity and current fastest Super CPU

A different measure of calculating processing capacity has been devised by Grace and Christiano who stated the following...

We can use Traversed Edges Per Second (TEPS) to measure a computer’s ability to communicate information internally. We can also estimate the human brain’s communication performance in terms of TEPS, and use this to meaningfully compare brains to computers. We estimate that the human brain performs around  0.18 – 6.4 * 1014 TEPS. This is within an order of magnitude more than existing supercomputers. TEPS = synapse-spikes/second in the brain

= Number of synapses in the brain * Average spikes/second in synapses

= Number of synapses in the brain * Average spikes/second in neurons

= 1.8-3.2 x 10^14 * 0.1-2

= 0.18 – 6.4 * 10^14

So the brain operates at around 18-640 trillion TEPS, while closest supercomputer is 2.3 * 10^13 TEPS (23 trillion TEPS).
Memory has been calculated to be around 2.5 petabytes (2.5 * 10^15 bytes), as reported here (seems to be based upon speculation by Prof P Reber). Another estimate has the neural memory capacity at 8∙10^19 bits--that's over 8 quintillion (10^18) bytes. Some researchers at Berkeley have suggested a relatively small 10-100 terabytes (10^13 to 10^14 bytes). All these estimates are based on variations in calculations relative to neuron density and and synapse connections across the whole brain. The larger estimates take addition account of other factors involved in neural communication. But the overall criticism I have is that we can't simply say that one synapse is 1 byte or 200 calculations per second.
The term estimate is generous here; guesstimate would be far more accurate. Individual neurons are complicated enough; moving to distributed and interconnected networks in the brain is just another level. Neurons do not conduct calculations independently; they rely heaving on context and information types. So we can say the processing of the brain is modular, in fact we already know this to be true to initial sensory processing. There is also no clearly obvious separation of memory from processing, although we know in motivation for instance certain areas will activate (the so called 'reward system') when assessing motivational objects. We won't say this is memory but it relies on it previous associations in memory. So some areas of the brain are used to assess rather than recall but they will activate together. The point being that we can't bundle all neurons together to calculate memory or processing. We just don't know what the vast amount of neurons are doing right now.
I highly recommend this article, for more information and references regarding computational and memory estimates.


The internet is flooded with anecdotal reports of 'Tian' relating to the drug's addictive potential after recreational use, for example here, here and here. Often, though, these reports come from people already addicted to other illicit drugs. Notably, tianeptine is used for rehab purposes, just like the partial opioid agonist naloxone. So anecdotal reports can be misleading.

Scientific reports however also indicate the drug's addictive potential. Vadachkoria et al. (2009) report

  Supposedly, Tianeptine, in contrast to other anti-depressants, stimulates release of neurotransmitter dopamine in nucleus Accumbens, that probably determine[s the] addictive potential of this drug.

Addiction can be defined as a syndrome characterized by compulsive substance abuse. In a more verbose definition:

  Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences.† It is considered a brain disease because drugs change the brain—they change its structure and how it works. These brain changes can be long-lasting, and can lead to the harmful behaviors seen in people who abuse drugs

It is generally accepted that the antidepressant drugs do not cause addiction. However, tianeptine, among some other antidepressants do have addictive potential (Lapsekili & Yavuz, 2014).

Reference
-  Lapsekili & Yavuz, J Psychiatry Neurol Sci (2014); 27: 81-4
- Vadachkoria et al., Georgian Med News (2009); 174:92-4


How many participants are needed for online reaction time studies?

There are four variables of interest in a statistical power analysis: power (often chosen as 0.8 or 0.9 by convention, this is the probability of correctly rejecting the null hypothesis if it is false), tolerated false-positive rate (alpha, often chosen as 0.05 by convention), sample size, and the effect size (which in turn depends on the variability of the observations and the difference between groups).
When you do a power analysis, you can choose any one of those variables to calculate provided you have all the others. In your case, you want to know the sample size you need so you need to choose or estimate the other numbers.
If you know what statistical test you are using, there are numerous online calculators to help you choose a sample size. Personally, I like to use the free software G*Power.
Power and alpha are typically chosen by convention, so what you still need to know to determine your necessary sample size is the effect size you are looking for. If you have an experiment that you expect to have a large impact on reaction times, you don't need as many participants. If you are looking for a subtle effect, you need more. You can choose that threshold based on what is reasonably interesting/clinically relevant (this is ideal but sometimes frustratingly difficult to settle on), or you can base it on pilot data (can be dangerous when pilots are based on small sample sizes).
If you don't have any preliminary data, the best way to estimate the variance in observations would be to look at other similar studies collecting online reaction time data.
Overall, if you want to make sure you have a sufficiently powered study, it's good to use conservative estimates. If you guess that your effect is smaller and the variability is larger than what you hope, then you have a better chance of a sufficiently powered study.


Is neuroplasticity limited to the cerebral cortex in the brain?

Short answer
Subcortical structures can definitely show neuroplasticity in adults. Most likely, all brain structures can show plastic changes to some degree.

Background
The question is rather broad, as there are many subcortical structures and neuroplasticity is age-dependent. I will therefore restrict my answer to three examples I dug up from the literature.

For example, in primates it has been shown that thalamic and brainstem areas projecting to the somatosensory cortex are plastic and change their projections to the cortex to aid in the rearrangement of the somatotopical map (Jones, 2000).

Changes in the connectivity between hemispheres has been associated with plastic changes in the callosal pathway (corpus callosum) after somatosensory lesions in the cortex (Duffau, 2009).

As a last example, subcortical plasticity has been shown after lesioning the spinal cord in monkeys and rats. By interrupting the ascending projections of mechanoreceptor afferents of the forelimb and the rest of the lower body the corresponding part of the somatotopic representation of primary somatosensory cortex becomes completely deafferented and unresponsive to tactile stimuli. If some of the afferents from the hand remain intact after such dorsal column lesions, the remaining afferents will extensively reactivate portions of somatosensory cortex formerly representing the hand over the course of a month. This functional reorganization has been linked to the sprouting of preserved afferents within the cuneate nucleus of the dorsal column–trigeminal complex in the medulla, also subcortical brain structure (Kaas et al., 2009).

In terms of structures that are resilient to plasticity, Aguire from USC argues that every brain structure has the potential for neural plasticity to occur. Basically, because the term plasticity is pretty much all-encompassing, and I quote:

  [N]europlasticity is the ability of elements in the brain to show structural and functional changes in response to internal and external events. Neuroplasticity occurs at different levels: structural[ly], functional[ly] and [through] all the molecular and cellular mechanisms that accompany these changes. [...] At all times, these players are constantly changing [...].

Admittedly it is a popular-scientific and broad answer to this question, but I do agree with it.

References
- Duffau, Neurosci Res(2009); 65: 131–5
- Jones, Annu Rev Neurosci (2000); 23:1-37
- Kaas et al., Exp Neurol (2000); 209(2): 407–16


How repeatable are cognitive science findings within the same individual?

Humans are, as you would expect, much noisier than physical systems. As such, replication of experiments in psychology is very important. Replication provides evidence that the original results were not spurious.

As pointed out in the comments, replication with the same subject pool is not always the way to go. Many tasks have learning effects, and so you would not expect to achieve the same results by re-administering the experiment.

There is a vast statistical literature on reliability testing. A good place to start would be at the Wikipedia article for Reliability (psychometrics)


Human memory - remembering sequences of letters vs numbers

I am not sure I completely understood your question but I will try to answer it. Different numbers and different letters can be easier or harder to remember based on the order, meaning that, depending on their sequence, it can be either way.
Ex.
a r d q
is easier to remember than
9 4 6 0
but
z n k r
is harder to remeber than
9 8 3 0.
This is because the letters are used in the English language in a way that allows you to make them into a certain sound but only if you have the right letters.

I hope that was helpful (even though it has been almost two years),


Comprehensive encyclopedia of nootropics for medical researchers and practitioners

Edit (09/14) -- Two years after writing this answer, I need to alter it slightly.  Examine.com is a website dedicated to aggregating information on nootropics and other supplements/chemicals.  It is often incomplete, but having a singular hub for academic/industrial research is nearly indispensable.   I don't know if it satisfies what you're looking for, OP, but if you haven't, take a look at it.

I am not a "medical professional", but honestly I strongly doubt something like this exists.

"clinically-researched and tested" would require huge amounts of money and time in a coordinated fashion.  This isn't something often performed for 'nutritional supplements'.  Ever seen the warning on vitamin bottles, something along the lines of "These statements have not been verified by the FDA"?

That's only for the supplements.

For newer pharmaceuticals, the process is HUGELY complicated.  Multiple animal trials, regulatory approval, multiple courses of human trials, more regulatory approval, and even more hoops to jump through before it can be sold by pharmacies (this process is easier in Countries will more lax regulation - hence why, for example, Modafinil is obtainable in a number of countries outside the US; well, that and lax patent laws).

Moreover, nootropic supplements are more touchy/personalized than most drugs.  For example, we don't exactly know how SSRI drugs work, yet we prescribe them by the millions (if not billions).  We know even less how some nootropics work.

And finally, we have not reached a point of diagnostic science to be able to say, "You could use a course of DrugA and DrugB, but stay away from DrugC and Foods fA, fB, and fC".

Until we're closer to that point, it's all a guessing game.

(one last thing - from my understanding, a lot of doctors have no idea of the deeper details of the drugs they prescribe; they're given all the 'info they need to know' by the pharma reps - another reason why a comprehensive compendium doesn't exist)


How does emotional stress cause skeletal muscle rigidity?

Short answer
The stress response included norepinephrine release, in turn increasing blood pressure. This may cause muscle tension.

Background
What an interesting question. To my surprise, I couldn't find convincing causal explanations, linking emotional stress and muscle tension.

In one study, study participants were exposed to emotional stress. The authors found a positive correlation between muscle (EMG) activity and blood pressure. They also found a significant positive correlations between stress and norepinephrine (NE) release. The latter plays an important
role in blood pressure homeostasis and is released during stress as part of the HPA axis response. These results seem to indicate that stress results in NE release, followed by increase in blood pressure (this is a known stress response). The increase in blood pressure could then lead to muscle tension. However, as the authors explain, the results do not explain whether these associations represent the effect of a general underlying factor (e.g., psychological arousal) or a more direct interdependence of blood pressure and muscular tension. In other words, a correlation was found, but no causal relationships can be deduced.

Reference
- Lundberg et al, International J Behav Med (1994); 1(4): 354-70


Memory is only a psychological construct. In reality there is only the brain, and the physiological functions of the brain. "Memory" is just a way to conceptualize some of these functions. For this reason, it's unlikely that a law will ever emerge. Part of the reason is that memory can refer to so many different things, biologically.

Even when you get down to the actual biology, laws are not really the standard. Biology is a messy thing and virtually no laws exist that couldn't be contradicted. Something as basic as the cell theory could be reasonably argued against. Viruses are not cellular, yet an argument could be made for them being alive. It isn't the current thinking, but it's not an absurd proposition either. If psychological phenomena are a result of biology, and no laws exist in biology, I think it's reasonable to say no laws will exist in psychology either.

Perhaps one of the strongest ideas about memory is Hebbian learning. But even that is just a simplification.