Does the brain generate identical words in different languages similarly?

Here's an article talking about exactly what you are asking:
EEG decoding of spoken words in bilingual listeners: from words to language invariant semantic-conceptual representations

I can say that the brain obviously has the ability to invariantly represent different stimuli as being the same abstract concept, not even from stimuli in the same domain (such as auditory to auditory) but even across different domains of knowledge (identifying astract conceptual relationships between visual signals and motor signals)! Whether this can be derived purely from EEG, I doubt it because it lacks the precision necessary (which would require single cell recordings of millions of cells at the same time). I should also note that EEG can't tell us much on how the brain generates the spectral graphs that we record, just what the electrical activity is. We also don't even know what exactly causes the signals. Electrical activity may not even be the only indication of invariance, because other underlying mechanisms may be involved. But the idea of invariance, itself, is the very idea of what you are talking about and this phenomenon is found in lots of ways. In fact, anytime anyone relates two different stimuli as the same concept, it's clear that somehow the brain has an invariant representation of the event. There exists some kind of mechanism in the brain to recognize and store abstract concepts, removed from the concrete signals from which the concepts are learned.

"Mirror" neurons are an example of the domain crossing invariance, and something you can Google. These neurons demonstrate invariance by being similarly activated when an animal witnesses another animal performing an action and when the animal performs the action itself (e.g. eating).

However, your question about bilingual invariant representations and the mirror neurons are simply specific examples of a more general phenomenon. In fact, the ability for humans to have such incredible invariance is a major substrate that makes our intellectual capabilities so distinctly advanced compared to even the latest and greatest artificial intelligence attempts.

In the auditory language vs. language example you provided, the differences in auditory signals are ignored and our perception of the concept being communicated remains invariant. The same thing happens in vision. Even though the objective visual signals received by the brain are different, objects can be conceptually related. Just look at one face, then look at another one. You will still be able to identify both objects as the singular concept, "face". You might say "but the general structure of the face is still there". Yet, if you actually look at firing patterns of the neurons, they are still completely different. It's just as mysterious how the brain does this as it is that we can identify differing audio signals as the same concept. Humans possess a variety of invariant abilities in object recognition, such as scale invariance (different sizes), rotational invariance, translational invariance, skew invariance, color invariance, contrast invariance, and many others.

Just keep in mind that even though we possess these invariant abilities, we also maintain the distinctions in parallel. So the answer to your question is both yes and no. We generate both an invariant representation and a variant representation of whatever the stimulus is. Theoretically, both representation types are present in the EEG. However, EEG is not powerful enough to identify the specifics of how this works in language and whether this is even true.


For a neuroscience focused overview I enjoyed:

"Making up the Mind" by Chris Frith

For a psychology textbook ( I think this is used in undergraduate level):

"Psychology 2nd Edition" by  Daniel L. Schacter, Daniel T. Gilbert, Daniel M. Wegner


What cognitive strategies diminish bias in decision-making beyond those outlined by Larrick?

One possible strategy is to phrase decision-making problems as questions in a foreign language. There's evidence that this attenuates at least certain kinds of cognitive bias (making you more rational and consistent) by distancing the cognitive and affective baggage that comes with the problem. See the following:

Keysar, B., Hayakawa, S.L., & Sun, G.A. (2012). The Foreign-Language Effect: Thinking in a Foreign Tongue Reduces Decision Biases. Psychological Science, 23 (6), 661-668.


Wikipedia's answer is a better answer than I could offer as to what the higher self is, because that's all you've used to define it, and as Wikipedia says, it's "a term associated with multiple belief systems," and probably differs rather widely across the gamut. Regardless of how odd some of those beliefs might get, it probably shouldn't be synonymous with the prefrontal neocortex or basal ganglia, each of which has multiple functions that couldn't simply be equated to what most people mean when they say "higher self."

In one aspect at least, there may be some overlap between the "higher self" concept and the prefrontal cortex. To whatever extent "higher self" means "self-awareness," the prefrontal cortex is probably involved in that...This article offers an interesting image from magnetic resonance tomography, and these quotes [emphasis added]:

  A specific cortical network consisting of the right dorsolateral prefrontal cortex, the frontopolar regions and the precuneus is...associated with self-reflective functions...

  By comparing the activity of the brain during...lucid periods with the activity measured immediately before in a normal dream, the scientists were able to identify the characteristic brain activities of lucid awareness.

So note that this is self-awareness in the context of dreaming. The original article (Dresler et al., 2012) is free, and mentions an interesting method for distinguishing lucid from normal dreaming, BTW. As for consciousness in general, we have some pretty interesting questions with richly informative answers here already, including:

What are current neuronal explanations and models of 'consciousness'?
Is there a region of cortex which over a period of development becomes the seat of self?
Research suggesting conscious control over brain region activation?
If someone becomes a split-brain patient, which side will "maintain" the continuity in their consciousness?

And as for the subconscious, Wikipedia again gives a pretty decent answer. Since the term is frequently misattributed to psychoanalysis, and may be most popular in pseudoscientific contexts, I prefer to point you directly to the section on Freud's answer and advocate his general practice of avoiding the term altogether (except for the sake of criticizing it). Freud used "preconscious" and "unconscious" in distinct ways that cognitive psychology has adopted somewhat as well, so those terms are generally much more useful and well-defined scientifically...though that's not saying all that much. However, thanks to @ArtemKaznatcheev, we also have a question here that says a little more: Subconscious vs Unconscious

Reference

Dresler, M., Wehrle, R., Spoormaker, V. I., Koch, S. P., Holsboer, F., Steiger, A., Obrig, H., Sämann, P. G., & Czisch, M. (2012). Neural correlates of dream lucidity obtained from contrasting lucid versus non-lucid REM sleep: A combined EEG/fMRI case study. Sleep, 35(7), 1017-1020. Available online, URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369221/. Retrieved January 25, 2014.


Difference between Instinct and Intuition

Intuition, as defined by Wikipedia:

  Intuition may be defined as understanding or knowing without conscious
  recourse to thought, observation or reason.

Intuition is currently understood to be the subliminal processing of information that is too complex for rational thought, e.g. mate choice. The processes that make up intuition are learned, not innate.

Instinct is not a feeling, but an innate, "hardwired" tendency toward a particular behavior. Instincts are automatic reactions to environmental stimuli that cannot be repressed and occur in every individual of a species. The current opinion in psychology (since Maslow) is that human beings have no instincts.

A Gut Feeling, according to the reference, arises from intuition.


How do some humans seemingly naturally have positive or mitigated appraisal of stressful events?

The interactions among several factors probably account for variability in reactivity to stressful events, including genetics, epigenetics, early life experience, and culture (e.g., Alexander et al., 2009; Boyce & Ellis, 2005; Francis, Frances, Liu, & Meaney, 2006; Gunthert et al., 2007; Meaney, 2001).  And individual differences are observable at multiple levels of analysis, including behavior, physiology, and brain structure and function.

On the one hand, there is a huge literature on the development of emotion regulation in children (e.g., positive appraisal of stressful events).  For example, there are models charting the complex influence of the family on emotion regulation development, where parenting practices interact with child characteristics to influence emotion regulation success and strategy use (Morris et al., 2007):

Positive (re)appraisal requires good cognitive control and working memory (McRae et al., 2012), which is associated with functional and structural integrity of cortical areas, most notably prefrontal cortex (Goldsmith, Pollack, & Davidson, 2008; Levesque et al., 2004; Lewis & Stieben, 2004; McRae et al., 2012).  And the ability of PFC to dampen negative affect seems to be mediated by functional connectivity with subcortical areas, notably bilateral amygdala (Banks et al., 2007; Buhle et al., 2014; Wager et al., 2008).

Positive reappraisal also benefits from practice, which forms part of the basis of cognitive-behavioral therapy (Beck, 2011; Goldin et al., 2012; Goldin et al., 2013).

Additionally, there is emerging evidence that genes (and gene-environment interactions) are related to emotion regulation strategy use and effectiveness (e.g., 5-HTT, OXTR; Canli & Lesch, 2007; Hariri & Holmes, 2006; Kim et al., 2011).  So genetic factors may promote resilience even in stressful environments.

Conclusion

So as you can see, there is a large host of factors that contribute to one's tendency to appraise (negatively or positively) a stressful situation. And indeed, you may see large within-person variability in the tendency to make positive appraisals, especially as the context changes (Aldao & Nolen-Hoeksema, 2012). Not to mention, positive appraisal may not always be a beneficial way to mitigate stress, and may instead sometimes be harmful or ineffective (Troy, Shallcross, & Mauss, 2013).


Where can I find open data for psychology research on meditation?

Kaggle has a dataset of an EEG conducted on a meditation group versus a control.
Other than that, if you are looking for the raw datasets of fmri meditation studies, that may be a little more difficult. If you are fine with summary statistics, and some inferential tests (data that has already been analysed), then Google Scholar has many open source papers on the topic.


Does this recent twin study contradict Anders Erricson's view on the hereditary basis of talent?

Ericsson’s studies have repeatedly ignored the genetics of performance in any field. His favourite study of expert performance - the London taxi driver experiment - also failed to control for prior genetic attributes that may have led these taxi drivers into their professions in the first place. A good place to start perhaps:

Hambrick et al 2014 Deliberate practice and performance in music, games, sports, education, and professions: A meta-analysis


Why do people look in the face or eyes while communicating?

Eye contact is one of the principal cues humans use to evaluate where other people direct their attention. A special issue on the use of eye tracking in the Infancy journal and other studies reported that infants' eyes are useful measures of attention over a range of task domains including object perception (Johnson, Slemmer, & Amso, 2004), faces (Hunnis & Geuze, 2004), and categorization (McMurray & Aslin, 2004).

This relationship between eyes and attention begins developing as early as within the first couple of neonatal weeks (Lohaus, Keller and Voelker, 2001). For the same reason, eye- and gaze tracking are central measures in many areas of the cognitive sciences, including developmental (neuro)psychology, perception and working memory.

Because gaze is such a good general indicator of attention, mutual eye contact between myself and someone indicates that we are both attending to one another, if not always, then at least often enough to depend on.

References

Lohaus, A., Keller, H., & Voelker, S. (2001). Relationships between eye contact, maternal sensitivity, and infant crying. International Journal of Behavioral Development, 25(6), 542-548.
Hunnis , S. and Geuze , R. H. 2004. Developmental changes in visual scanning of dynamic faces and abstract stimuli in infants: A longitudinal study. Infancy, 6(2): 231–255.
Johnson, S. P., Slemmer, J. A., & Amso, D. (2004). Where Infants Look Determines How They See: Eye Movements and Object Perception Performance in 3‐Month‐Olds. Infancy, 6(2), 185-201.
McMurray , B. and Aslin , R. N. 2004. Anticipatory eye movements reveal infants' auditory and visual categories. Infancy, 6(2): 203–229.


Background:

There is abundant research linking childhood attachment styles and adult attachment styles. This doesn't mean that an individual's attachment style is set in stone for life; it is a good indicator of how a child will fare as an adult.

The advent of Attachment theory:

A Brief Overview of Adult Attachment Theory and Research
R. Chris Fraley | University of Illinois

  ... Bowlby postulated that these attachment behaviors, such as crying and searching, were adaptive responses to separation from with a primary attachment figure--someone who provides support, protection, and care. Because human infants, like other mammalian infants, cannot feed or protect themselves, they are dependent upon the care and protection of "older and wiser" adults. Bowlby argued that, over the course of evolutionary history, infants who were able to maintain proximity to an attachment figure via attachment behaviors would be more likely to survive to a reproductive age. According to Bowlby, a motivational system, what he called the attachment behavioral system, was gradually "designed" by natural selection to regulate proximity to an attachment figure.

John Bowlby was the father of Attachment Theory; Mary Ainsworth tested and developed  this theory.

  ... John Bowlby formulated the basic tenets of
  the theory. ...
  Mary Ainsworth’s innovative
  methodology not only made it possible to test some of Bowlby’s ideas empirically hut also
  helped expand the theory itself and is responsible for some of the new directions it is now
  taking.

THE ORIGINS OF ATTACHMENT THEORY:
JOHN BOWLBY AND MARY AINSWORTH,
INGE BRETHERTON Developmental Psychology (1992), 28, 759-775.

John Bowlby - Attachment Theory

It is difficult to separate more recent attachment theory from its progenitor; as this is the source from which all attachment theory has evolved.

Attachment style categorisation:

Any style of attachment, that is not a healthy or secure attachment style is classified as an insecure attachment style or an attachment disorder.

This answer here addresses attachment disorders, in particular, ambivalent attachment disorder in detail.

Maryland's Source for
Attachment Disorder Related Information
Note I've added bold for emphasis.

  AVOIDANT ATTACHMENT DISORDER

  The predominant emotion internally, in Avoidant AD {AvAD} children is sadness. However, the world sees little or none of their sadness. AvAD children believe their sadness is infinite, and should they lapse into it, they see no exit. Hence, they go to extraordinary lengths to avoid any expression of it, and usually effectively shield themselves from even recognizing their sadness. Their internal shields work so well that they often truly do not think they are sad. What AvAD children do feel is an anxious edge in quieter moments. They rarely relax, lest their sadness “creep up” on them. Their hypervigilance is more about deflecting anything that might activate their sadness rather than simply scanning for direct hostile threats. As physical / emotional closeness carries a high potential for triggering their sadness, AvAD children avoid it. Attitudinally, AvAD children are contemptuous of sadness- they define it as the “stuff of sissies”. AvAD children present themselves as omnipotent and without need for others. About half of these children lie somewhere along the spectrum of depressive disorders.

  ANXIOUS ATTACHMENT DISORDER

  The primary emotion Anxious AD {AxAD} children feel is anxiety ...

  DISORGANIZED ATTACHMENT DISORDER

  The characteristic emotion of children with Disorganized Attachment Disorder {DAD} is overwhelming and unmanageable anxiety.

A cross over of avoidance and anxiety attachment disorders:

  AMBIVALENT ATTACHMENT DISORDER

Note: my answer gives a more comprehensive overview of Ambivalent Attachment Disorder and how it is classified as an Reactive Attachment Disorder.

  Reactive attachment disorder

  What is reactive attachment disorder?

  In reactive attachment disorder, DSM-IV considers two basic types of behavior. Representative of the hindered type of attachment disorder, is a child who “constantly refuses to initiate or respond to social activity, as it is expected of children in his age and level of development. It’s expressed in too depressed, too sensitive or highly controversial reaction, for example, a child may respond differently to the teacher: to avoid and refuse caress or to express increased vigilance (“frozen vigilance”).

Highlights of Changes from DSM-IV-TR to DSM-5

  Reactive Attachment Disorder
  The DSM-IV childhood diagnosis reactive attachment disorder had two subtypes: emotionally withdrawn/inhibited and indiscriminately social/disinhibited. In DSM-5, these subtypes are defined as
  distinct disorders: reactive attachment disorder and disinhibited social engagement disorder. Both of
  these disorders are the result of social neglect or other situations that limit a young child’s opportunity
  to form selective attachments. Although sharing this etiological pathway, the two disorders differ in
  important ways. Because of dampened positive affect, reactive attachment disorder more closely resembles internalizing disorders; it is essentially equivalent to a lack of or incompletely formed preferred
  attachments to caregiving adults. In contrast, disinhibited social engagement disorder more closely
  resembles ADHD; it may occur in children who do not necessarily lack attachments and may have established or even secure attachments. The two disorders differ in other important ways, including correlates, course, and response to intervention, and for these reasons are considered separate disorders

A Brief Overview of Adult Attachment Theory and Research
R. Chris Fraley | University of Illinois

  Recent research on adult attachment has revealed some interesting complexities concerning the relationships between avoidance and defense. Although some avoidant adults, often called fearfully-avoidant adults, are poorly adjusted despite their defensive nature, others, often called dismissing-avoidant adults, are able to use defensive strategies in an adaptive way. For example, in an experimental task in which adults were instructed to discuss losing their partner, Fraley and Shaver (1997) found that dismissing individuals (i.e., individuals who are high on the dimension of attachment-related avoidance but low on the dimension of attachment-related anxiety) were just as physiologically distressed (as assessed by skin conductance measures) as other individuals. When instructed to suppress their thoughts and feelings, however, dismissing individuals were able to do so effectively. That is, they could deactivate their physiological arousal to some degree and minimize the attention they paid to attachment-related thoughts. Fearfully-avoidant individuals were not as successful in suppressing their emotions.

This figure from Attachment as an Organizational Framework for Research on Close Relationships Cindy Hazan Cornell University, Phillip R. Shaver University of California, Davis; shows the basis of cause and effect underlying attachment.

Attachment anxiety and attachment avoidance.

This figure shows how this cause and effect is classified into attachment styles. Defensiveness leading to avoidance, fear leading to anxiety.

Attachment orientations

This figure taken from A Brief Overview of Adult Attachment Theory and Research gives a nice representation of how defensiveness and fear translate into attachment styles or attachment orientations.

These diagrams also give a good representation of childhood cause and adult attachment style affect.

images courtesy of Attachment Styles
By Kendra Cherry, About.com Guide

The Experiences in Close Relationships-Revised (ECR-R) Questionnaire
Fraley, Waller, and Brennan (2000) - Iive added emphasis within this quote.

  Scoring Information: The first 18 items listed below comprise the attachment-related anxiety scale.  Items 19 – 36 comprise the attachment-related avoidance scale.  In real research, the order in which these items are presented should be randomized.  Each item is rated on a 7-point scale where 1 = strongly disagree and 7 = strongly agree.  To obtain a score for attachment-related anxiety, please average a person’s responses to items 1 – 18.  However, because items 9 and 11 are “reverse keyed” (i.e., high numbers represent low anxiety rather than high anxiety), you’ll need to reverse the answers to those questions before averaging the responses.  (If someone answers with a “6” to item 9, you’ll need to re-key it as a 2 before averaging.)  To obtain a score for attachment-related avoidance, please average a person’s responses to items 19 – 36.  Items 20, 22, 26, 27, 28, 29, 30, 31, 33, 34, 35, and 36 will need to be reverse keyed before you compute this average.


How do hallucinations appear through reversing goggles?

Karl Jaspers describes clinical reports in which patients hallucinatory perception was changed in accordance with the optical distortion. For example, a prism would double the images of devils, binoculars enlarge or decrease the image, colored glasses make it colored, etc. He refers "Seppilli, Contributo allo studio delie allucinazioni unilaterali. Riv. sper. di fren. 16, 82. 1890" and "Pick. Beitrage zur Lehre von den Halluzinationen. N. C. 11. 329. 1892" Now, the question is, has anyone done a study on that in the 20th century.


Is the Neanderthal Theory of Autistic brain a reasonable scientific theory?

I don't know if it's a reasonable scientific theory, but here's some more info:

Autism: The Eusocial Hominid Hypothesis

ASDs (autism spectrum disorders) are hypothesized as one of many adaptive human cognitive variations that have been maintained in modern populations via multiple genetic and epigenetic mechanisms. Introgression from "archaic" hominids (adapted for less demanding social environments) is conjectured as the source of initial intraspecific heterogeneity because strict inclusive fitness does not adequately model the evolution of distinct, copy-number sensitive phenotypes within a freely reproducing population.

Evidence is given of divergent encephalization and brain organization in the Neanderthal (including a ~1520 cc cranial capacity, larger than that of modern humans) to explain the origin of the autism subgroup characterized by abnormal brain growth.

Autism and immune dysfunction are frequently comorbid. This supports an admixture model in light of the recent discovery that MHC alleles (genes linked to immune function, mate selection, neuronal "pruning," etc.) found in most modern human populations come from "archaic" hominids.

Mitochondrial dysfunction, differential fetal androgen exposure, lung abnormalities, and hypomethylation/CNV due to hybridization are also presented as evidence.

A short video introduction


Is there a reliable memory-retention guidance chart?

I think you can use this graphic:

It is taken from an article from WIRED, Want to Remember Everything You'll Ever Learn? Surrender to This Algorithm. It talks about Piotr Wozniak and his spaced repetition software SuperMemo.


What's the relationship between priming and anchoring?

Priming: Stimulus A influences perception/processing of stimulus B. E.g. you walk past an Italian restaurant and smell pizza. When you enter the supermarket and consider what you want to make for dinner, you might be more strongly inclined to bake a pizza, then when you hadn't smelled the delectable pizza from the restaurant.

Anchoring: The first information in a series if informations influences your processing of the whole of this information. E.g. if you are asked to guess (not calculate) the result of 8 x 7 x 6 x 5 x 4 x 3 x 2 x 1 you might guess a higher number compared to your guess of the result for 1 x 2 x 3 x 4 x 5 x 6 x 7 x 8, because the first number in that calculation (1 versus 8) influences your judgment.

So the theoretical difference is that while in priming one stimulus influences the processing of another, later stimulus, in anchoring the form of the beginning of the information influences the processing of the whole information.

Nevertheless it has been suggested that anchoring is caused by an underlying priming (Mussweiler & Strack, 1999; from the abstract):

  Results of four studies support the notion that anchoring effects are mediated by
  mechanisms of hypothesis-consistent testing and semantic priming. ... Study 4 suggests that self-generation of knowledge contributes to the robustness of the effect, thus resolving the seeming inconsistency that anchoring effects are at the same time remarkably robust and mediated by typically fragile semantic priming mechanisms.

Sources:

Mussweiler, T. & Strack, F. (1999). Hypothesis-consistent testing and semantic priming in the anchoring paradigm: A selective accessibility model. Journal of Experimental Social Psychology, 35, 136-164. doi:10.1006/jesp.1998.1364 Available online at http://www.communicationcache.com/uploads/1/0/8/8/10887248/hypothesis-consistent_testing_and_semantic_priming_in_the_anchoring_paradigm-_a_selective_accessibility_model.pdf


Why this guilt discrepancy in human beings?

Lack of guilt is related to psychopathy, although there could be other reasons for it, e.g. ideological self-justifications, like breaking a law you don't agree with. Psychopathy is partially inheritable, which means the genetically-unexplained variance is usually attributed to enivronmetal differences.

The propensity for guiltlessness is part of a narrower trait (of psychopathy) called "callous-unemotional traits", and these can be identified around the age of 7, according to one (fairly cited) study of Viding
 et al. (2005). Although the abstract of this paper is a bit... abstract, its intro is a bit more insightful what it is talking about:

  ‘Mark does not feel guilty if he has done something
  wrong, he does not show feelings or emotions, and he
  is rarely helpful if someone is hurt.’ This description
  of one of the 7-year-old children (name changed) in
  our twin study captures the core emotional impairment
  of individuals with psychopathy. Psychopathy
  in both childhood (psychopathic tendencies) and
  adulthood involves both affective-interpersonal
  impairment (callous-unemotional traits; e.g., lack of
  empathy, lack of guilt, shallow emotions) and overt
  antisocial behaviour.


Should fantasy distractors be avoided in multiple choice questions

I would say no, there's no reason not to, and in fact it might be better, based on the following rather speculative reasoning.

In general, despite the general benefits of testing for learning, multiple choice testing can also lead to subsequent memory for incorrect responses, i.e. it can cause students to learn false responses.

  Marsh, Roediger, Bjork, & Bjork (2007) "The memorial consequences of multiple-choice
  testing." Psychonomic Bulletin & Review, 14(2) 194-199

This doesn't explicitly compare fantasy answers to other misleading answers, but intuitively, it seems that such "false learning" would be MORE likely to be reinforced in the future for plausible responses than for fantasy responses.  The reason is that fantasy responses are unlikely to ever be encountered again, while plausible responses might be, leading to reinforcement of the false learning.

See also here regarding avoidance of false learning from multiple choice testing:

  Little and Bjork (2012) "The persisting benefits of using multiple-choice tests as
  learning." Proceedings of the 34th Annual Conference of the Cognitive Science Society.


Color constancy works only if the incident illumination contains a range of wavelengths. The different cone cells of the eye register different but overlapping ranges of wavelengths of the light reflected by every object in the scene. From this information, the visual system attempts to determine the approximate composition of the illuminating light. This illumination is then discounted in order to obtain the object's "true color" or reflectance: the wavelengths of light the object reflects. This reflectance then largely determines the perceived color.

Source

It is also known that the color constancy of humans is subject to individual differences. The perception of painters like Claude Monet but also landscape photographs illustrate that attention and learning processes play a role while performing color constancy.

Anya Hurlbert: Colour vision: Is colour constancy real? Curr Biol. 9(15): 1999: R558-561, Review Article


The travel experience etc, are episodic memories. The duration of these memories mostly depend on emotion and novelty.

The typing and singing, are procedural memories. They are formed with practice. Repetition and consistency are the two most important factors for this type of memory. We do not have any conscious access to procedural memory, we simply perform what we know.

The PIN memory can be explained with cued recall. The image of the post office is associated with the PIN, so whenever you imagine the post office the PIN number is also activated.


What is the optimal mean correct on a multiple choice test in order to maximise the measurement of individual differences?

My understanding is that in general a percentage correct of 50% is optimal where there is no scope for guessing.
However, on multiple choice tests there is a certain number of response options. Thus, the probability of getting the correct answer if you know nothing, is one over the number of response options.

In this case I believe that the optimum is:

$$1/k + \frac{1 - 1/k}{2}$$

where k is the number of response options.

So the optimum for different values of k would be:

k = 2: optimum proportion correct = 0.75
k = 3: optimum proportion correct = 0.67
k = 4: optimum proportion correct = 0.625
k is infinite: optimum proportion correct = 0.50

That said, I'd still like to find the classic references where I obtained these ideas from. And I imagine item-response theory might have a little more to say about this, particularly regarding the common recommendation to vary the proportion correct over a range.

Furthermore, none of the above recommendations address the issue that setting the difficulty at the above level for most items can be intimidating for some test takers.


At what age a child would develop a sense of racism or a minority discrimination?

Children as young as two to three years old are able to pick up on racial categories and stereotypes, and to infer that others' behavior is driven by race (also gender and other categories).

Of course, at that age children are actively exploring causes in the world of all types, so a comment asking about Arabic language does not mean that a child is experiencing extensive discrimination due to race - on the other hand, I think it would be naive to think anyone with any minority characteristic is not experiencing any discrimination ever, especially in comments from other kids who are themselves learning about the world and other people. It also could have been something overheard on TV, it could have been from a discussion of discrimination rather than an experience, etc.

Corenblum, B., & Annis, R. C. (1993). Development of racial identity in minority and majority children: An affect discrepancy model. Canadian Journal of Behavioural Science/Revue canadienne des sciences du comportement, 25(4), 499.

Hirschfeld, L. A. (2008). Children’s developing conceptions of race. Handbook of race, racism, and the developing child, 37-54.

Katz, P. A., & Kofkin, J. A. (1997). Race, gender, and young children. Developmental psychopathology: Perspectives on adjustment, risk, and disorder, 21, 51-74.

Pauker, K., Ambady, N., & Apfelbaum, E. P. (2010). Race salience and essentialist thinking in racial stereotype development. Child Development, 81(6), 1799-1813.

Taylor, R. G. (1966). Racial stereotypes in young children. The Journal of Psychology, 64(2), 137-142.


Are there any programmes to identify modular "NeuroBricks"?

Assuming that by "neurobricks" you imply the ability to design systems using modular neuronal components, then I think the Neurological Engineering Framework (NEF) and Nengo, the software used to leverage the NEF, is what you're looking for.

Essentially, groups of neurons fire together as a way to encode information from various sources. So you can get simple things like an integrator or something that keeps track of where to move a joystick (like in the research by Georgopolous), but that can scale up (because it's just a group of neurons) all the way to a complex model of the brain like Spaun.

In terms of engineering applications, there's a lot of things that these neurons are particularly good at, such as robotic arms, as shown in Spaun.


What is the current status of tetrachromacy in humans?

Jordan et al. (2010) tested humans that carry the genetic predisposition for having 4 classes of cone receptors. However, only one of their 24 subjects was able to discriminate three color dimensions, thus, demonstrated tetrachromacy.

  Jordan G, Deeb SS, Bosten JM, Mollon JD. (2010). The dimensionality of color vision in carriers of anomalous trichromacy. Journal of Vision. 10(8):12. [Free PDF]

  Abstract

  Some 12% of women are carriers of the mild, X-linked forms of color vision deficiencies called "anomalous trichromacy." Owing to random X chromosome inactivation, their retinae must contain four classes of cone rather than the normal three; and it has previously been speculated that these female carriers might be tetrachromatic, capable of discriminating spectral stimuli that are indistinguishable to the normal trichromat. However, the existing evidence is sparse and inconclusive. Here, we address the question using (a) a forced-choice version of the Rayleigh test, (b) a test using multidimensional scaling to reveal directly the dimensionality of the participants' color space, and (c) molecular genetic analyses to estimate the X-linked cone peak sensitivities of a selected sample of strong candidates for tetrachromacy. Our results suggest that most carriers of color anomaly do not exhibit four-dimensional color vision, and so we believe that anomalous trichromacy is unlikely to be maintained by an advantage to the carriers in discriminating colors. However, 1 of 24 obligate carriers of deuteranomaly exhibited tetrachromatic behavior on all our tests; this participant has three well-separated cone photopigments in the long-wave spectral region in addition to her short-wave cone. We assess the likelihood that behavioral tetrachromacy exists in the human population.


Can alter-personas of a person with MPD/DID have mental diseases of their own that other 'alters' don't have

Yes.  For example, people suffering from DID can also suffer from depression.

See DID

Since, by definition "dissociative identity disorder is characterized by the presence of two or more distinct or split identities or personality states that continually have power over the person's behavior. ... ", then the other disorder (e.g. depression) can be unique to a persona.


Is there any plausible answer for naturally explaining veridical perception in near death experiences?

There is no evidence that "the mind is a soul". This is what's known as the "hard question of consciousness".

There has been some research conducted on "out-of-body" experiences. The only one I can remember offhand was a couple of years ago where words and numbers were placed on top of cabinets in operating theatres. The logic behind this was that if anyone genuinely had an out-of-body experience while under anaesthesia, they would be able to read, and later recall, these words and numbers. I hope I'm not misquoting the findings (I'm doing this from memory), but I seem to recall that they found no evidence whatsoever for these experiences.

It is far more likely that experiences prior to death are hallucinatory and caused by chemical changes, or degradation, of the brain. In a similar way, out of body experiences in an operating theatre are almost certainly the result of similar hallucinations.


What's the most appropriate statistical analysis to run for a correlational study?

Although you have two times of testing, you really just have two binary variables and you'd like to know if they are associated, there are no repeated measures here. You'd like to know if the value of one binary variable depends on the value of the other binary variable. I'll call them A,B and X,Y.
If there is no relationship between A,B and X,Y, then you expect the ratio of X:Y to be the same for A as it is for B (this is your null hypothesis). You can examine your data by building a 2x2 contingency table with cells AX, AY, BX, and BY.
You can test the null hypothesis described with a chi-square test for independence, or Fisher's exact test if the sample size is fairly small.


Are different types of long term memories stored in different parts of the brain?

Just to add to Jens answer, opinion is still divided regarding whether memory is subserved by distinct systems, or is a distributed, emergent property of perceptual, navigational and semantic systems. Whereas patient data has always strongly implicated distinct memory systems (e.g., declarative vs non-declarative), multivariate fMRI studies have provided good support for reinstatement theories, where successful retrieval of memories involves reinstatement of perceptual states. Moreover, there is growing evidence that regions that are thought to be amodal memory structures (e.g., hippocampus, perirhinal cortex), are involved in perceptual discrimination judgements and show preferences for different categories of visual input. For example, damage to the hippocampus can impair scene discrimination judgements whereas damage to the perirhinal cortex can impair face and object discrimination judgements. So it could be the case that there really aren't any dedicated memory structures per se, but memory is the co-ordinated reactivation of mechanisms involved in perception and action (probably via top down signals from frontal lobes).

The references provided by Jens provide good coverage of the distinct systems view of memory so I'll just provide some references for the distributed and reinstatement views.

References

Murray, E. A., Bussey, T. J., & Saksida, L. M. (2007). Visual perception and memory: A new view of medial temporal lobe function in primates and rodents. Annual Review of Neuroscience, 30, 99-122.

Graham, K.S., Barense, M.D. & Lee, A.C.H. (2010).  Going beyond LTM in the MTL: a synthesis of neuropsychological and neuroimaging findings on the role of the medial temporal lobe in memory and perception.  Neuropsychologia, 48, 831-853.

Polyn S.M., Natu V.S., Cohen J.D., & Norman K.A. (2005) Category-specific cortical activity precedes recall during memory search. Science, 310, 1963-1966.

Johnson, J. D., McDuff, S. G. R., Rugg, M. D., & Norman, K. A. (2009). Recollection, familiarity, and cortical reinstatement: A multivoxel pattern analysis. Neuron, 63, 697-708

Xue G, Dong Q, Chen C, Lu ZL, Mumford JA, Poldrack R (2010). Greater Neural Pattern Similarity Across Repetitions is Associated with Better Memory. Science, 330, 97-101.


You will have to investigate quite a few factors:

There must be a genetic/epigenetic factors to this because we know that personality trait neuroticism has genetic and environmental factors.
You should also investigate into stress - biological and psychological stress.
Investigating theories of psychological development can also come in handy, especially, Freudian theories.

In my personal view, I think a combination of genetic and environmental factors should play role in shaping irritability tolerance, however, additionally environment plays a role of stressor.

In other words, you should have genetics, epigenetics and upbringing as a predictors of general irritability. Immediate state of being can also have influence, but stressor is like a trigger.


How far can a signal travel in the neocortex without passing through the white matter?

The distance of horizontal communication depends on species, cortical region, and cortical layer. Very few combinations of those 3 factors have ever been studied. For the combinations with which I am familiar, most horizontal connections are limited to a few hundred microns, though some are as long as a few millimeters. Most of that distance is axonal because dendrites are generally much shorter than axons. Of all the connections I've read about, none span an entire region. To get across a region, a connected series of signals would have to make several hops through several neurons and across several synapses, as you suggested in your question.

The direct path of an axon connecting two cortical areas (or an axon from a subcortical area to a cortical area) is through the white matter, but sometimes an axon will additionally ascend to layer I of the target area before branching, presumably to save space. This is the main use of layer I, and the lengths of these connections is several millimeters or centimeters.

I have never heard of the longer-distance horizontal connections that you suggest occur in layer II; layers II through VI contain neurons with short horizontal and vertical connections.

References

  Alonso, J.-M. (2002) Neural Connections and Receptive Field Properties in the Primary Visual Cortex. The Neuroscientist. 8(5): 443-456.
  Feldmeyer, D. (2012) Excitatory Neuronal Connectivity in the Barrel Cortex. Frontiers in Neuroanatomy. 6: 1-22.
  Rockland, K.S. and Virga, A. (1989) Terminal Arbors of Individual Feedback Axons Projecting from Area V2 to V1 in the Macaque Monkey: A Study Using Immunohistochemistry of Anterogradely Transported Phaseolus vulgaris-leucoagglutinin. The Journal of Comparative Neurology. 285: 54-72.


Here's a quick answer from general background knowledge, not from any specific knowledge of "Bayesian Program Synthesis (BPS)"

In general, Bayesian models can use strongly informed priors or diffuse "could be anything" priors. Strong priors specify that a lot of parameter values are very unlikely, while a few other parameter values are possible descriptions of the data. With a strong prior, it takes relatively little data to winnow down the possibilities (i.e., faster learning). Weak priors allow for a much broader range of possibilities, but it takes a ton of data to narrow down the possibilities (i.e., slower learning).

Many Bayesian models of mind use strong priors. Such models come pre-set with particular structure or parameter dependencies that are tuned for the type of problem that needs to be learned. This is not "cheating;" the prior is a crucial part of the theory. Another example comes from computer vision: Figuring out what objects and lighting produced a pixelated 2D image can only be done by assuming strong prior knowledge of the types of objects and types of illumination "out there" in the world, otherwise it's an unsolvable problem. An introductory article is here or here (specifically, see the section on "Prior Knowledge" starting on p. 17).

Deep learning, however, is (as far as I know) a generic approach that can learn just about any possible relationship among variables. The cost of this weak prior is that it takes a ton of training to narrow down the parameter distribution.


Is there a metric of the overall excitation of the brain or nervous system?

MEGs using SQUIDs can detect magnetic flux density measured in teslas. Away from sleep studies and epileptic brain activity, this should be a useful indicator of relative brain arousal. Readings from two different people on this scale should be comparable  based on the orders of magnitude for the unit measurement. As for comparative measurements of brain arousal, I don't think Actigraphy would be useful, nor any other method of measuring somatic motion. These can certainly determine weather a person is sleeping, sedentary, or exercising, but discriminating between different sedentary behaviors would be difficult and determining relative brain activity for those behaviors would be reliant on more traditional methods (EEG,MEG, etc). MRI methods might be useful, as the total change in blood oxygen volume from a base state or inactive state can be distinguished from a more active state.


Sleeping is a usual, necessary process for memorization and brain rest. It is commonly known that there are two phases of sleeping: rapid eye movement sleep (REM) with high brain activity and non-rapid with low activity and usually without dreams. When you get tired and fall asleep, you enter directly into second, non-rapid phase, and your internal discourse stops. Obviously, this brain state doesn't differ faster processes.

During REM sleep there are some images, dreams in your head, combinations of ideas, memories and worries, which aren't useful, since brain erases most of it. But there is one interesting technic, lucid dream. Using that you can keep consciousness when falling asleep or get it while sleeping. You can control dreams, do whatever you want, even control memories, if you got high skill.

And what about speed of this REM condition? Despite the rapid eye-movements, this condition also doesn't provide high speed of thinking. Sometimes (e.g. during a nap or while awakening) you can have dreams and feel, hear things round you; and you can observe that your dreams and real world go at the same speed. However, when you awoke, thanks to special chemical mechanisms you forget dreams, it seems dim and far - that makes the illusion of fast feelings.

So, the answers are:

No, it is just another kind of brain work.
You can learn lucid dreaming. Also you may just try remember dreams every morning, e.g. I keep dreams diary for a few years and now can remember about 5 dreams per night, when I started from 1 dream per month.

I'd like to add, from mine and friends experience, there is nothing very interesting or useful about remembering or controlling dreams. It is a real trash for mind, although unusual trash.


Does sugar change our short-term behaviour?

You are what you eat right? I guess that would probably apply with how internal physiological responses to food consumption may result in various behaviours.

According to Flora and Polenick (2013), there are some counter-intuitive evidence about sugar and its effects on human behaviour:

  "To this point, what is known about the effects of sugar consumption on
  human  behavior and performance is that sugar consumption, even in
  high amounts, does not  contribute to hyperactivity, inattention,
  juvenile delinquency, reductions in cognitive  performance, or other
  behavior problems in children or adults. Instead, a high level of
  glucose, or sugar, consumption actually improves athletic, academic,
  and cognitive  performance, and may enhance self-control. Sugar
  consumption may reduce aggressive  behavior, and sugar consumed during
  breakfast and in afternoon snacks improves  performance during a wide
  range of activities."

Notably, they indicate that sugar can reduce aggression in both children and adults and implied aggressive behaviour:

  "Just as Bachorowski et al. (1990) observed improved behavior of
  juvenile delinquents  after they consumed a sugar-filled breakfast,
  research suggests that sugar consumption  may reduce aggressive
  behavior in adults, as well as in children. Benton and Owens (1993)
  found that, compared to undergraduate participants who consumed a
  placebo non-sugar  beverage, participants who consumed a sugar
  beverage were less likely to show aggression,  use profanity, or bang
  on the computer while playing a frustrating and intentionally
  impossible computer game."


Is it reasonable to have a factor with only two levels in a carry-over design for an fMRI study?

I'm not an expert in neuroimaging, so I had to search a little bit to learn about how carry-over designs apply to fMRI (I found Aguirre, 2007). Thus, feel free to correct me if there is something specific about this problem domain that influences the correct answer to this question.

However, based on general principles of experimental design of repeated measures experiments, you always have to choose

how many factors you want,
how many levels you want for each factor,
what levels you have for each factor, and
what factors you hold constant.

The particular levels you choose are directly tied to your research question. There are often trade-offs between the cost of resources required to have more experimentally manipulated levels and the benefit of additional questions that can be answered. Thus, I don't think a black and white answer can be given. You need to weigh up the pros and cons.

And presumably you have already made many experimental design decisions to get to this point. There's nothing magical about 3 levels to a factor. If anything, in experimental psychology two levels seems more common. And you could have four or five or more.

References

Aguirre, G.K. (2007). Continuous carry-over designs for fMRI. Neuroimage, 35, 1480-1494. HTML


What does "dimensionality of power distance" mean?

Hofstede has developed a cultural dimensions theory to compare countries, which uses factor analysis to assign values across 6 dimensions of culture.
These dimensions are:

Power Distance Index
Individualism vs Collectivism
Masculinity vs Femininity
Uncertainty Avoidance Index
Long Term Orientation vs Short Term Orientation
Indulgence vs Restraint

That's all their seems to be when it comes to defining the term 'dimension': a measurable aspect of a situation. As for power distance, as you have already quoted as "the extent to which the less powerful members of institutions and organisations within a country expect and accept that power is distributed unequally", basically means how readily the people of the culture accept hierarchies and inequalities of power. A larger power distance would imply a wider gap between people at different levels of the hierarchy, and greater acceptance of this gap with lesser questioning or asking for justifications.


Why does a neuron choose to connect to another?

Donald Hebb originally formulated what would later come to be known as spike-time dependent plasticity by famously stating "neurons that fire together wire together". In actuality, the firing has to be sequential (not simultaneous) and causal: if a neuron A fires and causes B to consequently fire, the synaptic strength between them increases. This is how the brain implements learning and memory. [1] This principle fits with the idea that the brain essentially learns causal relationships that exist in the world, as formalized in the Bayesian brain hypothesis [2].

[1] Markram et al., "A history of spike-timing-dependent plasticity": http://infoscience.epfl.ch/record/168812/files/fnsyn-03-00004.pdf

[2] Clark et al., "Whatever next? Predictive brains, situated agents, and the future of cognitive science": http://www.fil.ion.ucl.ac.uk/~karl/Whatever%20next.pdf


Is it possible to think in a second language?

It is possible for some people to think in a second language. And given that you are asking about possibility, to some extent anecdotes are evidence.

Many children who change linguistic communities at a young age lose the ability to talk in their first language. This is particularly the case where the first language is different to the language in which parents speak to their children.
In less extreme cases I have friends who came to an English speaking country at a young age, but still retained the ability to speak in their native language. Nonetheless, the vast majority of the time, they speak English. I assume that at a certain point, they switched from primarily thinking in their native language to primarily thinking in English. One friend mentioned the experience of when at around age 14, his dreams began to switch from being in Polish to being in English.

I guess the interesting question is whether there are limits to this, such as when the second language is not learnt until teenage years or adulthood.

In terms of a few hypotheses, I would think that ability to think in a second language would be linked to (a) greater fluency with the second language which in turn would be linked to experience and training and (b) specific primary training in the content of the thoughts in the second language (e.g., if you study a subject at university in the second language and thus you may know the terms better in the second language). Also from my limited experience of learning French, it felt like there was a degree of choice whereby I could actively try to think in French. That said, the cognitive associations between underlying concept, English word, and French word were pretty strong. Thus, the subjective experience of thinking in French and translating from English to French was often subtle.

Note also that I'd still be interested in any research that has specifically studied this phenomena.


Is cognitive science a concentration of psychology?

It's the other way around: Psychology is a discipline within Cognitive Science, which includes Artificial Intelligence, Neuroscience, and possibly Philosophy of Mind.  Research work in Psychology presumably makes you a Cognitive Scientist.


Do bodily manifestations (e.g. jerking) and intense euphoric sensations (e.g. "heat", "electricity") always co-occur in spiritual experiences?

An inherent problem with the line of investigation is that the exhibited behaviours are inconsistent with the claimed emotions.  In no other situation do the emotions of love, peace, ecstasy and euphoria result in the performance of behaviours such as glossolalia, collapsing, fainting, trembling, jerking, convulsing, contorting and shaking.  More likely causes of involuntary jerking, convulsing, contorting and shaking may include anxiety, seizure, and myoclonus. Given the incongruity and incompatibility of the emotions and behaviours, it may seem that they are entirely unrelated; however, it is possible that there is an antecedent cause of both. To assist with this analysis, the following mathematical notation is introduced:

Let R be the reporting of particular emotions (love, peace, ecstasy and euphoria).  Note, that the reported emotions may not be the actual emotions.
Let B be the performance of the behaviours (glossolalia, collapsing, fainting, trembling, jerking, convulsing, contorting and shaking).
Let C be the cause of R under certain conditions.
Let C be the cause of B under certain conditions.
Let A be the actual emotions (not necessarily the reported emotions R).

Analysis

If C always causes R and always causes B, then R and B will always co-occur.
If C causes B under certain conditions and C causes R under different conditions, then B and R will not necessarily co-occur.

Note: In this analysis, it is important to note that the reporting of emotions (R) is not the same as actually experiencing the emotions (A). For the reasons given above, it is asserted that the reported emotions (R) can not cause the behaviours (B), and by implication, the reported emotions (R) are never the same as the actual emotions being experienced (A). See dramaturgy and self-monitoring as a possible explanations of this.
In the answer to one of your earlier questions, eight strawman hypotheses were offered to explain the claimed emotions (R) and observed behaviours (B):

Unidentified invisible force.
Hysterical state induced by the leader
Hysterical state induced by the individual:
Conformance to the social norms
Functional Neurological Disorder (FND)
Paid actors
Hypnosis
Attention seeking

Of the eight hypotheses, six were excluded as being implausible, leaving only 4) Conformance to the social norms and 8) Attention seeking as being plausible explanations, which I will consider individually.
Conformance to the social norms:  In this case, the cause (C) is the desire to conform.  Whether C results in R and B would be governed by the social norms of the particular religious group.  It may be possible for one particular religious group to emphasise the reporting of emotions (R) and place less emphasis of the behaviours (B) (or vice versa), in which case, the answer to your question is “No”, that is, the observed behaviours and reported emotions do not necessarily co-occur.  However, in religious groups that emphasize both the reporting of emotions and the performance of the behaviours, then it is more than likely that both will co-occur.
Attention seeking:  In this case, the cause (C) is the desire to gain the attention of others.  Whether C results in R and B would be governed by whether the attention seeking individual assessed that either or both R and B are necessary to gain the desired attention. The attention seeking individual may be seeking the attention of only one person, a sub-group, or the entire religious group.  If the attention seeking individual is seeking the attention of the entire group, then the analysis is virtually identical to Conformance to the social norms analysed above.  If the attention seeking individual is seeking the attention of only one individual, then the attention seeking individual would assess whether B and/or R are necessary to gain the desired attention.  In this situation, it is not possible to say that R and B would always co-occur, however, if the interaction occurred in the confines of one of the relevant religious groups, then it seems more likely that the R and B would co-occur.
In conclusion, it is not necessary that the reported emotions (R) and observed behaviours (B) co-occur, however, it is likely in practice that they often do due to the social norms of the particular religious cults.


What human factors play part in traffic congestion?

Kesting, Treiber and Helbing (2000) created an Intelligent Driving Model (IDM) based on actual data on the German highway. The model is a single lane model, assuming that the trailing car tries to fixate the distance of the leading car by accelerating and decelerating only.

From Kesting, Treiber and Helbing (2008):

  The IDM acceleration is a continuous function incorporating different driving modes for all velocities in freeway traffic as well as city traffic. Besides the distance to the leading vehicle s and the actual speed v, the IDM also takes into account velocity differences ∆v, which play an essential stabilizing role in real traffic, especially when approaching traffic jams and avoiding rear-end collisions (see Fig. 3). The IDM acceleration function is given by:

work in progress. To be continued


Does long-term alcohol use permanently change one's thought processes?

I am only addressing the  extreme end of the spectrum of chronic alcohol abuse:
One syndrome that is known to develop from chronic alcohol abuse id Korsakoff's syndrome or Wernicke-Korsakoff syndrome.
It causes memory loss and a form of dementia. An irreversible brain damage that permanently disables the individual. The individual is unable to function within society and carry out the daily tasks necessary for functional living. It can also include psychosis.

  Korsakoff syndrome is most commonly caused by alcohol misuse,...//...

  Korsakoff syndrome causes problems learning new information, inability
  to remember recent events and long-term memory gaps. Memory problems
  may be strikingly severe while other thinking and social skills are
  relatively unaffected. For example, individuals may seem able to carry
  on a coherent conversation, but moments later be unable to recall that
  the conversation took place or to whom they spoke.

  Those with Korsakoff syndrome may "confabulate," or make up,
  information they can't remember. They are not "lying" but may actually
  believe their invented explanations. Scientists don't yet understand
  why Korsakoff syndrome may cause confabulation. (1)
  ....
  Scientists don't yet know exactly how Korsakoff syndrome damages the
  brain. Research has shown that severe thiamine deficiency disrupts
  several biochemicals that play key roles in carrying signals among
  brain cells and in storing and retrieving memories. These disruptions
  destroy brain cells and cause widespread microscopic bleeding and scar
  tissue. (1)

....

  Lack of vitamin B1 is common in people with alcoholism....//..
  Korsakoff syndrome, or Korsakoff psychosis, tends to develop as
  Wernicke symptoms go away. Wernicke encephalopathy causes brain damage
  in lower parts of the brain called the thalamus and hypothalamus.
  Korsakoff psychosis results from permanent damage to areas of the
  brain involved with memory.   (2)
  ....
   Symptoms of Wernicke encephalopathy include:
  - Confusion and loss of mental activity that can progress to coma and
  death
   - Loss of muscle coordination (ataxia) that can cause leg tremor
  -  Vision changes such as abnormal eye movements (back and forth
  movements called nystagmus), double vision, eyelid drooping
  Alcohol withdrawal Symptoms of Korsakoff syndrome:
  -  Inability to form new memories
  -  Loss of memory, can be severe
  -   Making up
  stories (confabulation)
  - Seeing or hearing things that are not really there (hallucinations) (2)

 (1) Korsakoff Syndrome
Alzheimer's Association
(2) A.D.A.M. Medical Encyclopedia.
Wernicke-Korsakoff syndrome
Korsakoff psychosis; Alcoholic encephalopathy; Encephalopathy - alcoholic; Wernicke's disease
Last reviewed: February 27, 2013.


Quoting from one paper, which doesn't say all that much:

  The experience of nakedness under the gaze of others is highly diverse, and
  important background differences will affect the relative comfort with which one
  might strip in front of others.

Cover, R. (2003). The naked subject: Nudity, context and sexualization in contemporary culture. Body & Society, 9(3), 53-72. DOI: 10.1177/1357034X030093004

And from one of the few studies of nudists in the US, back when this was more common over there (that is 1964):

  Among changes reported by nudists were “less concern
  with appearance,” “reduced anxiety,” “more benevolence,” and “less inhibition.”

Casler, L. (2010). Some Sociopsychological Observations in a Nudist Camp: A Preliminary Study, The Journal of Social Psychology, 64:2, 307-323

Fairly similar findings from a nude group therapy "marathon" (24hrs session):

  Nudity apparently facilitates group interaction in a marathon. 17 of 20 participants felt that the factor of nudity increased their ability to open up to each other emotionally and to achieve a greater degree of authenticity and transparency. The group integrated and seemed to become therapeutically functional more rapidly than clothed marathon groups

Bindrim, P. (1968). A report on a nude marathon: The effect of physical nudity upon the practice of interaction in the marathon group. Psychotherapy: Theory, Research & Practice, 5(3), 180-188

And a pretty interesting discussion contrasting the German and UK cultural differences in how sexuality relates to social nudity is found in
Smith, G., & King, M. (2009). Naturism and sexuality: Broadening our approach to sexual wellbeing. Health & place, 15(2), 439-446.


i once wrote a paper doing biophysical modeling of neurons that could create plateau potentials.  While the paper itself is not exactly what you are looking for, there should be lots of good references in there:
http://www.jneurosci.org/content/33/2/424.short
Sanders H, Berends M,
Major G,
Goldman MS,
Lisman JE. (2013) NMDA and GABAB (KIR) Conductances: The “Perfect Couple” for Bistability. J. Neurosci. 33, 424–429

also, check other articles that cited that paper: https://scholar.google.com/scholar?cites=2120401607202660739


Depression Causing Body Dysmorphic Disorder (BDD)

TLDR version: it appears depression-as-a-risk-factor-for-BDD hasn't actually been studied, so the quoted UK NGO claims might stem from a blurring of risk factors and comorbidity.

Let's start by recalling what risk factor actually means (it does not mean cause):

  Risk factors are characteristics at the biological, psychological, family, community, or cultural level that precede and are associated with a higher likelihood of negative outcomes.

So support the quoted passage in your question, one would only have to show that depression (from whatever cause) can happen before BDD in some individuals. If someone is predisposed to "go off the deep end" because of their body, they could possibly do that for any other perceived insufficiency in themselves (like thinking they're not being smart enough). The criteria to BDD are extremely specific, only a preoccupation with physical appearance counts; if someone ruminates or obsesses or over their (perceived) lack of intelligence, that doesn't qualify for BDD. With this in mind, depression being a risk factor for BDD doesn't so improbable.

Alas, I came up empty for an actual longitudinal study where depression got worse before BDD... but I did find one close enough:

  We found several significant longitudinal associations between BDD and the comorbid disorders we examined. The association was strongest for depression. Time-varying associations showed that improvement in BDD and major depression were closely linked in time, with significant associations in both directions: improvement in major depression predicted BDD remission, and improvement in BDD predicted major depression remission. This finding suggests that the same etiologic processes contribute to both BDD and major depression in some subjects.

The reason they could only talk of improvements (and not deterioration) is that this study had a treatment-based time frame. So there's wasn't much in the way of naturalistic observation sans treatment. That would probably require a much longer time scale... and I'm not convinced someone could get funding for that... especially since it raises ethics questions like observing depression getting worse in some patients but not doing anything about it, just so BDD aggravation could be observed.

On the other hand, the common sense logic (that you had) that depression might usually come after BDD, turns out to be supported by this study (well, again based on remission):

  in our sample depression may be largely secondary to BDD for many subjects, as a substantial proportion remitted from major depression following BDD remission. Conversely, after remission of depression, BDD tended to improve but less markedly. Our findings additionally suggest that BDD is not simply a symptom of depression. If it were, BDD would be expected to remit around the time of depression remission and during subsequent months.

Frankly, I suspect that the NGO page in question might have simply confused (or amalgamated) risk factors with comorbidity. I'm saying this because a 2015 research paper notes that very little is know about risk factors for BDD. According to that paper, the only things which have been investigated as risk factors for BDD being:

"perceived teasing about general appearance"
"emotional, physical, or sexual abuse or neglect resulting in poor
attachment and body shame"
"a genetic predisposition for a need for symmetry or order"
"being excessively self-conscious about appearance changes during adolescence"

So, my conclusion from all this: it sounds somewhat plausible that depression is a risk factor for BDD (based on the common etiology [in some people] hypothesis), although it doesn't seem to have been formally/directly investigated, and the reverse occurence of events (BDD first, then depression) sounds a bit more common/likely.


What is the concordance rate for schizophrenia in monozygotic and dizygotic twins?

The Wikipedia article seems to provide a summary of this information with links to the primary literature

http://en.wikipedia.org/wiki/Causes_of_schizophrenia#Genetics

  Concordance rates between monozygotic twins vary in different studies,
  approximately 50%; whereas dizygotic twins was 17%. Some twin
  studies (Koskenvuo et al; Hoeffer et al) have found rates as low as 11.0%–13.8% among
  monozygotic twins, and 1.8%–4.1% among dizygotic twins, however.

References

Koskenvuo M, Langinvainio H, Kaprio J, Lönnqvist J, Tienari P; Langinvainio; Kaprio; Lönnqvist; Tienari (1984). "Psychiatric hospitalization in twins". Acta Genet Med Gemellol (Roma) 33 (2): 321–32. PMID 6540965.
Hoeffer A, Pollin W; Pollin (November 1970). "Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs". Arch Gen Psychiatry 23 (5): 469–77. doi:10.1001/archpsyc.1970.01750050085012. PMID 5478575.


Is there evidence of suppression of the frontal cortex during herding behavior?

This is probably not a complete answer to your question.

There have been a few studies on this relationship.

This article from the Journal of Neuroscience "Downregulation of the Posterior Medial Frontal Cortex Prevents Social Conformity" (Klucharev et al. 2011) approach the research (from their abstract):

  Here we demonstrate that the transient downregulation of the posterior medial frontal cortex by theta-burst transcranial magnetic stimulation reduces conformity, as indicated by reduced conformal adjustments in line with group opinion.

This article may also be of interest


What is the conceptual difference between causal inference and 'prediction'

Correct me if I'm wrong here, but after some more reading and thinking this is what I took away: both the term 'prediction' and 'cause' here refer to the maximum likelihood of a distribution ($Y$), meaning the probability of an event ($X$), given sensory data ($Y_{1}$) and the likelihood given prior data ($Y_{2}$) .
Even though maybe seemingly orthogonal to some (like me), the terms here would actually represent the same thing (i.e. no difference).
Please post a better answer if this is partially or completely incorrect =)


What is the difference between Cognitive Bias and Cognitive distortion?

Wikipedia has articles on both of these terms, so that would be one place to start. Although you may not be able to cite Wikipedia as a source, both of these articles have good References sections.
Here are the Wikipedia definitions (emphasis added):

Cognitive bias: "a systematic pattern of deviation from norm or rationality in judgment."
Cognitive distortion: "an exaggerated or irrational thought pattern involved in the onset or perpetuation of psychopathological states, such as depression and anxiety."

So both of these terms apply to thought patterns that deviate from a theoretical rational standard. But cognitive distortions apply specifically to states considered psychologically abnormal, while cognitive biases refer to properties of human thinking that tend to affect everyone. The examples given in the articles seem to support this distinction.
As you mentioned, cognitive distortions could be seen as a subset of cognitive biases, specifically the subset that leads to psychopathological conditions.


How well are neurotransmitters used in SPA?

At this point in time, the difference in neurotransmitter types affect the synaptic time constant (i.e. the filter on the incoming spike train) between neurons in Nengo. See Neural Engineering p.112 and these notes (see the section called "Biologically plausible filter") from a course covering the book.

Neurotransmitters are also leveraged more theoretically. For example, in connection between neurons that involve learning, dopamine is often said to modulate this learning. For example, see Dan Rasmussen's neural hierarchical reinfrocement learning implementation (PHD link pending).

Hypothetically, it would be possible to implement a back-end to Nengo using a more biologically detailed software such as Neuron to take into account neurotransmitter generation, concentration and consumption. Although I can attest anecdotally that this has been attempted with mixed success, there has been no formal release or publication of this approach.


Is there a scientific term for when you fall asleep because you can't handle something?

I'm not completely sure, but you may be referring to Syncope, a medical term which describes events such as fainting or passing out which occurs upon low blood flow to the brain. As a result it can occur when under shock or trauma or a post-effect of stress.

Obviously, one would expect the opposite to happen in half the events, such as after vomiting, however when you said

  have some major upheaval in their life, or experience some other trauma (e.g., a bad breakup, losing a job, etc.). When the mind can't cope it simply shuts off and they fall asleep or pass out.

I realised you may be relating to someone feeling a depressed, in which case lowering of blood pressure is possible and thus he or she could suffer from syncope.

In all honesty it is simply a technical term for fainting, and is more commonly used for people who suffer a disorder which will cause them to faint often.


Can humans really successfully multitask?

"Trying to do two things at once is usually a recipe for doing both badly, according to a long line of research. We’re slower and less accurate when we try to juggle two things."

Generally, it is thought that multi-tasking is just the brain rapidly shifting its focus from one matter to another instead of doing both (or several) things simultaneously. This is very straining and distracting for the brain, and so it ends up doing less well on both tasks than it would if the tasks were done separately.https://www.apa.org/research/action/multitask.aspx

However, there is an interesting article that says there might be more going on that that. The article explains 2 studies done that seem to indicate that our ability to perform a task might depend on the context in which we learnt to perform the task. E.g. " If you’re typing while listening to a conference call, maybe you’re less likely to make mistakes if you were equally distracted when you originally learned to type."
https://hbr.org/2015/01/the-curious-science-of-when-multitasking-works


Is is possible to "delete" a memory permanently?

There is still much that is not completely understood about the process of memory and forgetfulness, and the following is what I have been able to find out.
It is understoood that physiologically, the establishment of long-term memory involves a process of physical changes in the structure of neurons (or nerve cells) and their synapses in the brain, through a process known as long-term potentiation (LTP). (Mastin, 2018; Science Direct, 2018a).
Short-term memory can become long-term memory through the process of consolidation, involving rehearsal and meaningful association (strengthening the physical structure of neurons and their synapses). Unlike short-term memory (which relies mostly on an acoustic, and to a lesser extent a visual, code for storing information), long-term memory encodes information for storage semantically (i.e. based on meaning and association).
The opposite to LTP is long-term depression (LTD) (Dharani, 2015), whereby the neuronal and synaptic structures are weakened, and forgetfulness develops, after a certain triggering activity. (Science Direct, 2018b).
There are several forms of LTP and LTD classified by their mechanisms and their mode of induction (Hammond, et al. 2015), and LTD can be temporary or permanent.

LTD synergistically functions with long-term potentiation (LTP) to generate a balanced, stable memory mechanism. Although LTP plays a major role in the associative type of learning that occurs in the hippocampus and neocortex, LTD is a major player in the error-driven learning that occurs in the cerebellar cortex. Recent studies have revealed complex signal transduction processes underlying LTD. In the long run, LTD may lead to a loss of synapses, or to preservation as silent synapses that have recently been found to prevail in the cerebellar cortex (Ito, 2009).

To answer your question

is it possible to purposefully and permanently forget a specific memory

It seems possible, and Hammond, et al. (2015) discusses induction of LTD, however induction of LTD to forget a specific memory would be impossible at this present time that I can find.
References
Dharani, K. (2015). Chapter 3 - Memory. The Biology of Thought: A Neuronal Mechanism in the Generation of Thought–A New Molecular Model p.53-74. doi: 10.1016/B978-0-12-800900-0.00003-8
Hammond, C., Goaillard, J-M., Debanne, D. & Gaiarsa, J-L. (2015). Chapter 18 - Synaptic Plasticity. Cellular and Molecular Neurophysiology (Fourth edition) p361-389. doi: 10.1016/B978-0-12-397032-9.00018-2
Ito, M. (2009). Long-Term Depression: Cerebellum. Encyclopedia of Neuroscience, p533-539. doi: 10.1016/B978-008045046-9.00807-X
Mastin, L. (2018). Long-Term Memory [Online]Retreived from: http://www.human-memory.net/types_long.html
Science Direct (2018a). Long Term Potentiation [Online]Retreived from: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/long-term-potentiation
Science Direct (2018b). Long Term Depression [Online]Retreived from: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/long-term-depression


Why might a person get widely varying scores on different online IQ tests?

Firmin et al. (2008) tested the validity of a handful of online IQ tests by having college students complete IQ tests at three different websites and also complete a validated lab measure, the Reynolds Intellectual Assessment Scales (RIAS). They found that there were moderate correlations ($r$ values were around 0.4 to 0.5) between some of the online tests and the RIAS, though other tests did not have a significant correlation with the RIAS. Thus, there was some evidence that online IQ tests are measuring the same kinds of things as lab-based IQ tests, but the correlations were weak and some tests were better than others.

In short: online IQ tests are widely variable in their validity, and even the good ones are probably not all that accurate.

Reference

Firmin, M., Hwang, C., Burger, A., Sammons, J., & Lowrie, R. (2008). Evaluating the concurrent validity of three web-based IQ tests
and the Reynolds Intellectual Assessment Scales (RIAS). Eastern Education Journal, 37, 20-28.


In principle, could a brain be rewired to experience more pleasure and/or pain?

This is a difficult question to answer and likely can generate a variety of equally valid (or invalid) answers.
I thought to tackle this from a pathological vista - namely that of sensory processing sensitivity (SPS), which seemingly resembles your area of interest.
SPS can be defined as (Acevedo et al., 2018)

[A] genetically based trait associated with greater sensitivity and responsivity to environmental and social stimuli. [It] is characterized by greater empathy, awareness, responsivity and depth of processing to salient stimuli.

In their article the authors review the structural underpinnings as observed by fMRI scanning of SPS, alongside the brains of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder who also exhibit SPS alongside their other symptoms.
Common activated regions in all disease types were shown in the precentral gyrus.
SPS was associated with activity in reward processing centers (ventral tegmental area (VTA) and substantia nigra (SN), centers for regulation of bodily physiology and pain (hypothalamus and periaqueductal gray (PAG); self versus non-self recognition and empathy (inferior frontal gyrus (IFG) and insula), awareness and self reflection (temporoparietal junction (TPJ)) and self-control (prefrontal cortex (PFC)).
In terms of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder the authors continue with multiple brain regions that are activated commonly and uniquely with respect to SPS proper. I refer to the review referenced below for details.
I reckon, but am unsure, that re-wiring of the pathways or altering the structures themselves with, e.g., transcranial stimulation or with ablation techniques can emulate SPS symptoms, including pain and emotion processing. The practical ways to do this are difficult, given the complexity of the brain.
References
- Acevedo et al., Philos Trans R Soc Lond B Biol Sci (2018); 373(1744): 20170161


A good overview on the topic is Metacognition: A Literature Review (E. R. Lai), page 27 has a section assessing the measures of Metacognition.

  Flavell (1979) describes
  assessment tasks that asked children to study a set of items until they were sure they could
  remember them completely. Children were then tested on their ability to recall all the items.

  Another common task was to read a set of written instructions and indicate any omissions,
  mistakes, or areas of ambiguity. Schneider (2008) observes that the most studied type of
  procedural metamemory is self-monitoring. Assessments designed to capture this ability include
  ease of learning judgments, judgments of learning, and feelings of knowing. For example, ease
  of learning judgments typically ask students to study a set of test materials for a short amount of
  time and then assess their abilities to remember the material. After the students are tested on the
  material, their performances are compared to their initial predictions.

Generally assessments focus on one specific area of Metacognition like Metamemory.

See also Development and Validation of an Objective Measure of Metacognition that assess four studies evaluating metacognitive abilities.

Searching around on Google Scholar finds a great deal of studies using and proposing various measures for Metacognition. There's certainly no "standard" like an IQ test, as Metacoginiton: A Literature Review notes, part of the challenge in studying and teaching Metacognitive abilities is due to the lack of focus on them in traditional school curriculum.


Can hypnotherapy help to change my tastes in food?

As a professional hypnotist, I would start by asking you to consider if your body perhaps needs one or more nutrients in those snacks, or maybe there is a component of salad that really doesn't work for your body? There's the possibility of aversion to salad due to a negative association at some point in your life, say as a child you were forced to eat it. And of course there's the positive association of lardy snacks that the salad has to compete with! Sugar and fat are powerful motivators.

I don't think any respectable hypnotist would set about 'making' you like or dislike anything without seriously considering the ramifications of such an approach, and I doubt that hypnotic suggestion would be enough to overcome the messages coming from your enteric nervous system in the case of it not being an emotionally-based negative association.


When we are sad, why do we feel pain in our stomachs?

I certainly wouldn't say "everything is in the brain"; even the central nervous system is defined more broadly than that (to include the spinal cord)...and then there's everything else in the peripheral nervous system to consider...

I also wouldn't say that feeling pain in one's stomach when sad is normal (you didn't say this either, but it's implied by your phrasing, so I think you might've assumed it), but this and the many other varieties of somatization aren't necessarily abnormal either, in as much as it may occur for most people in some way at some point in life (an intuitive guess informed by personal experience; don't quote me on this). From Wikipedia: "Somatization is a tendency to experience and communicate psychological distress in the form of somatic symptoms," which includes bodily pain of pretty much any variety. Note that this definition raises some interesting questions, e.g.:

How do you know if it's psychosomatic or not?
Can psychosomatic reactions be completely unconcious?

Setting these aside and assuming sadness is your original source of stomach discomfort, there are a number of ways this could occur, and the stress of strong negative emotion (which includes sadness) could exacerbate it. Stress in general can cause ulcers (e.g., stress from head injury; Li et al., 2010). Here's a good (and very long) section from The Cortisol Connection (Talbott & Talbott, 2007) [bolding added]:

  The phenomenon of stress-induced ulcers and other digestive problems has been documented in the medical literature for more than fifty years. From a physiological point of view, we know quite clearly that any stressful event will cause digestion to cease. Blood flow is diverted from the digestive organs to the heart and muscles, secretion of saliva and digestive enzymes is slowed, and intestinal contractions and absorption of nutrients stop. This rapid shutdown of the digestive process makes perfect sense, because from the standpoint of long-term survival it is more important to get away from the dangerous stressor (the lion) than to fully digest all your food...However...even while stress hormones are signaling the body to shut down digestion, these same hormones, when kept elevated for more than a few minutes, are telling us to eat...

  Medical evidence shows quite clearly that ulcers of the stomach (gastric ulcers) and intestine (duodenal ulcers) are much more common in people who are anxious, depressed, or under chronic or repeated stress. In the face of these conditions, which are all also examples of chronic stressors, many of the digestive actions are curtailed, and the body also backs off from its production of other protective measures—such as the mucus that lines the stomach, and the bicarbonate that counteracts the highly acidic gastric juices...The problems start to occur when a person experiences the repeated cycles of high stress followed by low/normal stress...This sets up the digestive system for total confusion. Most of the time the body won't be able to secrete enough digestive enzymes to properly digest food (producing nausea, constipation, gas, and bloating). During the "lucky" times when a body can secrete enough digestive enzymes to properly break down food, the protective mechanisms are far from fully operational—which puts the person at risk for damage to her gastrointestinal tract (because the food enzymes digest the gut's lining in addition to digesting the food). This scenario says a lot about why several bouts of intense stress are known to cause more ulcers than a longer continuous period of heightened stress.

  To compound the problem, other factors, such as immune-system function and the body's control of inflammation and wound healing, come into play. It is well described in the medical literature that both repeated periods of acute stress and continuous periods of chronic stress are associated with suppressed immune-system activity. This has a direct bearing on ulcer development, because less immune-system activity means more growth and higher activity of a bacterium called Helicobacter pylori, which infects the stomach and causes ulcers in 80 percent of the people infected with it. Compounding the tissue damage caused by the accelerated growth of H. pylori is a suppression of the body's ability to heal that tissue damage because of an inhibition in prostaglandin synthesis. Prostaglandins are typically produced in response to tissue damage, where they help reduce inflammation and accelerate healing. During times of stress, however, the synthesis of prostaglandins is curtailed, which suggests that stress not only increases the rate at which ulcers may form, but also slows the rate at which they are repaired.

  Aside from ulcers, the most common stress-related gut disease may be irritable bowel syndrome (IBS). Most of us will experience some degree of IBS during our lifetime. The name "IBS" is really a catchall for a variety of intestinal disorders...The majority of the gastrointestinal conditions falling under the IBS umbrella are either caused by or exacerbated by periods of heightened stress. Irish researchers have solidified the link between stress, inflammation, and gastrointestinal diseases such as IBS through a series of experiments involving 151 subjects that showed IBS to be clearly exacerbated by stressful psychological events, with cortisol and inflammatory cytokines such as IL-6 and IL-8 elevated in all forms of IBS...

  So, again, we have bad news about stress and cortisol for an important bodily system. Stress leads to poor digestion, ulcerated stomachs, and inflamed intestines—not a pretty picture. These effects tend to result in poor dietary choices, suboptimal nutritional status, and a drop in energy levels and overall feelings of well-being. Getting stress and cortisol levels under control can help to reverse these problems.

Pardon the wall of text; I could hardly shorten it further without cutting out directly relevant material or supportive explanation of the responsible anatomical mechanisms. Anyway, given that sadness (a form of stress) can cause our stomachs to go haywire when it's intense or chronic enough, haywire stomachs can then reduce energy and well-being, which forms a wicked little feedback loop between emotional and gastrointestinal distress. Feeling stomach pain can also cause one to clench the abdominal muscles, leading to cramping, which itself also leads back to pain and stress, so that's two feedback loops! Severe and chronic stress can also lead to rumination among those without better coping mechanisms, which is another cognitive-emotional feedback loop unto itself: the more you worry about your stress (both emotional and physiological) is the more you have to worry about!

Given at least these three, distinct, vicious cycles, it's not hard to imagine how a person can spiral out of control and into true disorder. Somatization disorder (SSD) is one such possibility; pain disorder is another. Both involve physical pain that is largely, sometimes completely caused by psychological stress, and are sometimes comorbid with mood disorders, among others. SSD is also sometimes comorbid with IBS.

Extreme cases might best relate to the sentiment expressed in your question, but that doesn't mean your case is extreme or even abnormal necessarily. If you or anyone else is concerned that you might have a disorder such as pain disorder, SSD, IBS, or if you're in any way concerned about how depressed you feel, I'd encourage you to talk to a counselor or therapist (some help is even available for free), seek diagnosis only from licensed professionals, and focus on what you can do about it instead of how bad it might be right now. Most psychological problems can at least be improved through patience, persistence, and positivity, so don't worry about labeling your problem or yourself; focus on finding and pursuing improvements and hope.

Here are some ideas that may help break feedback loops that exacerbate psychogenic stomach distress:

Dietary choices that ease digestion (including anti-inflammatory, low acidity foods)
Nutritional improvement (e.g., vitamins & minerals for stress response, probiotics for digestion)
Stress reduction (as via lifestyle choices, R & R, social support, counseling, etc.)
Cognitive behavioral therapy and biofeedback
Limited, careful, pharmacist-supervised medication of some physical and neurochemical problems
General mindfulness of automatic negative thoughts and unconscious muscle tension
Exercise, recreation, and positivity—generally spending more time looking on the bright side of life!

References

Li, Z. M., Wang, L. X., Jiang, L. C., Zhu, J. X., Geng, F. Y., & Qiang, F. (2009). Relationship between plasma cortisol levels and stress ulcer following acute and severe head injury. Medical Principles and Practice, 19(1), 17-21.

Talbott, S. M., & Talbott, S. (2007). The cortisol connection: Why stress makes you fat and ruins your health - And what you can do about it (pp. 120-122). Hunter House.