When does a fear of something constitute a phobia?

The DSM-5 criteria for Specific Phobia are:

A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals, receiving an injection, seeing blood).
Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, or clinging.
B. The phobic object or situation almost always provokes immediate fear or anxiety.
C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
G. The disturbance is not better explained by the symptoms of another mental disorder, including fear, anxiety, and avoidance of situations associated with panic-like symptoms or other incapacitating symptoms (as in agoraphobia); objects or situations related to obsessions (as in obsessive-compulsive disorder); reminders of traumatic events (as in posttraumatic stress disorder); separation from home or attachment figures (as in separation anxiety disorder); or social situations (as in social anxiety disorder).

The parts I would highlight are that the fear has to be intense and out of proportion to the actual risk, it has to cause some sort of impairment, and it can't be classified as part of a broader mental disorder.
So, if someone sees a spider at work and is startled by it, you wouldn't call that a phobia by itself from a clinical perspective. You might joke about it among friends and say you have a phobia of spiders, but that's just using embellishing language, it's not a diagnosis.
If someone lives in an area where dangerous spiders are present, and takes reasonable precautions to defend themselves (for example, not walking barefoot outdoors), that would not be a phobia: it's not out of proportion.
However, if someone sees a spider at work and then experiences intense symptoms while at work that interfere with their performance, make them constantly preoccupied that there is going to be another spider, and it's a sustained rather than passing experience, then that's closer to the DSM-5 definition of phobia.
In either case, it's really up to a professional to assess the situation and determine if a diagnosis is warranted.


How many bits of data would it take to represent an entire life as a film?

This is a tough question, and there's a few routes to go. When we are watching this life played back, do we want to be able to go to any arbitrary moment and observe what was happening, or do we only want to watch life as we watch it? This would be the difference between recording all information that bombards our brain, or just the information that we are attending to.

We'll go with the first one, as this will be easier.

I'm going to ignore 'thoughts', and just look at information as it enters the body.

We need to know a couple things before we start.

What is the data rate of our eyes?
What is the data rate of our ears?

As these are our most dominant senses, if we want a few orders of magnitude for information, we will get it from these two.

Researchers at the University of Pennsylvania School of Medicine say that the data rate for the eye is about 10 million bits per second, or about 1.25 Mb/s.

Our eyes have about 120 million cells, and they sample at roughly 30 Hz. Determining the number of 'bits' is hard, as eyes have a nonlinear response, so the amount of information they are transmitting is dependent on what the cells are observing. I will trust their number.

As vision is our most powerful sense, and accounts for over 40% of the processing in our brain, we know that the majority of the information will be from the eyes. (EDIT: This is incorrect, see the data below.)

Now onto the ears - our ears can hear up to about 20 KHz, and to actually pick up these sounds we need to sample at twice that frequency, or 40 KHz.
That doesn't tell us how much information we actually get though.
This question on Yahoo! Answers goes a little bit deeper, specifying that ears cannot distinguish information that is represented in more than 16 bits.

This is kind of an interesting way to determine the sensitivity of our ears, as we don't have to wonder 'well, how well can I distinguish what I hear?', rather the question is 'We have these samples of audio, and people can't hear the difference between them, therefore our ears cannot transmit this much information'.

So we have eyes and ears, and we now need to do some math.

I'm going to assume all these rates are fixed, the actual information that is transmitted is nonlinear as the spike trains from our cells change depending on what they are sensing.

I wrote a little python program, available here.

  With the information from above in hand, we have the following:

  Eyes data rate is 2.4 MB per second.

  Ears data rate is 687.5 MB per second.

  over 60 years, our eyes will transmit 4.2 PB

  over 60 years, our ears will transmit 1.2 EB

  The total information we will receive will be upwards of...

  1.2 Exabytes

Now this sounds a little silly, do our ears really transmit more information than our eyes? Actually yes, because they are sampled so much more frequently.
The eyes sample at roughly 30 Hz, whereas the ears sample at 44 KHz.

This analysis ignores the number of cells, and is likely incorrect for a number of reasons. We ignore the other senses, as well as information being sent between brain regions (processing of information).

This question brings up an interesting point though, the raw information that we receive is meaningless, only through successive iterations of information abstraction (what neural networks do, they operate on regions of information, gaining a higher and higher level picture) can we begin to distinguish the world as it is. When we see something, we can immediately break the world apart into segments, we know what can move, we know where things are, we know when we put them there. This isn't information that we were given at our current place in time, it's rules that we have learned about what we see in the world through a lifetime.

Additional source of information:
How many colors and shades can the human eye distinguish in a single scene? This Photography.SE question goes into logic about how much information we can discern, more closely matching the analysis on the Ears, rather than the research data that we used.


If a specific neuron is present in my brain, will it be present in another person's brain?

No, unless you are a C. elegans (or have a similarly simple nervous system), and even then maybe not quite.

Wild-type C. elegans has exactly 302 neurons and they are the same neurons in different members of the species. However, even then, learning can change their nervous system so that it isn't exactly identical in two individuals.

Mammals including humans, however, have brains that are much more shaped by experience and learning. Only the general structure is the same, and even that differs somewhat. It has even been shown that different parts of the brain can be different sizes in individuals with different occupations (see Maguire et al., 2000, for example).

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

White, J. G., Southgate, E., Thomson, J. N., & Brenner, S. (1986). The structure of the nervous system of the nematode Caenorhabditis elegans. Philos Trans R Soc Lond B Biol Sci, 314(1165), 1-340.


Is a drop in intellect necessary for one to be diagnosed with psychosis?

This question pertains to the perception of psychosis by psychiatrists and not to up-to-date interpretation of research data on psychosis classification. So I'll focus on how pure psychosis is roughly conceptualised by the average psychiatrist.

First of all, some diagnosis such as bipolar disorder or schizo-affective disorder, while usually being considered psychotic, have the additional component of problematic affective or mood states attached to it. I'll therefore leave that out to focus on the "pure psychosis" part of psychiatric diagnoses.

The notion of pychosis is usually presented as "being out of touch with reality". A more operational description of it would be to say that a psychiatrist perceives that (1) there is something about reality or your perception thereof or your lack of perception thereof that has a damaging impact on your life and (2) he does not objectify that item.

I purposely rephrased that definition since people are sometimes "persecuted" or "deluded" (or whatever else there may be, such as hypocondria, erotomania, et ceterae) in a way that is real though not objectifiable. Or at least not objectifiable at first glance.

That being said, clinical observations of psychosis have led, broadly, pure psychosis to be conceptualised as lying qualitatively on a linear spectrum extending from psychosis typical of the schizophrenia spectrum to psychosis typical of persistent delusional disorder.

Simply put, persistent delusional disorder psychosis pertains to a very well logically structured system of thought, where the patient adamantly holds some claim that seems self evident for him, and where evidence presented by him or to him is perceived discordantly by psychiatrist and patient.

On the other end of the psychosis spectrum lies schizophrenia-like psychosis. Which broadly speaking is a pattern of thought that is perceived by the psychiatrist as inconsistent, loosely organised, wishful thinking or otherwise unsupported "bullshit". This can range from "my parents are assholes, screw school" to "yeah, I've had a revelation, I can help save the world but I do not know how or why and it bothers me".

Persistent delusional disorder psychosis is a fixed set of thought pattern met by patients around 40 and that, aside from co-occuring depression or other form of distress, does not impact per se the ability to meet family obligations or job expectations. Intellect does not seem to be affected, and it is indeed used vigorously to fuel the persistent pattern of thought.

Schizophrenia-like psychosis on the other hand is considered a disorganised pattern of thought that will lead the patient into hardships family-wise or job-wise. To diagnose schizophrenia, a usual criterion is that this pattern of thought happens at the same time as a job loss, family dysfunction, or academic or school underachievement. It is conceptualised as an impairment of intellect that will get worse the more the patient undergoes further or future life hardships. Also known as "persecutions".

That is why schizophrenia-like psychosis is supposed to be diagnosed with the crucial symptom of functional impairment with respect to so-called pre-morbid intellectual or social baseline functioning. Usually, in practice, determining this premorbid baseline depends on what parents or relatives say to the psychiatrist. IQ tests are not currently used for that.

In a nutshell, if a psychiatrist meets a patient who is not on the delusional disorder side of the psychosis spectrum, with no intellectual impairment compared to its premorbid baseline functioning, he should be confused as to why the patient is now in front of him in the first place. Every medical intervention is indeed triggered one way or another by someone asking for something... He might or should be confused as to what that motive really is or was.


The psychology of disproportioned people in artwork

I have been drawing for more than twenty years and have observed many people learn how to draw. Getting human (or any) proportions right is the one most difficult part for most people, and that Hitler, who made a living as an artist for years and produced two to three thousand drawings, sketches, watercolors, and oil paintings (Price, 1983), maybe drew people too large in some of them does, it would seem, not reflect anything but his level of artistry – or the expressionistic and new objectivist styles popular at the time: other expressionistic and post-expressionistic artists didn't paint very realistic, either.

Deducing psychopathology from artistic output is at least difficult. "The primary assumptions of art psychopathology theories are unreliable since, as Prinzhorn shows, emotionally troubled people are capable of producing wondrous artworks which compare favorably with the creations of artists and children." (Betts, 2006) Hans Prinzhorn, a German psychiatrist and art historian, was entrusted with caring for the collection of art by mental patients begun by Emil Kraepelin in 1919 and expanded it to more than 5000 works in the following years. He published a book, Artistry of the Mentally Ill (1922), in which he analysed the paintings from his collection and found no differences to "normal" art.

Prinzhorn attempted to discern the differences between art by healthy individuals and "outsider art", as the artistic output by mentally ill people came to be called, in a more subjective manner. But first experimental results were contradictory as well. In an experiment, art teachers, mental health professionals, and laypeople, were all unable to discriminate drawings by schizophrenic or healthy children (Rubin & Schachter, 1972). The same group of researchers again found that judges discriminated at levels of chance when they were presented with art by schizophrenic and healthy mothers (Rubin, Ragins, Schachter & Wimberly, 1979). But in other experiments by another research group (Ulman & Levy, 1968, 1984; Levy & Ulman, 1974), judges were able to identify art by mentally ill adults and could even be trained to increase discriminative accuracy.

Discriminative ability seems to depend on what aspect of the artwork the judges look at. In a meta-analysis, Susanne Hacking and David Foreman (2001) identify a number of scales (thematic, quality, shape, color, reality, energy, complexity, composition etc.) and found that two of them (content and body detail, with effect sizes of 0.88 and 0.84 respetively) were able to discriminate patients and healthy controls. Using her own instrument, Hacking (1999) was able to correctly identify psychopathology from artwork with 80-90% accuracy by looking at use of color, line quality, and use of the drawing space.

Even in successful experiments, proportion does not seem to be a distinguishing characteristic of psychopathological art. And it is unlikely that other aspects of Hitler's art would show aspects of psychopathology, because, as he himself stated, as a professional artist his works were dictated by this customers: "I paint that which the people want to buy." (Price, 1983)

Sources:

Betts, D. J. (2006). Art therapy assessments and rating instruments: do they measure up? The Arts in Psychotherapy, 33, 422-434.
Hacking, S. (1999). The Psychopathology of Everyday Art: A Quantitative Study (doctoral dissertation), University of Keele. Available online at http://www.wfmt.info/Musictherapyworld/modules/archive/stuff/papers/Hacking.pdf
Hacking, S., & Foreman, D. (2001). Psychopathology in paintings: A meta‐analysis of studies using paintings by psychiatric patients. British Journal of Medical Psychology, 74, 35-45.
Levy, B. I., & Ulman, E. (1974). The effect of training on judging psychopathology from paintings. American Journal of Art Therapy, 14, 24-25.
Levy, B. I., & Ulman, E. (1984). An experimental approach to the judgment of psychopathology from paintings. American Journal of Art Therapy, 23, 47-52.
Price, B. F. (1983). Adolf Hitler als Maler und Zeichner: Ein Werkkatalog der Ölgemälde, Aquarelle, Zeichnungen und Architekturskizzen. Zug: Gallant.
Prinzhorn, H. (1922). Bildnerei der Geisteskranken: Ein Beitrag zur Psychologie und Psychopathologie der Gestaltung. Berlin: Springer.
Rubin, J. A., Ragins, N., Schachter, J., & Wimberly, F. (1979). Drawings by schizophrenic and non-schizophrenic mothers and their children. Art Psychotherapy, 6, 163–175. doi:10.1016/0090-9092(79)90040-1
Rubin, J. A., & Schachter, J. (1972). Judgments of psychopathology from art productions of children. Confinia Psychiatrica, 15(3-4), 237-250.
Ulman, E., & Levy, B. I. (1968). An experimental approach to the judgment of psychopathology from paintings. Bulletin of Art Therapy, 8, 3-12.


Does the time required to read a word grow linearly with the number of characters?

To answer your question, we must first understand what you mean with "read". Since you ask in the context of speed reading, you appear to be interested in extracting meaning from written text. So we can rephrase your question as:

Does the time to recognize and understand a word increase with word length?

The effect of word length has been studied for two tasks, lexical decision and naming. In a lexical decision task participants are presented with words or nonwords (e.g. "dftrpg") and have to quickly press one specific key for words, and another for nonwords, on the keyboard. The time between the presentation of the stimulus and the key press (the reaction time) is registered. Since you are reading a text in which there are no nonwords, lexical decision is irrelevant in the context of your question.

A naming task is similar to a lexical decision task, with the exception that participants read the words aloud, and their responses trigger the computer via a microphone ("voice key"). Again, the reaction times between the presentation of the stimulus and the spoken word are registered. Since we cannot directly measure understanding, we assume that naming reflects understanding. (Of course you can speak words that you do not know, and even nonwords, but the reactions times would be significantly longer, so we would notice the difference. As long as RT is reasonably short, we may probably assume that the participant knows that word and has understood it.)

Not every time a participant names a word will he or she do so in the exact same time. Sometimes someone will be a bit slower to react, sometimes a bit faster. So we calculate the average reaction time for each word. What we note is that these average reactions times are not the same for different words, that is: the reaction times vary. Now, what we want to do, is explain this variance. Is it in some way related to word length? Or does it correlate to other characteristics of the words, such as number of syllables, word type (noun, verb, adjective), word frequency (how often a word is actually used in everyday spoken language), and so on.

After a number of calculations on the data, we find that all these aspects explain a part of the variance in reaction times (Baayen, Feldman & Schreuder, 2006). Here is a table of the different word characteristics (the predictors), and how much of the variance in naming speed they predict. Only those predictors are listed that had a significant effect. The numbers are adjusted R2 × 100, i.e. the percentage of variance uniquely accounted for by each predictor over and above all other predictors. You don't have to understand the meaning of these numbers, but they show the relative strength of the effect each predictor has on naming speed.

Lower bounds for the percentage of variance (adjusted R2 × 100)
explained by the significant predictors in word naming

Frequency                           6.08
Initial diphone 2                   4.33
Initial diphone (syllable-based)    3.88
Frication/Length first phoneme      2.24
Voicedness first phoneme            1.73
PC2 Consistency                     1.28
Length                              1.14
PC1 Consistency                     0.91
Written-to-spoken ratio             0.59
Neighborhood density                0.36
PC3 Consistency                     0.36
Inflectional entropy                0.34
Residual familiarity                0.31

In all, the results are:

The overall variance in reaction times is small. In young adults they range from around 300 to around 700 ms, with about two thirds of the RTs falling into a narrow slot of only 100 ms.
All the predictors together explain only half of the variance in reaction time (R2 = 0.4999), the rest of the variance must be attributed to unknown predictors or, more likely, are artifacts of the testing situation (distraction, boredom, etc.).
The single strongest predictor of naming speed is word frequency.
The contribution of each of the other single predictors is tiny (a few microseconds each).
Word length predicts only a few microseconds in variance.
There is a word length effect only if words are presented individually, not in a text context (Meyer, Roelofs & Levelt, 2003).

  To answer your question, we can say that the length of the words has probably no noticeable effect on your text reading speed.

Sources:

Baayen, R. H., Feldman, L. B., & Schreuder, R. (2006). Morphological influences on the recognition of monosyllabic monomorphemic words. Journal of Memory and Language, 55(2), 290-313.
Balota, D. A., Cortese, M. J., Sergent-Marshall, S. D., Spieler, D. H., & Yap, M. (2004). Visual word recognition of single-syllable words. Journal of Experimental Psychology: General, 133(2), 283.
Meyer, A. S., Roelofs, A., & Levelt, W. J. (2003). Word length effects in object naming: The role of a response criterion. Journal of Memory and Language, 48(1), 131-147.


Answering the question in the manner that you are asking for would require quite an exhaustive list.  However, a fundamental concept in all of this is having a "leak" channel.

NALCN is the only nonselective channel found in the 24-TM channel family and is equally permeable to Na+, K+, and Cs+. [1]

The majority of the ions transported by the channel are sodium.  This slow influx will have the same effect on voltage over a longer period of time as would a rapid influx, a depolarization of the membrane.

NALCN is found in all animals studied, from humans to D. melanogaster, C. elegans, snails, sea urchins, and the placozoan Trichoplax adhaerens.

So, it is likely that this channel is conserved in the evolutionary ladder.

NALCN mutant mice have a severely disrupted respiratory rhythm and die within 24 hours of birth. Brain stem-spinal cord recordings reveal reduced neuronal firing. The TTX- and Cs(+)-resistant background Na(+) leak current is absent in the mutant hippocampal neurons. [2]

This addresses your other question, this leakage makes the membrane voltage more permissive to initiation of rhythmic discharge and other oscillatory behaviors.
As to whether anything fires "randomly", I would say that neurons can fire with a given distribution [3], but this is governed by all the different channels which operate and their conductances (inverse of resistance) rather than just by chance alone.  Remember, if a neuron fires randomly, it's not likely to have much effect on a post-synaptic cell unless it's time-locked to a series of other action potentials arriving at the same spot.

[1] Ren, D. (2011).  Sodium Leak Channels in Neuronal Excitability and Rhythmic Behaviors.  Neuron, 72(6):899-911. http://www.ncbi.nlm.nih.gov/pubmed/22196327
[2] Lu B, Su Y, et al (2007). The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm. Cell, 129(2):371-83. http://www.ncbi.nlm.nih.gov/pubmed/17448995
[3] Webb TJ, Rolls ET, Deco G, Feng J. (2011) Noise in attractor networks in the brain produced by graded firing rate representations. PLoS One, 6(9):e23630. Free PDF


Comparison between IO psychology, Arbeitspsychologie and Psychologie du travail et des organisations

In this case, wikipedia is not such a good starting point, because at least the German and the French articles do not seem very well developed and are unlikely to be representative of the research in the respective countries. This is in part my subjective opinion, but can also be seen in their length, which is very short compared to the English article.
Nevertheless, there are differences between research traditions in these countries. A good introduction is Peter Warr's chapter “Some Historical Developments in I-O Psychology Outside USA" in Koppes (2007) which compares US and European approaches.
For example with regard to differences between research in the US and Germany, Warr observes that

In general, German psychologists have been more sympathetic to broad conceptual frameworks (...) This German preference is illustrated by the development of broad "action theories". Those (...)[view] the concept of action as integrating otherwise unrelated issues of job performance, stress, errors, skill development, and other processes.
Whereas American I-O psychology has focused more on abilities, motivation, and similar precursors, action theory examines knowledge, cognitive understanding, mental strategies, and processes of self-regulation. (...) This traditional focus on regulatory processes between an environmental input and behavior has been different in both style and content from most American theorizing. (p. 85).

References
Laura L. Koppes (Ed.). Historical Perspectives in Industrial and Organizational Psychology. Mahwah, NJ: Lawrence Erlbaum Associates, 2007.


Consciousness is a broad concept.

In a binary world (conscious/not conscious), biological evidences are irrefutable. For example, a 2009 Brain article stated that "Impaired consciousness during temporal lobe seizures is related to increased long-distance cortical-subcortical synchronization." (Arthuis et al.). A 2012 Lancet Neurology article had the following sentence "the consciousness system,a specialised set of cortical-subcortical structures, maintains alertness, attention, and awareness" (Blumenfeld) - a system that is described on wikipedia. Here, we can see that the binary view of consciousness can be divided into smaller pieces.

Dehaene et al. ("Conscious, preconscious, and subliminal processing: a testable taxonomy", Trends in cognitive science, 2006) proposed a more complex view within a 2 by 2 frame: consciousness is a product perception (weak and strong) and top-down attention (absent and present) - the fully conscious experience arising in the "strong perception/present attention" case. Here again, biological evidences are strong, but the type of the published article (opinion, not a review-type article) says that consciousness is far from being well understood - not even well defined.

An interesting aspect: the first two articles cited here (1st paragraph) are written by neurologists - meaning pure biology. Dehaene et al. (2nd paragraph) are cognitive psychologists and philosophers - a wee bit more of humanities but still biologically grounded. When it comes to philosophy alone, consciousness can completely loose its biological link: William Lycan, for example, argued in his book Consciousness and Experience that at least eight clearly distinct types of consciousness can be identified (organism consciousness; control consciousness; consciousness of; state/event consciousness; reportability; introspective consciousness; subjective consciousness; self-consciousness) (from wikipedia). And when it comes to non-science, the views on consciousness are purely spiritual (The 144 Levels of consciousness).


What evidence is there to suggest that delayed gratification is taught and learned and not genetic?

whilst the nature-nurture issue in mammalian (and particularly human) behaviour is a perennially-fascinating topic, we have learned to be cautious about attempting to construct any strict dichotomies between learned and innate behaviour. suppose you had asked: "did I learn English or just have it?".

successful delayed gratification most likely involves cognitively-mediated inhibition channeled via the frontal lobes. the behaviour must be learned, but it relies on a genetically encoded neural substrate. since it has been claimed (on the basis of longitudinal studies) that the degree of success in delayed gratification tasks persists over time, it may be interesting to ask a related question: if a person has a below-average ability to successfully delay gratification, to what extent is this due to poor teaching and to what extent is it based on neurological factors?


What is the "static" in human vision called?

It's essentially shot noise.

  In optics, shot noise describes the fluctuations of the number of photons detected (or simply counted in the abstract) due to their occurrence independent of each other. This is therefore another consequence of discretization, in this case of the energy in the electromagnetic field in terms of photons. In the case of photon detection, the relevant process is the random conversion of photons into photo-electrons for instance, thus leading to a larger effective shot noise level when using a detector with a quantum efficiency below unity.

Researchers have taken notice of this as early as the 1960s See [2]  I was unable to access this, but the abstract notes that it is probably not ideal shot noise, but I don't know what the De Lange filter adds to the shot noise model, it may be a small corrective factor.

  A noise model incorporating the De Lange filter is applied to visual threshold performance. The model gives better agreement with the experimentally observed Weber-Fechner relation than does the ideal shot noise limited model, and it predicts that the critical time duration for integration of threshold stimuli depends upon the mean luminance level of the background field.

As noted in the introduction to [1], the noise stems from the transduction stage in the retina:

  On the other hand, people working on vertebrate photoreceptor believe that the responses of rods to single photons are locally saturated and that the "quantum" responses in
  rods are surprisingly stereotyped. Thus the variability in responses to dim light flashes is believed to be basically due to the absorption of one, two, . .. , few photons [they cite (Baylor et al., 1984)].

Refs:

  [1] Petracchi D., Cercignani, G., Lucia, S. (1996) Photoreceptor Sensitivity and the Shot Noise of Chemical Processes.  Biophysical Journal, 70: 111-120.
  pdf

  [2] Ruddock, K.H. (1969)Some aspects of human visual threshold performance in relation to temporal frequency response characteristics.  Optics Communications 1(4): 173-179.doi


After how much time should we review a particular study material after once studying it thoroughly so as to retain it longer?

Memory is a complex phenomenon with a number of variables for which we don't have yet the whole picture, let alone specific recommendations, a lot of research is also disputed since we tend to be different from human to human, perhaps that is why it hasn't been used in academia,i.e. we don't teach how to learn. Having said that here's a brief overview of your situation.
The first step is information encoding, a number of variables are at play here, but in short: "The retention of briefly presented information depends on past experience,context, and it's perceived importance"1, very little information is new ( you are not re-learning the periodic table every time you are presented with a new molecule), rather you are learning a new association and your physical situation (like where you are, distractions, motivation,emotional state, stress levels) influence the process.
The second step is information consolidation, that is transferring your newly formed associations from a short term memory to a longer term storage, a continual process. Any new conflicting information will negatively impact this first short( day to day)  to medium (weeks) bridge.Sleep: (non REM,slow wave or even naps) after information encoding seem to be both critical and helpful at this stage, diet,stress levels and lack of sleep work against this process.2

Is there a specific time interval after which you must review things after first learning them so that you can retain them longer?

Caveat emptor: A quirk of human memory, specially during early consolidation, is that retrieval ( or rehearsal ) alters the state of previously stored information, so an incorrect rehearsal session has the probability of affecting you previously well formed memories.3
Beyond that and previously mentioned variables, the consensus seems to be:

Rehearsals are only effective if they involve successful retrieval, in other words, if you can't remember the lesson, you are mostly at square one4 and need to relearn.
Number of successful repetitions (rehearsals) increases chance of recall.
The optimal spacing strategy is  as far apart as possible.
Each successful retrieval/rehearsal gives you a cumulative bonus.

How many times should I review it before I could remember it for an extended period of times(at least 5-6 months) ?

Memory in general stabilizes 3 to 5 years after the acquisition period3.2 ( so as many times as possible during that time based on the above recommendations seems reasonable) with the emphasis that (another memory quirk)  in a process similar to how it is originally stored and rehearsed for consolidation, it becomes easier to recall something as you try to retrieve it.5

What percentage of a particular study material could I forget after not reviewing it for 2-3 weeks?

Depends on the aforementioned initial encoding and subsequent stabilization plus the particular study material, ( is it a list of elements, a concept, a multi step process).In general memory tasks with unique multivariate associations (mnemonic devices for instance) fare better than less complex or even similar/competing memories. So each particular study material is expected to have a different forgetting curve in specific circumstances. Ebbinghaus forgetting curve which skirts these issues and a lot of newer research non the less can still be considered a good general estimate and starting point for how memory fades:

The plot is exponential, which means that the initial conditions greatly influence future retention rates, ( I've used a mix of subjects/conditions for an average), But as mentioned your starting point and specific situation  can greatly influence memory strength (your exponent over time ), so under bad learning conditions, no interest on the subject and a very hard to discern subject matter, your curve would look like this:

I am leaving aside flashbulb memories (aliens landed during your study session !, good luck thinking about anything but aliens for the next 3 weeks!), which are a separate topic and do not seem to obey normal memory consolidation rules.

How much time does our brain take to forget things?

As mentioned the initial conditions are critical and influence the process, there is a period of consolidation (more variables) which further influences consolidation and then one of relative stability, this period in a general simplified way looks this:

So you get a nice long sub exponential tail thanks to long term consolidation.
Just a quick note before wrapping up, in general people are overconfident, specially at the high end when it comes to memory retrieval 3.3.

how much time it should take for me to gain the same amount of confidence about that chapter as I had a couple of weeks ago?

Due to all the above variables, it is hard to give you a definitive answer, beyond the obvious one that 2-3 weeks under your initial learning conditions are inadequate and you will have to relearn (albeit you will be doing it a slightly faster rate), there are a number of strategies for sequential learning that pair our basic understanding of memory into a studying regime, here is one such strategy:

This is an oversimplification, in order for you to answer your own question, you need to standardize your learning environment and subject matter in as much as possible (don't forget to adjust for overconfidence), come up with your own decay rate and then plan your studying regime based on your learning curves which would need to be updated as you relearn and specialize, sounds like a lot, but it's basically jotting down a couple of numbers and perhaps the hardest part making sure you have the correct learning environment.
Finally, I haven't talked about learning aids, the effect of mnemonics as well as other strategies is well researched and I believe can be beneficial to anybody,specifically students, but I believe it should be used as a sort of extra boost rather than a foundation for learning. (i.e. An understanding of the material should come first) Use at your own risk.6

Notes, reference & sources:
The overarching note is that memory research stands in stark contrast to most academic programs and learning environments, practices and popular myths.
1. Neuroscience (Purves)
2. The Secret World of Sleep (Lewis).
3. The Oxford Handbook of Memory(Tulving,Craik) 3.2 Strictly speaking there are a number of other variables that influence memory stability, a high emotional context for instance seems to solidify them earlier. 3.3 Not trivial either and something like 20% of errors can be observed in high confidence reporting.
4. You still have the benefit of the priming effect and other temporal benefits, so it's not all wasted, you can catch up faster.
5. What is sometimes called Spontaneous recovery.
6. Your Memory: How it works and how to improve it (Higbee) has a lot of useful advice aimed mostly at students.


Psychopaths' Response to Expected Losses?

I do not normally respond negatively about a cited study. This study you have cited is rather glib and very flawed. It could be a better evaluation of a person's mathematical ability as opposed to:

  Fear seemed to play a large role in risk-avoidance behavior of the
  normal participants.

The other flaw in this study, is to even attempt to correlate giving subjects the money (as it is no personal loss) and using  a rather trivial amount, $20.

Any person with a basic understanding of mathematics, would know that the odds were in favor to betting each time. This cannot be compared to real life risk aversion, where there are unknown risks associated with return, and the financial investment is far greater (as it is coming from the individual's pocket).

My views are supported by the following study In fact the results could be accounted by this study
 Mathematical-Verbal Ability Differentials and Somatic Expressions of Situational Anxiety.

Are there any observations of psychopaths' responses to negative expected values?

The following study would demonstrate that on an emotional level, a person with clinical psychopathy would have no response to negative expected values, but the cognitive  (purely intellectual) awareness of negative expected values would be intact. This could play out in many ways given the circumstances, as life itself is never so clear cut.

Suffice to say, if it involves the fear of harming another of self harm, this would not be consideration for average psychopath.

  CONTEXT: Psychopaths belong to a larger group of persons with
  antisocial personality disorder and are characterized by an inability
  to have emotional involvement and by the repeated violation of the
  rights of others. It was hypothesized that this behavior might be the
  consequence of deficient fear conditioning.

  OBJECTIVE: To study the cerebral, peripheral, and subjective
  correlates of fear conditioning in criminal psychopaths and healthy
  control subjects.

  RESULTS: The healthy controls showed enhanced differential activation
  in the limbic-prefrontal circuit (amygdala, orbitofrontal cortex,
  insula, and anterior cingulate) during the acquisition of fear and
  successful verbal and autonomic conditioning. The psychopaths
  displayed no significant activity in this circuit and failed to show
  conditioned skin conductance and emotional valence ratings, although
  contingency and arousal ratings were normal.

  CONCLUSION: This dissociation of emotional and cognitive processing
  may be the neural basis of the lack of anticipation of aversive events
  in criminal psychopaths.

Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study.

I do not see how you have made the following deduction:
The quoted study's only valid if it shows that psychopaths respond properly to expected losses.

Mathematical-Verbal Ability Differentials and Somatic Expressions of Situational Anxiety
Robert L. Milliken and Bernard Spilka
The Journal of Experimental Education
Vol. 31, No. 1 (Sep., 1962), pp. 3-26
Published by: Taylor & Francis, Ltd.
Article Stable URL: http://www.jstor.org/stable/20156598

Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study.
Birbaumer N, Veit R, Lotze M, Erb M, Hermann C, Grodd W, Flor H.
Source
Institute of Medical Psychology and Behavioral Neurobiology and Section of Experimental Resonance Imaging of the CNS,
 Department of Neuroradiology,
 University of Tübingen,
Tübingen, Germany.


What is the standard way to analyze EEG data in a mismatch negativity paradigm?

Programs/packages for EEG analysis
There are decent MatLab toolboxes with good tutorials for for the analysis of EEG data. The EEGLAB toolbox (tutorial) can be operated by both GUI and command-line (and script). The fieldtrip toolbox (tutorial) is mainly operated by command line / script.

Of course there are also (commercial) software packages for EEG analysis that do not require Matlab (e.g., BESA, Brain Vision Analyser, eeprobe), but I am not familiar with them.

Are there techniques to avoid averaging out small ERPs whose latencies might vary?
No, probably not. ERPs are calculated by averaging across multiple trials because this averaging cancels out all components that jitter in time (that is, mostly noise), i.e. the thing you want to avoid (canceling out of jittering components) is actually the purpose of calculating ERPs.

However, to be sure you should have a look at reviews or tutorials for the measurement of the mismatch negativity. See for instance

Duncan CC, Barry RJ, Connolly JF, Fischer C, Michie PT, Näätänen R, Polich J, Reinvang I, Van Petten C. (2009) Event-related potentials in clinical research: guidelines for eliciting, recording, and quantifying mismatch negativity, P300, and N400. Clin Neurophysiol. 120(11):1883-908.  (pubmed)


What are the major structures of the medial temporal lobe?

The MTL consists of (note that some structures overlap):

cortical areas, which can be categorized in at least three ways:

portions of two gyri

entire parahippocampal gyrus
anterior medial side of fusiform gyrus

five named cortical areas:

perirhinal cortex
parahippocampal cortex (see parahippocampal gyrus)
entorhinal cortex
presubiculum*
parasubiculum*

five Brodmann areas: 27, 28, 34, 35, 36

hippocampus
amygdala*

* indicates that not all literature includes this component in the MTL

I didn't find a diagram of only the MTL. The best diagrams I found were (not shown here because I don't own the copyright):

Figure 1
Figure 2
Figure 3

References

  Brodmann, K. (1909) Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des
  Zellenbaues. Leipzig : Johann Ambrosius Barth.
  Squire, L.R., Stark, C.E.L., & Clark, R.E. (2004) The Medial Temporal Lobe. Annu. Rev. Neurosci. 27:279–306
  [pdf]


Is the Thatcher Face Illusion only limited to face recognition?

Short answer
According to a study by Boutsen et al. Thatcherization of objects (houses in this study) did not reveal the Thatcher effect, while faces did.

Background
The Thatcher-face illusion (Fig 1) is, in my opinion, not really an illusion. Instead, it is a phenomenon where in-congruent features are more apparent when observed in their normal everyday context and orientation. In Fig. 1, for example, ms Spears appears normal, but upside down in the left panel, while her face appears hugely distorted when the left panel is turned upside down.

Your question whether this also occurs in objects other than faces. According to a study by Boutsen et al. (2006), it doesn't. Boutsen et al. manipulated images of faces and houses. Houses did not show effects of thatcherization. The authors discuss the why behind this finding and mention that a number of factors may explain the lesser salience in objects, namely a higher variability in the number of manipulated house features and  their perceptual salience or relevance. Because of their more stable feature structure and configuration, inversion of house elements was thought to be less salient with houses than with houses. Unlike the parts of a building, facial features are highly relevant to an observer to determine identity or expression, thereby rendering configural manipulations of buildings less disruptive.

Fig. 1. Thatcher illusion of Britney

Fig. 2. Thatcherized face and house. source: Boutsen et al., 2006)

Reference
- Boutsen et al., NeuroImage (2006); 32: 352 – 67


The subject of gender can be a very personal subject and the subject of gender is discussed among the LGBTQIA+ community.
The LGBTQIA Allyship is

the practice of confronting heterosexism, sexism, genderism, allosexism, and monosexism in oneself and others out of self-interest and a concern for the well being of lesbian, gay, bisexual, transgender, queer, intersex and asexual people.  Is founded on the belief and believes that dismantling heterosexism, monosexism, trans oppression/trans misogyny/cissexism and allosexism is a social justice issue (see the UCDavis link above)

The social sciences have a branch devoted to gender studies. Other sciences, such as sexology and neuroscience, are also interested in the subject.
The social sciences sometimes approach gender as a social construct, and gender studies particularly do, while research in the natural sciences investigates whether biological differences in males and females influence the development of gender in humans; both inform debate about how far biological differences influence the formation of gender identity. In some English literature, there is also a trichotomy between biological sex, psychological gender, and social gender role. This framework first appeared in a feminist paper on transsexualism (Yudkin, 1978).
Genders
There is the binary gender (male or female) and some identify themselves under a third (non-binary) gender of either:

non-binary,
genderqueer,
gender fluid,
bigender,
trigender,
pangender,
agender,
nongendered,
genderless,
genderfree, or
neutrois

See also: Gender Identity
Gender identity vs Sexual Orientation
Gender identity is separate from sexual or romantic orientation, and non-binary people have a variety of sexual orientations, just as transgender and cisgender people do.
A non-binary gender is not associated with a specific gender expression, such as androgyny. Non-binary people as a group have a wide variety of gender expressions. People who are non-binary have gender identities that are not exclusively masculine or feminine. They may identify as having an overlap of gender identities, having two or more genders, having no gender, having a fluctuating gender identity, or being third gender or other-gendered. Recognition of non-binary genders is still somewhat new to mainstream Western culture (McGee & Warms, 2011).
Gender Identity and Society
Historically, many if not most societies have recognized only two distinct, broad classes of gender roles, a binary of masculine and feminine, largely corresponding to the biological sexes of male and female.

Most cultures currently construct their societies based on the understanding of gender binary—the two gender categorizations (male and female). Such societies divide their population based on biological sex assigned to individuals at birth to begin the process of gender socialization. (Nadal, 2017).

In addition to these traditionally recognized third genders, many cultures now recognize, to differing degrees, various non-binary gender identities.
Gender neutrality is a movement to end discrimination of gender altogether in society through means of gender-neutral language, the end of sex segregation, and other means.
Quantifying genders
Genders can only be quantified to a certain extent.  As indicated, there are binary and non-binary genders.  Binary being male or female and non-binary being others which don’t follow the binary convention. So, you could say there are three genders, but that is oversimplified.  The genders in the third (non-binary) gender category is numerous, and can be bigger than the list I provided.  It is all down to how people identify themselves in the way of gender.
References
McGee, R. J. & Warms, R. L. (2011). Anthropological Theory: An Introductory History. New York: McGraw Hill.
Nadal, K. L. (2017). The SAGE Encyclopedia of Psychology and Gender
Yudkin, M. (1978). Transsexualism and women: A critical perspective. Feminist Studies. 4(3): 97–106. doi:10.2307/3177542 jstor: 3177542


Best meditation techniques to overcome Behavioral Addictions?

Several years ago, I was unsuccessfully searching for a study that evaluates the efficacy of many different interventions in the context of addictions. However, I did find a cognitive behavioral therapy (Copeland et al. 2001) that included a mindfulness technique called urge surfing and it was compared to other CBT interventions in cannabis use disorders. A definition follows from Marlatt (2002):

  Other clients have described the successful use of "urge surfing" as a
  mindfulness technique (Marlatt, 1985, 1994). Clients are taught to
  visualize the urge as an ocean wave that begins as a small wavelet and
  gradually builds up to a large cresting wave. As the urge wave grows
  in strength, the client's goal is to surf the urge by allowing it to
  pass without being "wiped out" by giving into it. I tell clients that
  urges are often conditioned responses triggered by cues and high-risk
  situations. Like a wave, the conditioned response grows in intensity
  until it reaches a peak level of craving. Giving in to the urge when
  it peaks only serves to further reinforce the addictive behavior. Not
  acting on the urge, on the other hand, weakens the addictive
  conditioning and strengthens acceptance and self-efficacy. Like any
  skill, learning how to "urge surf" takes practice and improves over
  time as the client attains greater balance on the mindfulness
  surfboard.

Copeland et al. mention the use of urge surfing in their program:

  The second session discussed urge management strategies such as‘‘urge
  surfing’’ and nonreinforcement.

and reported

  significantly better treatment outcomes than those receiving
  notreatment. They were more likely to report abstinence during the
  follow-up period, were significantly less concerned about their
  control over cannabis use (as measuredby the SDS), and were more
  likely to have significantly fewer cannabis-related problems than
  those in the delayed treatment control group. Further, those receiving
  six sessions of treatment significantly reduced their level of
  cannabis consumption. These outcomes were unaffected by the therapist
  delivering the intervention, but were affected by treatment
  compliance.

Note that the study included a lot of other lessons. Regarding how often it should be done: The subjects were advised to use this technique whenever the urge appeared.

More info about urge surfing can be found in the freely accessible book Cognitive behavior therapy: Applying empirically supported techniques in your practice (2003) in Chapter 67.

Regarding the question about lifestyle factors, there have been countless studies (some cited in McGonigal's book) that indicate a positive effect of cardiovascular exercise, sufficient sleep, low-glycemic diets on self-regulation and so I will not cite them here.

Sources

Copeland, J., Swift, W., Roffman, R., & Stephens, R. (2001). A randomized controlled trial of brief cognitive–behavioral interventions for cannabis use disorder. Journal of substance abuse treatment, 21(2), 55-64. doi:10.1016/S0740-5472(01)00179-9

Marlatt, G. A. (2002). Buddhist philosophy and the treatment of addictive behavior. Cognitive and Behavioral Practice, 9(1), 44–50. doi:10.1016/s1077-7229(02)80039-6

Lloyd, A. (2003). Urge Surfing. In W. O'Donohue, J. E. Fisher & S. C. Hayes (Eds.), Cognitive behavior therapy: Applying empirically supported techniques in your practice (pp. 451-455). New York: John Wiley & Sons Inc.


Due to Gestalt Psychology, is the face an illusion?

Dependent on your definition of an illusion, there is truth in your claim.

A definition of an illusion is:

  [A] perception, as of visual stimuli (optical illusion) that represents what is perceived in a way different from the way it is in reality.

But then - what is reality?

First off, Bach-y-Rita famously proclaimed, 'We don't see with our eyes, we see with our brains' (Abrams & Winters, 2003). The reason he said that is that everything we perceive is generated within our brain; it's a synthesis of visual information (photons) flowing from the photoreceptors in the eye (rods & cones) to the visual cortices. For instance, color and shape are mere reflections of brain activity. Colors do not exist - the brain synthesizes them by combining information from three classes of photoreceptors, each sensitive to another peak wavelength.

Secondly, the rabbit hole goes a lot deeper than the Gestalt Principles. The retinal image is actively completed by the brain (Ramachandran & Ramachandran, 2005). There are two relatively large gaps in each of our retinae, namely the place where the optic nerve head leaves the retina, called the optic disc, or the blind spot. No sensations, and hence no conscious perceptions can be generated by these regions which are devoid of photoreceptors. Yet, we do not notice those gaps in the visual field, because the brain interpolates what it guesses might be there in the visual field and actively fills up the empty spaces in the conscious image.

As a consequence of this, people suffering from retinal degeneration might not even notice it, only when they start hitting street signs and bump stuff from the table. Even then, they often do not perceive the patchy dead regions in their retinae, instead, they know there must be a gap, because they are hitting things. The brain simply fills the gaps such that they are not noticeable in the visual percept. Nonetheless, entire road signs or entire crystal bowls or glasses on the table might be erased, as the brain simply extends the table image in our minds.

References
- Abrams & Winters, Discover, June 2003
- Ramachandran & Ramachandran, Sci Am, April 2005


researched with "sensory cortex latency" on google:

according nowak et al, latency in macaque v1 is ~75 ms, although there are cells with latency as short as 30 ms.  according to camalier at al, latency in macaque A1 is more like 15-25 ms.

Also, see shriki et al for a computational perspective on latency coding in V1.

There is research into the latency of population responses recorded at the skin called "evoked potentials", reviewed by Nuwer. He says that there are evoked potentials over somatosensory cortex 20 ms after stimulus, whereas the potential over V1 is more like 100 ms after stimulus.  All taken together, it does seem that the visual system is slower


When using APA style citations, is it acceptable to have page numbers for everything?

In APA style, when you cite a work, you add an in-text citation in the body of the work and you add the full reference to the reference list at the end of the work.

End of text references for book chapters, journal articles, and similar works include the page range of the work in the reference. This  refers to the start and end page of the cited work (and not to the particular pages that contain the content most relevant to your citation).
In-text citations need to include page numbers when you are quoting a passage of text.
APA stye encourages but does not require the use of page numbers in in-text citations where you are paraphrasing a specific passage of text (i.e., putting a passage of text in your own words). That said, I rarely see this practice in journals, and don't be surprised if someone marking your paper is unaware of this rule.
The more common rule is that if it is not a quote, then you don't use page numbers in in-text citations.

Rationale

As @Josh points out, most citations in psychology refer to overall works. For example, a journal article may present the results of an experiment, and these results and communicated and discussed in multiple points in the article. Thus, you are citing the work as a whole, and it does not make sense to refer to specific page numbers.

That said, I think there are times where authors cite an entire book written by one author for a reference, and some form of page reference would make the citation more useful for the reader (e.g., a particular chapter might be most relevant).

Tutorials

Purdue OWL APA Format


Psychological explanation for perceptions of the Loch Ness monster

Herd mentality and hallucinations can explain many things like the Loch Ness monster, ware wolves, vampires and ghosts.

  Hallucinations involve sensing things while awake that appear to be real, but instead have been created by the mind.

Extreme emotional states can cause psychosis which leads to hallucinations and delusions and other thoughts which are removed from reality. Many things can stir an otherwise normal person into a frenzy which then provides the vulnerability for psychosis. Then at the sight of wave their imagination is more real than what their eyes see and the image of a monster is imprinted in their memory. If the monster is attacking them or something else it might be an intrusive thought as well.

After the initial hallucination the story is repeated and herd mentality will cause others to experience something similar at the sight of the wave. As more people experience the sighting it becomes more popular continuing and expanding the myth.


Is there any research about effect of unfamiliar environment on stress?

I have found the following

Older people's cardiac responses as indicators of stress in familiar and unfamiliar environments (Lewis & Phillips, 2012)

I also found:

Padilla, A. M., Alvarez, M., & Lindholm, K. J. (1986). Generational status and personality factors as predictors of stress in students. Hispanic Journal of Behavioral Sciences, 8(3), 275-288.
DOI: 10.1002/dev.420220608

  stressful events center on loss of familial and cultural ties as well as on relative discomfort in an unfamiliar social environment

References

Lewis M. J. & Phillips J. E. (2012). Older people's cardiac responses as indicators of stress in familiar and unfamiliar environments. Psychophysiology, 49(4): pp. 478-483
DOI: 10.1111/j.1469-8986.2011.01321.x PMID: 22176515


How to best prepare the mind for a problem identification brainstorm?

I'm wondering if your approach to "identify[ing] problems, not solutions," will include so-called reverse or negative brainstorming, in which participants are directed to consider "what can be done to break something instead of focusing solely on narrow-minded fixes,"1 to be "highly critical, rather than highly creative."2 If this is the case, the group could "warm up" by applying this technique to some other area: their own lives, their favourite sports teams, public policy issues, etc.

1 Stephen C. Harper. How to Solve Problems with Reverse Brainstorming, posted on his TalentSpace Blog, December 14, 2011.

2 Harper. Extraordinary Entrepreneurship: The Professional's Guide to Starting an Exceptional Enterprise (Google eBook), 2005, p.78.


What is the diagnosis when someone suffers only from negative symptoms of schizophrenia?

Short answer
Many people in the general populace suffer one or more negative symptoms that are associated with schizophrenia, but are not diagnosed with a mental illness whatsoever.

Background
Indeed, for a diagnosis of schizophrenia, negative symptoms alone are not enough. According to the Diagnostic and Statistical Manual of Mental Disorders, (DSM-5), to meet the criteria for diagnosis of schizophrenia, the patient must have experienced at least 2 of the following symptoms:

Delusions
Hallucinations
Disorganized speech
Disorganized or catatonic behavior
Negative symptoms

Werbeloff et al. (2015) note that, similar to psychotic experiences, negative symptoms are common in the general population, namely between 20–22%. The vast majority of these people do not manifest a clinically diagnosed psychiatric disorder. Negative symptoms do appear to be associated with the development of schizophrenia later in life, and to other non-psychotic disorders. However, neither negative symptoms nor psychotic experiences alone predicted later schizophrenia in their study. It was only the combined presence of both strong positive psychotic experiences and negative symptoms together that showed a statistically significant risk for later schizophrenia.

Reference
- Werbeloff et al., PLoS One (2015); 10(3): e0119852


What is the most effective treatment for ADD and ADHD that excludes chemical prescriptions from a doctor?

Not much seems to work; psychotherapy appears questionable when the patients are re-evaluated by someone else. The only thing with a minor but generally applicable effect is free fatty acid supplementation, although the effect may be so minor as to have no clinical value.
Of course, most of these findings come from a meta-analysis (Sonuga-Barke 2013) published in a psychiatry journal...

Two different analyses were performed. When the outcome measure was based on ADHD assessments by raters closest to the therapeutic setting, all dietary (standardized mean differences=0.21-0.48) and psychological (standardized mean differences=0.40-0.64) treatments produced statistically significant effects. However, when the best probably blinded assessment was employed, effects remained significant for free fatty acid supplementation (standardized mean difference=0.16) and artificial food color exclusion (standardized mean difference=0.42) but were substantially attenuated to nonsignificant levels for other treatments.
CONCLUSIONS:
Free fatty acid supplementation produced small but significant reductions in ADHD symptoms even with probably blinded assessments, although the clinical significance of these effects remains to be determined. Artificial food color exclusion produced larger effects but often in individuals selected for food sensitivities. Better evidence for efficacy from blinded assessments is required for behavioral interventions, neurofeedback, cognitive training, and restricted elimination diets before they can be supported as treatments for core ADHD symptoms.

The editorial that accompanied this paper had this pull-out:

Behavioral treatments have been
demonstrated to be helpful for children
with co-occurring disorders and
symptoms, although this blinded
analysis did not show efficacy for core
ADHD symptoms.

And it's worded that way because a prior meta-analysis (Fabiano 2009) using less stringent criteria (no blinging required) found (of course) that behavioral interventions work.
Regarding food colorants, only about 8% of ADHD children are estimated by a different meta-analysis (Nigg 2012) to be affected/sensitive.
And a meta-analysis of diet interventions Pelsser 2017 was quite skeptical of most stuff:

Considering the small average ESs [effect size] PUFA [poly-unsaturated fatty acid] supplementation is unlikely to provide a tangible contribution to ADHD treatment, while further research is required for AFC [artificial food color] elimination before advising this intervention as ADHD treatment. The average FFD [Few Foods Diets] ES is substantial, offering treatment opportunities in subgroups of children with ADHD not responding to or too young for medication.

So the cool new thing is FFD now. Since the last paper is freely available... I won't say much more, except that it may take a year to permute food choices until the right few foods are determined. They do say in the (body of the) paper that (owing to this time-scale issue):

large-scale implementation of the few-foods approach would not be a realistic recommendation.

I have to wonder why that didn't make it into the abstract.


What is the meaning of semantics to cognition?

Logical semantics is one of the three sections of logical semiotics (in addition to syntax and pragmatics) dealing with the relations between signs (in particular the expressions) and reality, to which they refer. In addition to basic semantic functions, we can include, e.g. semantic connotation, determination and denotation, where the basic terms of semantics are meaning and truth.
For example, I recommend Benthem (1986) and maybe Wikipedia's definition at the beginning of your journey. For further reading I can also recommend Friedenberg & Silverman (2012).

How can the relation between signs, expressions, symbols, and reality, in which semantics works so hard, be referred to in cognitive science? One very simple (at the beginning) answer - representations. It is one of the fundamental processes in cognitive science; a representation is something that stands for something else. Single words can be good examples here, e.g., apple. When we say it, then in the mind of someone who knows English, the concept of a particular type of fruit will pop up. One will see it, taste it, and maybe touch it in his/her imagination.

There are other types of representations. For example there are propositions, which are statements about the world and which can be illustrated with sentences. The sentence, e.g John is eating a red apple is a proposition, that is itself made up of a few concepts. There are also rules, which are another type of representation, and they can specify relationships between prepositions. Let's say the rule, If it is raining, I will not go with you to ZOO makes the second proposition contingent on the first one. Also, there are analog representations, which help us make comparisons between two similar situations, objects, etc.

References:

Benthem, J.V. (1986). Essays in Logical Semantics.
Wikipedia
Friedenberg, J., & Silverman, G. (2012). Cognitive Science. An Introduction to the Study of Mind.


What causes fear of failure to lead to lack of effort and actual failure?

Is there a name for the phenomena of not putting effort into study because of fear of failure which in turn results in actual failure?

Yes, this is called self-handicapping.

  Self-handicapping is the process by which people avoid effort in the hopes of keeping potential failure from hurting self-esteem.

  What causes this?

The main and most relevant reason here is the preservation of your own self-image and/or managing your public image. If you were to try your very best and still fail, then the only causal attribution would have been dispositional, that is, the only way to explain it to yourself would have been that, you are just not good enough.

However, when you place impediments in your path and essentially prevent yourself from performing to your fullest, you are creating scapegoats for your failures. This will allow you to attribute the failure to situational factors and not dispositional ones, allowing you to maintain your image of self-competence and/or self-efficacy.

  Are there any strategies for overcoming this cycle?

Self-handicapping occurs in many different fashions but most of them tend to be variations of procrastination and lack of effort/practise. So, by tackling either of these, you will be able to reduce the chances of handicapping yourself.

Other than that, research has shown that by focussing on long-term mastery in a field that you like, self-handicapping behavior can be reduced.

  In three studies with German high-school and college students, we found empirical evidence for the assumed moderator effect of mastery goals. In studies 1 and 3, performance-avoidance goals were remarkably lower associated with self-handicapping in the group of students highly endorsing mastery goals compared to students who proved to be less mastery oriented. In studies 2 and 3, moreover, individuals' self-esteem was less related to self-handicapping when students strongly emphasized mastery goals.


What benefit is responsible for human preference of one food over another?

Reasons why we do or do not like certain foods:

1. Taste

I may want to eat foods that taste pleasantly: chocolate, cakes, fried chicken and...sweet cabbage (?!).

2. Bowel regularity

I discover that whole-grain bread makes wonders to my bowel regularity, which makes my stomach to feel good, which overweights a bit bitter taste of such bread in my mouth, so I start to like it.

3. Health concerns

I read that fast food may not be healthy, so I stop eating it and start to feel better in general, and, with time, I will actually stop liking fast food.

4. Nutrient deficiencies

If I have a period in which I eat very few plant foods, I'll start to crave things, like green salad. I believe, I can start craving foods that contain certain minerals and vitamins I'm missing (iron, potassium, vitamin C, protein...).

Salt craving may be due to low sodium diet or habitual high sodium diet, or zinc deficiency.
Sugar craving may be due to need for immediate energy or due to addiction to sweet taste.
Potato craving can be due to potassium deficiency (potatoes are high in potassium).
The association between food cravings and consumption of specific foods in a laboratory taste test (PubMed, 2008). According to the study, you may crave for a certain food just because you regularly eat it.
Eating everything except food (PICA) can be due to iron or zinc deficiency.

5. Medical conditions

Addison's disease (adrenal insufficiency) is often associated with salt craving.
Postprandial hypoglycemia (low blood sugar after meals), diabetes mellitus type 1 and heroin withdrawal can be associated with sugar craving.

6. Beliefs

I can just hear or believe that certain food is "not good to eat" or "not good for me" and, just because of this, I might find that food disgusting.

7. Genetics and environment

Genetic and environmental factors can influence food preferences, especially in children and adolescents (PubMed, 2016).

8. Depression

Depression can be associated with craving for foods high in carbohydrates and fats, such as chocolate and chips (PubMed, 1995).

In conclusion: Nutrient deficiencies can be one of the factors for food preference.


Can one neuron spike inhibit and excite at the same time?

The textbook convention is that neurons release only one type of chemical from their synaptic terminals. This is known as Dale's Principle (https://en.wikipedia.org/wiki/Dale%27s_principle), and would exclude the possibility that neurons can release both inhibitory and excitatory neurotransmitters.

Examples have been found of neurons which co-release two types of neurotransmitters, such as Glutamate and Dopamine [1] or GABA and Dopamine [2]. The effect of Dopamine depends on the types of Dopamine receptors in the target neuron, is generally modulatory, and can not be classified as purely excitatory or inhibitory [3], which is what your question asked. There is no evidence for neurons which release purely inhibitory and excitatory neurotransmitters, such as GABA and glutamate respectively.

References:

[1] Sulzer, D., and S. Rayport. "Dale's principle and glutamate corelease from ventral midbrain dopamine neurons." Amino acids 19.1 (2000): 45-52.

[2] Tritsch, Nicolas X., Jun B. Ding, and Bernardo L. Sabatini.
"Dopaminergic neurons inhibit striatal output through non-canonical release of GABA." Nature 490.7419 (2012): 262-266.

[3] Romanelli RJ, Williams JT, Neve KA (2009). "Chapter 6: Dopamine receptor signalling: intracellular pathways to behavior". In Neve KA. The Dopamine Receptors. Springer. pp. 137–174. ISBN 1-60327-333-6.


In light of a recent question in MedicalSciences.SE, I thought I would update this answer to include some information from my answer there.

Autism spectrum disorder (ASD) now affects one in 68 births in the United States and is the fastest growing neurodevelopmental disability worldwide (Edmiston, et al. 2017) [free access paper with links to cited papers].

Alarmingly, for the majority of cases, the causes of ASD are largely unknown, but it is becoming increasingly accepted that ASD is no longer defined simply as a behavioral disorder, but rather as a highly complex and heterogeneous biological disorder (Edmiston, et al. 2017).

With information available, the genetic and environmental causes of Autism is open to speculation and interpretation.

The NHS webpage on Autism states (Emphasis mine)

  Most researchers believe that certain genes a child inherits from their parents could make them more vulnerable to developing ASD.

  Cases of ASD have been known to run in families. For example, younger siblings of children with ASD can also develop the condition, and it's common for identical twins to both develop ASD.

  No specific genes linked to ASD have been identified, but it may be a presenting feature of some rare genetic syndromes, including Fragile X syndrome, Williams syndrome and Angelman syndrome.

On environmental causes the NHS say that

  Some researchers believe that a person born with a genetic vulnerability to ASD only develops the condition if they're exposed to a specific environmental trigger.

  Possible triggers include being born prematurely (before 35 weeks of pregnancy), or being exposed in the womb to alcohol or to certain medication, such as sodium valproate (sometimes used to treat epilepsy during pregnancy).

  No conclusive evidence has been found linking pollution or maternal infections in pregnancy with an increased risk of ASD.

Research Autism has some referenced information on leading research into the causes of Autism from the Medical Research Council, National Autistic Society and the Autism Society of America; and the crux of the matter from what is said here is that the causes are still being investigated and

  There is no known single cause for autism, but it is generally accepted that it is caused by abnormalities in brain structure or function

The site also provides a list of publications on the possible causes of Autism

There has been research into autoimmune disorders causing ASD.

Edmiston, et al. (2017) stated (emphasis mine):

  there are likely multiple, biologically defined subgroups within the ASD spectrum(3–7). Specifically, there is growing evidence that supports maternal immune dysfunction may underlie the behavioral abnormalities observed in a subset of children affected with the disorder(8). Several immunologic risk factors have been described including: genetic associations with immune-related genes(9–16), family history of autoimmune disease(15, 17–21), maternal inflammation and infection during pregnancy(22–27), and altered immune responses in the children, and are associated with increased impairments in core and associated features of ASD(28). More specific to this review, maternal anti-brain autoantibodies, which are thought to access the fetal compartment during gestation, have been identified as one risk factor for developing ASD and are proposed to contribute to early neurodevelopmental perturbations in the developing fetus(29–31).

  References

  Lord C, Risi S, Lambrecht L, Cook EH, Leventhal BL, DiLavore PC, et al. The autism diagnostic observation schedule-generic: a standard measure of social and communication deficits associated with the spectrum of autism. Journal of autism and developmental disorders. 2000;30:205–223.
  Newschaffer CJ, Croen La, Daniels J, Giarelli E, Grether JK, Levy SE, et al. The epidemiology of autism spectrum disorders. Annual review of public health. 2007;28:235–258.
  Snow AV, Lecavalier L, Houts C. The structure of the Autism Diagnostic Interview-Revised: diagnostic and phenotypic implications. Journal of child psychology and psychiatry, and allied disciplines. 2009;50:734–742.
  Ousley O, Cermak T. Autism spectrum disorder: Defining dimensions and subgroups. Current Developmental Disorders Reports. 2013;1:20–28.
  McDougle CJ, Landino SM, Vahabzadeh A, O’Rourke J, Zurcher NR, Finger BC, et al. Toward an immune-mediated subtype of autism spectrum disorder. Brain Research. 2015;1617:72–92.
  Onore C, Careaga M, Ashwood P. The role of immune dysfunction in the pathophysiology of autism. Brain, Behavior, and Immunity. 2012;26:383–392.
  Warren RP, Singh VK, Cole P, Odell JD, Pingree CB, Warren WL, et al. Increased frequency of the null allele at the complement C4b locus in autism. Clinical & Experimental Immunology. 1991;83:438–440.
  Warren RP, Odell JD, Warren WL, Burger RA, Maciulis A, Daniels WW, et al. Strong association of the third hypervariable region of HLA-DRβ1 with autism. Journal of Neuroimmunology. 1996;67:97–102.
  Torres AR, Sweeten TL, Cutler A, Bedke BJ, Fillmore M, Stubbs EG, et al. The association and linkage of the HLA-A2 class I allele with autism. Human immunology. 2006;67:346–351.
  Campbell DB, Li C, Sutcliffe JS, Persico AM, Levitt P. Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder. Autism Research. 2008;1:159–168.
  Thanseem I, Nakamura K, Miyachi T, Toyota T, Yamada S, Tsujii M, et al. Further evidence for the role of MET in autism susceptibility. Neuroscience Research. 2010;68:137–141.
  Mostafa GA, Shehab AA. The link of C4B null allele to autism and to a family history of autoimmunity in Egyptian autistic children. Journal of Neuroimmunology. 2010;223:115–119.
  Jung JY, Kohane IS, Wall DP. Identification of autoimmune gene signatures in autism. Translational psychiatry. 2011;1:e63–e63.
  Torres AR, Westover JB, Gibbons C, Johnson RC, Ward DC. Activating killer-cell immunoglobulin-like receptors (KIR) and their cognate HLA ligands are significantly increased in autism. Brain, behavior, and immunity. 2012;26:1122–1127.
  Comi AM, Zimmerman AW, Frye VH, Law PA, Peeden JN. Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism. Journal of Child Neurology. 1999;14:388–394.
  Atladóttir HO, Pedersen MG, Thorsen P, Mortensen PB, Deleuran B, Eaton WW, et al. Association of family history of autoimmune diseases and autism spectrum disorders. Pediatrics. 2009;124:687–694.
  Vinet É, Pineau CA, Clarke AE, Scott S, Fombonne É, Joseph L, et al. Increased Risk of Autism Spectrum Disorders in Children Born to Women With Systemic Lupus Erythematosus: Results From a Large Population-Based Cohort. Arthritis & rheumatology (Hoboken, NJ) 2015;67:3201–3208.
  Wu S, Ding Y, Wu F, Li R, Xie G, Hou J, et al. Family history of autoimmune diseases is associated with an increased risk of autism in children: A systematic review and meta-analysis. Neuroscience and biobehavioral reviews. 2015;55:322–332.
  Chen S-W, Zhong X-S, Jiang L-N, Zheng X-Y, Xiong Y-Q, Ma S-J, et al. Maternal autoimmune diseases and the risk of autism spectrum disorders in offspring: A systematic review and meta-analysis. Behavioural brain research. 2016;296:61–69.
  Chess S. Autism in children with congenital rubella. Journal of autism and childhood schizophrenia. 1971;1:33–47.
  Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, et al. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006;26:4752–4762.
  Smith SEP, Li J, Garbett K, Mirnics K, Patterson PH. Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2007;27:10695–10702.
  Atladóttir HÓ, Thorsen P, Østergaard L, Schendel DE, Lemcke S, Abdallah M, et al. Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders. Journal of Autism and Developmental Disorders. 2010;40:1423–1430.
  Patterson PH. Maternal infection and immune involvement in autism. Trends in Molecular Medicine. 2011;17:389–394.
  Garay PA, Hsiao EY, Patterson PH, McAllister AK. Brain, Behavior, and Immunity Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development. 2012
  Ashwood P, Van de Water J. Is autism an autoimmune disease? Autoimmunity reviews. 2004;3:557–562.
  Braunschweig D, Van de Water J. Maternal autoantibodies in autism. Archives of neurology. 2012;69:693–699.
  Fox E, Amaral D, Van de Water J. Maternal and fetal antibrain antibodies in development and disease. Developmental Neurobiology. 2012;72:1327–1334.
  Fox-Edmiston E, Van De Water J. Maternal Anti-Fetal Brain IgG Autoantibodies and Autism Spectrum Disorder: Current Knowledge and its Implications for Potential Therapeutics. CNS Drugs. 2015;29:715–724.

In conclusion, they pointed out that Maternal autoantibody related (MAR) ASD:

  has been noted by numerous researchers describing the presence of maternal autoantibodies reactive to fetal brain proteins in a subset of mothers of children with ASD. Further, there is now an abundance of evidence supporting their deleterious role in neurodevelopment. For the most part, these studies have described similar experimental outcomes and, given the clinical and biological heterogeneity of ASD, there likely exists a complex relationship between the presence of maternal anti-fetal brain antibodies and developmental trajectory of exposed offspring. It is still unclear how and when these maternal autoantibodies arise, but studies currently underway may provide increased insight into their ontogeny.

References

Edmiston, E., Ashwood, P., & Van de Water, J. (2017). Autoimmunity, autoantibodies, and autism spectrum disorder. Biological psychiatry, 81(5), 383-390. Pubmed Central: PMC5373490


Any form of excessive secretion of dopamine, can not be good, be it drugs, learning, sex etc. workaholism is a form learning addiction,  workaholism is said to be as an addiction
very similar to alcoholism. Workaholic as a “person whose pleasure from learning things at work has become so extreme, that it indicates clear disturbances with his/her personal happiness, bodily health, and interpersonal relations, and with his smooth social functioning” . Therefore,  there are some perspectives related to workaholism. workaholism at least initially was formulated to be referred as addictive process (Sussman, 2012).
 Negative side effects of workaholism or the strive or need to constantly work towards gaining knowledge may include subjective emotional sorrow or feeling of “burned out” (Sussman, 2012).

Based on that search,
these authors induced that addiction includes:
(a) engagement in the behavior to achieve
appetitive effects
 (b) preoccupation with the behavior
(c) temporary satiation
 (d)loss of control
 (e) suffering negative consequences
hope my answer helped. if you want to read in depth on this. do refer to the reference for article.
reference :  Sussman, S. (2012). Workaholism: A Review. Journal Of Addiction Research & Therapy. doi: 10.4172/2155-6105.s6-001


Meditation for patients with neuroleptic induced tension

Akathisia is very difficult to handle. Sometimes akathisia responds to anxiolytic drugs such as benzodiazepines, propranolol, and even red wine. Amantadine, benztropine (for Parkinsonism) might also help. Mostly these are off-label prescriptions.

Meditation, exercise, and de-stressing measures are certainly helpful on general principle, though the best way to eliminate akathisia (if it is drug-induced) is to taper down the dosage or take a different medication. Finding a medication that treats the symptoms and provides a quality of life improvement despite side-effects is the job of the physician. You can think of it as quality of life improvement from reduction of symptoms plus quality of life improvement from minimization of side-effects, of which akathisia is one of the most common and unpleasant.

https://www.mdedge.com/psychiatry/article/89620/somatic-disorders/akathisia-restlessness-primary-condition-or-adverse-drug

King DJ, Burke M, Lucas RA. Antipsychotic drug-induced dysphoria. Br J Psychiatry 1995; 167:480–482.

Healy D, Farquhar G. Immediate effects of droperidol. Hum Psychopharm 1998; 13:113–120.

Jones-Edwards G. An eye-opener. OpenMind 1998; September:12,13,19.

Jones-Edwards G. On the receiving end. New Therapist 2000; 7:40–43.

Belmaker RH, Wald D. Haloperidol in normals. Br J Psychiatry 1977; 131:222–223.

Kendler KS. A medical student’s experience with akathisia. Am J Psychiatry 1976; 133:454.

Healy D, Savage M (1998) Reserpine exhumed. Brit J Psychiatry 172: 376–378.


When a person starts to scratch, why does this often start others to scratch?

There are two functions that I'm aware of that are involved, though there of course may be more I'm simply unaware of.

The first is so-called mirror neurons. Cognitively, neurologically, and evolutionary, we generally assume that the brain tends to be very efficient to be able to get its immense job done in so little space, so quickly, with so little 'power' (food). One result of this pressure is re-use, so that the same parts of the brain that are used in active experience of something are also used for recalling, thinking about, and indeed perceiving others experience similar things (thus the mirror neurons). To see someone else itch compels us to think about itching, and to recall/think about/understand itching is to activate the same parts of the brain that register the concept of itching in ourselves.

This then neatly leads into (and overlaps) with another set of effects: conscious awareness and selective attending. The nature of our conscious awareness is that it is limited - we can't consciously attend to everything at once. And thus we have perceptual and cognitive filters (and we have lots of theories over time that have developed this context - I think the "leaky filter" hybrid model being the most recent, but I can't recall the name of the researcher(s) who came up with it).

This set of functions give us the cocktail party effect and the invisible gorilla experiments, change blindness, and so many fun others. It also effects how we respond to "how happy are you" questions; another fun experiment was that finding a nickle on a copying machine before you get asked about your happiness and satisfaction in life causes one to respond more positively to even general questions.

But I digress...

In contagious yawning - and in itching! - the act of perceiving someone itching can direct our attention to personal comfort and any potential itchiness. For instance, if you are fully dressed right now (including socks): you know that 'seam' at the end of the sock down by your toes? Does that always go above your toes on the top of your foot, or does it sometimes kind of work it's way down so it's at the bend of your toes underneath your foot?

Well, I have gone all morning without thinking about it, but now I realize my sock is a little twisted, I think the heel of the sock has slid a bit off-center, and the top of my boot is rather tight while the lower part of the laces could be tighter. Also, my ankle kind of itches a little.

The fact of modern life is, quite frankly, there is always something that could use a good scratching! Like my back right now...answering this question is making me wish for a scratching post. Multiple layers of clothes of varying fibers, little skin folds, body hair, all those tiny little follicles and pores mean there's bound to be at least one little pimple somewhere, and even if you are very flexible there's always places that aren't terribly easy to reach...

So perhaps a better question is "why aren't we itchy all the time?!" Thankfully, most of us have filters that consider many of these sensations relatively unimportant, so they don't get passed over into something that captures our conscious awareness. Also, we are busy: there's lots to think about in the world, so we tend to only think about it when we are given a cue like trying on clothing, or looking at an irritated/injured piece of skin...or seeing someone else itching.

Given these are cognitive processes, we can also view what happens when they go wrong, as manifested in symptoms and disorders such as intrusive thoughts, "sensitive skin" or tactile sensitivity (especially common in the autism spectrum), etc.

TLDR;

First we perceive, then we imagine, then we experience - empathy! Sad songs can make us sad, in part because they remind us of the sadness that is an unavoidable part of life, and also in part because to think about sadness we can't help but feel at least a little sad; the only reason we aren't sad all the time is because there are happy things to think about, too.

Itching is like an elephant - try not to think about it. Oops, too late!


Why does it seems in similar cases sometimes classic conditioning happens and in others habituation?

The Wikipedia article on Habituation explains it fairly well:

  The habituation process is a form of adaptive behavior (or neuroplasticity) that is classified as nonassociative learning. Nonassociative learning is a change in a response to a stimulus that does not involve associating the presented stimulus with another stimulus or event such as reward or punishment.[4] (Examples of associative learning include classical conditioning and operant conditioning). Habituation is the decrease of a response to a repeated eliciting stimulus that is not due to sensory adaption or motor fatigue.

Classical Conditioning strengthens associations and elicits a response because the stimulus is associated with something. The bell means food, pay attention to it. Habituation happens when there's no association; why keep getting worked up by the church bells ringing when you know it doesn't mean anything important (as opposed to a tornado siren).

To generalize "classical conditioning" further into just "associative learning", they're two sides of the same coin; if something is important, connections in your mind strengthen; you remember and a response is illicited. If something isn't important, you stop caring about it and might fail to notice the stimulus at all. This is why excessive fire drills (and worse, false alarms) can be a bad thing; many college students end up being habituated against fire alarms rather than being classically conditioned to know "loud noise" -> "get the heck out".


Intuitive explanation of MBTI test and it's gender bias

From the data in the table, it is not possible to tell whether there is a meaningful difference between men and women with regard to the Judging trait, because it does not state the size of the sample, the effect size, and whether the difference is statistically significant. All differences could be just random noise. In fact, the data may just as well be more supportive of the idea that gender does not make a difference here.

Because the MBTI does not hold up to scientific scrutiny (and is hardly used by academic personality researchers), it should be difficult to find reliable data on gender differences. However, because the Judging dimension overlaps with the Conscientiousness factor in the Big Five, one can look at gender comparisons there. There do not seem to be strong gender differences with regard to Conscientiousness (see this earlier answer).


If we consider the field of psychiatry, usually a comorbidity is understood as the simultaneous occurrence of two or more mental disorders in the same person. But attention can also treat physical comorbidity, when there is coexistence of physical and mental pathologies for example. But that does not clarify your question. Sometimes DSM can help and sometimes cause confusion. What needs to be highlighted is the crucial role of clinical evaluation. It is through the evaluation process that we can understand the course of the disease development, its predisposing factors, current difficulties and the symptomatological evolution. A good assessment can see if and when there is a major disease and which diseases can act secondarily. Some symptoms may work together, some clinical conditions of comorbidity have a temporally defined course of action. Although the experience of the clinician counts a lot, we cannot ignore the remarkable role played by exams, tests and other diagnostic instruments. In the case of psychological assessment, which is my background, we can often see from the evidence that new insights are made into each case and from there, build a more effective intervention plan. Hope this helps. Good luck.Here you can find some more.


What are the current suggested models for Primacy Effect in memory recall or personality impression?

Primacy is one of several memory phenomenon often associated with serial recall--the other most common being the recency effect. There have been several computational models which attempt to establish an integrated account of serial recall (list memory). I will briefly cover to two such models, one ACT-R and one connectionist model.

ACT-R

ACT-R is a hybrid (symbolic and sub-symbolic) cognitive architecture used to model a variety of tasks. It contains a detailed memory module, which is the oldest and most well-validated component in ACT-R (though this distinction does not necessarily apply to its explanation of primacy specifically).

Anderson et al. (1998) explain the primacy effect as an interaction of two mechanisms:

  The tendency for the earlier items to receive greater rehearsal
  is one factor that is producing the primacy. The other factor is the lower positional confusions among items at the beginning of the list.

The first mechanism, greater rehearsal, refers to the fact that items that are encountered sooner have more time to be rehearsed in working memory. Rehearsal is considered an important component of many influential working memory models, such as Baddeley's model of working memory. Rehearsal in the ACT-R model is accomplished through production rules. Sub-symbolically, rehearsing an item leads to an increase in the base-level activation of a chunk according to the base-level activation equation:

  $\beta=ln(\sum_{j=1}^{n}t_j^{-d})$

In this equation, a chunk's activation is determined by the frequeny ($n$) with which a chunk is encountered and the recency of each occurence ($t_j$). Rehearsing an item increases $n$, and thus increases its activation level. Chunks are retrieved using the softmax activation function, and neural noise may lead to incorrect retrievals.

The authors justify the use of rehearsal mechanisms, arguing that

  In experiments where an effort is made to eliminate rehearsal the primacy effect goes away.

The second mechanism, positional confusion, relies on the fact that each item in the list is stored in a memory trace along with its neighbors. Thus, a memory "chunk" stores not only the item itself, but also the numbers that come before and after it in the list. The partial-matching mechanism in ACT-R leads to memory retrievals in which a neighbor is mistakenly retrieved in place of the item itself. The first and last items of the list have only one neighbor, while items in the middle of the list have two neighbors. Thus, there is an increased chance that numbers in the middle of the list will be transposed.

Neural Networks

Botvinick & Plaut (2006) used a recurrent neural network to model list memory. Recurrent neural networks are a common way to model temporal order of events in neural networks. They are also an increasingly popular explanation of how working memory might be implemented in the brain.

Like the ACT-R model, Botvinick & Plaut note the tendency to transpose items during recall:

  Note that elements at both the beginning and the end of a list have
  fewer positional near neighbors than items toward the middle. This
  makes it relatively unlikely that the positions of elements near the
  list boundaries will be mistaken for other, similarly represented
  positions.

Their model also leverages a second mechanism to model the primacy effect, but it is not explicit rehearsal. Instead, it relies on the dynamics of recurrent neural networks to encode earlier items with greater reliability:

  Consider that when the first element in a list is
  encoded, there are no other elements yet represented in the hidden
  layer. When the second item is encoded, there is only one other
  element represented there. With each successive element encoded,
  the number of elements already in memory continues to increase.
  This provides a partial explanation for the primacy effect. As noted
  a moment ago, the more items held in memory at any given time,
  the more difficult the overall representation becomes to decode.
  This means that items at early list positions have an advantage,
  because during the overall period from encoding to recall they
  share the hidden layer with relatively few other elements.

It is also worth reading Botvinick & Plaut (2006) for their comparison of their own model to several others in the literature, including an earlier version of Anderson's. Briefly, they state:

  It is difficult to compare this ACT-R
  account with the model we have presented [...]
  because several critical aspects of the account (such as the functioning of the position pointer and the basis for similarity between
  position representations) are directly stipulated, without an explicit
  account of the underlying mechanisms or representational structure. [...]
  This being said,
  the Anderson and Matessa model, unlike the context-based models
  we have cited, can also be viewed as portraying item and position
  information as being stored together, as part of a single, structured
  representation. If viewed from this perspective, the theory has a bit
  more in common with the account we have put forward.

Summary

In sum, the two models discussed share some similarities. Both models account for primacy partially through positional confusion during retrieval. The ACT-R relies on explicit rehearsal, whereas the neural network model does not. Though it ignores higher-level strategies, the neural network model can be seen as a lower-level explanation of the primacy effect because it provides a possible explanation of how the effect may arise through the interaction of real neurons.

References

  Anderson, J. R., Bothell, D., Lebiere, C., & Matessa, M. (1998). An integrated theory of list memory. Journal of Memory and Language, 38(4), 341-380. PDF

  Botvinick, M. M., & Plaut, D. C. (2006). Short-term memory for serial order: a recurrent neural network model. Psychological review, 113(2), 201. PDF