Is it possible to create a false memory by trying to remember something that eludes you?

A seminal paper by Roediger and McDermott (1995) observed that studying (similar to thinking about) materials was associated with a high likelihood of false recall and false recognition of materials similar to the studied items. This research has spawned hundreds of follow-up studies, none of which address your question entirely but converge on a plausible explanation: As you try to recall the specifics of the event, you likely recall a number of things that actually occurred (e.g., you were drinking rum, there was a pretty girl in the corner, and it was getting late). Considering these true specifics, however, according to this line of research, may introduce associated memories which never actually occurred (e.g., the pretty girl winked at you). Think these thoughts long enough and you'll have what's called a source monitoring error -- that is, you'll conflate thinking about the pretty girl winking with a memory that she actually did wink. That might be why you feel as if you had fewer false memories when you don't consider specifics -- there are fewer opportunities to make false associations. (It's also interesting to note that repeated testing, while improving "correct" memory, also enhances false memory. I can provide more links if you're interested.) If you're interested in other things that cause false memory (at least in these laboratory studies), here's a link.

Most of this is research my group is associated with, generally because I'm most familiar with that literature. I like this line of studies (called DRM studies) because they show false memories can be generated in a matter of moments (or "the morning after"). Loftus's work is fascinating, too, because she uses more naturalistic materials, those more pertinent to real life. Definitely two sides of the same coin.

Leave a comment if I can provide more info.


Is there a precise definition of "attitude"?

Have you considered Wikipedia's Definitions of attitude page? Here are some excerpts with which I agree...

An attitude can be defined as a positive or negative evaluation of people, objects, event, activities, ideas, or just about anything in your environment, but there is debate about precise definitions. Eagly and Chaiken [(1998)], for example, define an attitude "a psychological tendency that is expressed by evaluating a particular entity with some degree of favor or disfavor." Though it is sometimes common to define an attitude as affect toward an object, affect (i.e., discrete emotions or overall arousal) is generally understood to be distinct from attitude as a measure of favorability [(Ajzen, 2001)]. [Emphasis added.]

To me, this distinction means that affect exists apart from attitudes at the level of the person (e.g., "I feel [insert affect word $X$ here]"), but is influenced by affect at the level of the object (e.g., "I feel [insert affect word $Y$ here] toward [insert object $Z$ here]"). Thus affect at the object level would more or less constitute an attitude, yet remain distinct from affect per se, which can occur at many levels, and not necessarily be directed toward any specific object. Examples of $X,\ Y,\ \&\ Z\ $ could include:
$$X=Y=\text{"resentful"};\ Z=\text{"Obama"}$$
Thus, "I feel resentful," states an affect, whereas, "I feel resentful toward Obama" states an attitude. However, you might prefer to consult Ajzen's (2001) own reasoning on the matter (TBH, I haven't).
Further considerations from Wikipedia:

This definition of attitude allows for one's evaluation of an attitude object to vary from extremely negative to extremely positive, but also admits that people can also be conflicted or ambivalent toward an object meaning that they might at different times express both positive and negative attitude toward the same object. This has led to some discussion of whether individual can hold multiple attitudes toward the same object [(Wood, 2000)].
Whether attitudes are explicit (i.e., deliberately formed) versus implicit (i.e., subconscious) has been a topic of considerable research. Research on implicit attitudes, which are generally unacknowledged or outside of awareness, uses sophisticated methods involving people's response times to stimuli to show that implicit attitudes exist (perhaps in tandem with explicit attitudes of the same object). Implicit and explicit attitudes seem to affect people's behavior, though in different ways. They tend not to be strongly associated with each other, although in some cases they are. The relationship between them is poorly understood.

References
Ajzen, I. k. (2001). Nature and operation of attitudes. Annual Review of Psychology, 52, 27–58.
Eagly, A. H., & Chaiken, S. (1998). Attitude structure and function. In D.T. Gilbert, Susan T. Fisk, and G. Lindsey (Eds.), Handbook of Social Psychology, pp. 269–322. New York: McGowan-Hill.
Wood, W. (2000). Attitude change: Persuasion and social influence. Annual Review of Psychology, 51: 539–570.


What is the relationship between self-perceptions and actual driving ability?

The results are mixed.

It's well known that in general people will consider themselves above average in most areas, and driving is no exception Do expert drivers have a reduced illusion of superiority?

  Expert police drivers rated themselves as superior to equally qualified drivers, to the same degree as novices, Cohen’s d = .03 ns. Despite their extensive additional training and experience, experts still appear to be as susceptible to illusions of superiority as everyone else.

Drivers' Ratings of Different Components of Their Own Driving Skill: A Greater Illusion of Superiority for Skills That Relate to Accident Involvement also suggests that good appreciation for hazard perception results in higher self-percieved safety even when skill is controlled for:

  Also, ratings of hazard-perception skill related to self-perceived safety after overall skill was controlled for. We suggest that although drivers appear to appreciate the role of hazard perception in safe driving, any safety benefit to be derived from this appreciation may be undermined by drivers' inflated opinions of their own hazard-perception skill. We also tested the relationship between illusory beliefs about driving skill and risk taking and looked at ways of manipulating drivers' illusory beliefs.

Age differences in male drivers' perception of accident risk: The role of perceived driving ability suggests that younger (male) drivers consider themselves equal to older drivers, youunger drivers are involved in more accidents:

  Although young drivers' estimates of accident involvement in the next year were higher than those of older drivers, young drivers gave lower ratings of accident risk for specific driving situations which demanded fast driving reflexes or substantial vehicle-handling skills. Young drivers rated their own risk of an accident and driving abilities as being the same as for older drivers. However, they saw their peers as being significantly higher at risk and having poorer abilities than themselves.

The article Confidence in, and self-rating of, driving ability among older drivers suggests there is no correlation between confidence and driving performance for older drivers. This seems to go against most results but other studies were not focused on older drivers.

  No relationship was found between confidence and adverse driving events or driving performance. Understanding the relationship of confidence and self-rating of driving ability to driving patterns, adverse events and driving performance may provide additional insights into identifying older drivers at increased risk for problems and formulating intervention strategies to help lower risk.

Overall it appears that young drivers are likely to have excessively high confidence in their own ability. There isn't much evidence to suggest that higher or lower confidence actually correlates with a specific skill level.  Older drivers seem to have better driving skill and less overconfidence, but I have not seen results controlling for age and correlating driving ability with confidence except the study on older drivers which showed no correlation.


I don’t have a direct or a very reputable reference to answer this question, but I work in the clinical field and have seen many insomniacs, so I’ll offer you the answers based on the references and the experiences I have for you to consider in the meantime.

Melatonin’s principal function is to convey the message of darkness or information about timing of the day and night to the central circadian clock. [1-3]

  In mammals, a central circadian clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, tunes the innate circadian physiological rhythms to the ambient 24 h light–dark cycle to invigorate and optimize the internal temporal order. … Melatonin conveys the message of darkness to the clock and induces night‐state physiological functions, for example, sleep/wake blood pressure and metabolism. [1]

and

  The primary physiological function of melatonin, whose secretion adjusts to night length, is to convey information concerning the daily cycle of light and darkness to body structures. [2]

Melatonin does not have direct effects on sleep-wake cycles, which are governed by other complex neural circuits in the brainstem. It is not one of the neurotransmitters in the complex sleep-wake neural circuits, which utilize cholinergic, noradrenergic, and serotonergic neurotransmitters. Melatonin just influences the circuits by conveying the message of darkness or timing of the day and night to the SCN, the central circadian clock, which in turn, affects the sleep-wake neural circuits.

  The highly organized sequence of human sleep states is actively generated by nuclei in the brainstem, most importantly the cholinergic nuclei of the pons–midbrain junction, the noradrenergic cells of the locus coeruleus, and the serotonergic neurons of the raphe nuclei. The activity of the relevant cell groups controls the degree of mental alertness on a continuum from deep sleep to waking attentiveness. These brainstem systems are in turn influenced by a circadian clocks located in the suprachiasmatic nucleus and VLPO of the hypothalamus. The clock adjusts periods of sleep and wakefulness to appropriate durations during the 24-hour cycle of light and darkness that is fundamental to life on Earth. [4]

Clinically, melatonin seems to be neither necessary nor sufficient for sleep to occur. This is evident by the fact that when melatonin is high in the night and a person is about to fall asleep or even asleep, he /she can be awakened and remain awake by some strong stimulus despite the high level of melatonin at that time. Also, if melatonin is given to awake people, they may feel like sleeping, but, unlike strong sleeping pills (which mostly affect cholinergic, noradrenergic, and/or serotonergic neurotransmissions), they may not fall asleep if other things such as surrounding circumstances do not allow them to sleep. So, melatonin alone is not sufficient for sleep to occur or be maintained.

On the other hand, when a person is deprived of sleep for one or more nights, he/she can fall asleep during daytime even if the level of melatonin is low at that time. Or, if strong sleeping pills (which mostly affect those mentioned neurotransmissions) are given to awake people during daytime, when melatonin level is low, they will fall asleep despite the low level of melatonin. So, melatonin alone is not necessary for sleep to occur or be maintained.

In summary, the principal role of melatonin regarding sleep is to convey the message of darkness or information about timing of the day and night to the central circadian clock to influence the sleep-wake neural circuits so that the animal, including human, can sleep at appropriate time; but it is not necessary or sufficient for sleep to occur or be maintained.

References.

Nava Zisapel. New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation. Br J Pharmacol. 2018 Aug; 175(16): 3190–3199.
Claustrat B, Leston J. Melatonin: Physiological effects in humans.. Neurochirurgie. 2015 Apr-Jun;61(2-3):77-84. doi: 10.1016/j.neuchi.2015.03.002.
Pandi-Perumal SR1, Srinivasan V, Spence DW, Cardinali DP. Role of the melatonin system in the control of sleep: therapeutic implications. CNS Drugs. 2007;21(12):995-1018.
Purves D. Chapter 27.  Sleep and wakefulness. Neural circuits governing sleep. In Neuroscience. 3rd ed. Sunderland, Massachusetts: Sinauer Associates Inc; 2004. p 674-684.


Are reaction time and memory physiological measure or behavioral observation?

It may help considering whether the phenomenon is under some  control by the participant. Pupil dilation is a physiological measure, but the speed at which I hit a key (reaction time) is a behavioral measure. Memory is a phenomenon. If you meant recall, recognition, or another memory retrieval task, how could you measure that physiologically? Memory is generally measured through (somewhat controlled) self-report. However, it could also be probed through less controllable, more automatic reactions.


What is depersonalization and derealization disorder from a neurological point of view?

You ask for a very in detail analysis of depersonalization (DP) and derealization (DR) disorder. I'll try to meet your expectation.

Lets start with some definitions. Depersonalization and derealization happen after people have experienced great amounts of psychological stress or brain injury. The likes of which their coping measures fail to handle. The brain in an effort to contain the pain cuts off some contact with reality or self identity. DP/DR can be a sign of the onset of psychosis in bipolar or schizo type individuals; however it is not correlary to psychosis.  "it was like a dream" is how someone speaks of derealization and "did that happen to me or did I hear about it happening to someone else" is depresonalization.

DP/DR (not the disorder) is very common among those who have been in any way traumatized (especially head trauma) happening about half the time. (Hunter 2004) Basically when you hear on TV "He's going into schock". They mean the patient is experiencing an acute stress reaction one of which features is DP/DR.

Because DP/DR is oft encompassed by shock let me describe the physiological symptoms and treatment of shock before we discuss the psychological and neurological signs.

Appear as a living zombie.
Cool, clammy skin which may be pale or gray. Ie the blood drained out of their face.
Abnormally weak or rapid pules and breathing.
Low blood pressure.
Absent staring eyes with occasional pupil dilation.
Sometimes overly excited or catatonic

In response to shock always get professional medical help by dialing the emergency number of your town/nation like 911. Make the person as comfortable and still as possible with reassurances until professional help arrives. Do not give them any food or water as the body is unprepared to handle any additional input.

Shock happens before DP/DR disorder. When the specific features of DP/DR continue or reemerge longstanding after trauma it becomes a disorder. (Simeon 2006)  As a disorder it is the third most frequent. (Simeon 2004) A self administered intake survey or an hour long psychological interview following DSM guidelines allows a doctor to make the diagnosis.

The general guidelines provided by the DSM-IV-TR:

  Longstanding or recurring feelings of being detached from one's mental processes or body, as if one is observing them from the outside or in a dream.

  Reality testing is unimpaired during depersonalization
  Depersonalization causes significant difficulties or distress at work, or social and other important areas of life functioning.

  Depersonalization does not only occur while the individual is experiencing another mental disorder, and is not associated with substance use or a medical illness.

  The DSM-IV-TR specifically recognizes three possible additional features of depersonalization disorder:

  Derealization, experiencing the external world as strange or unreal.
  Macropsia or micropsia, an alteration in the perception of object size or shape.

  A sense that other people seem unfamiliar or mechanical.

-Wikipedia Depersonalization Disorder

Your first assertion that DP/DR is associated with spirituality is correct. As when psychotic hallucinations happen they typically have a DP/DR feature to them. It is common for something obviously psychotic like seeing an angel or devil to be associated with an out of body experience or vision type trance. Common is it for someone to experience a trip to the spirit world to see a loved one. Such events are to a limited extent drug induceable. (I do not like many other students of psychology believe that all spirituality is aberrant however much is caused by illness.) Psychologist typically teach a patient what is a hallucination and psychosis and allow the individual to label their experience as either spiritual or psychotic.

Now the neurological basis is diverse as it is not necessarily an organic originating condition but a response disease. I was able to find two main theories first a functional difference and the second based on lesions in the brain.

  On the basis of this, a new model is proposed according to which the state of increased alertness observed in depersonalization results from an activation of prefrontal attentional systems (right dorsolateral prefrontal cortex) and reciprocal inhibition of the anterior cingulate, leading to experiences of “mind emptiness” and “indifference to pain” often seen in depersonalization. On the other hand, a left-sided prefrontal mechanism would inhibit the amygdala resulting in dampened autonomic output, hypoemotionality, and lack of emotional coloring that would, in turn, be reported as feelings of “unreality or detachment.”

-Depersonalization: neurobiological perspectives

  Although DP/DR can occur as a primary condition, it often accompanies other psychiatric  or neurological diseases.

  Most of the neurological conditions associated with DP/DR, such as epilepsy, migraine, and mild head trauma etc have poor localisation value. However, DP/DR have also been described accompanying localised lesions. This raises the question if the study of such cases (the lesion method) might be a valuable approach to study the neurobiology of DP/DR.

-Separating depersonalisation and derealisation: the relevance of the “lesion method”

  Depersonalization appears to be associated with functional abnormalities along sequential hierarchical areas, secondary and cross-modal, of the sensory cortex (visual, auditory, and somatosensory), as well as areas responsible for an integrated body schema. These findings are in good agreement with the phenomenological conceptualization of depersonalization as a dissociation of perceptions as well as with the subjective symptoms of depersonalization disorder.

-Feeling Unreal: A PET Study of Depersonalization Disorder

To answer another one of your questions as the above papers show it may or may not be caused by organic brain damage. It is co-morbid to epilepsy but is its own distinct diseases. That is to say epilepsy is caused by overloads in neural pathways like a neural thunderstorm. DR/DP is what is left over after the storm starts destroying pathways. Likewise with oxygen deprivation and a stroke.

There are no drugs to treat all the symptoms of DR/DP instead antidepressants like Prozac and anti-anxiety like Klonopin are known to help sometimes.

Freud created a very basic and useful treatment for DP/DR called Reality testing which is a main component in CBT. In it you logically examine and reflect on your emotional responses and see how you correctly or incorrectly responded. The you make adjustments to become more rational. Rather than fixing the underlying problem it allows the sufferer to adapt to the disease.

DR/DP is not always associated with a delusion. So sometimes people can self identify the onset of an episode.

All things psychological are new but DP/DR is not very new. It was introduced in DSM-II in 1968. Yes DP/DR diagnostic is controversial in the psychological science. This is because it is used in criminal law. As it is a major question if someone who commits a crime in a DP/DR state should be held equally accountable. (Saks 2000)

References

Hunter EC, Sierra M, David AS (2004). "The epidemiology of depersonalization and derealisation. A systematic review". Social psychiatry and psychiatric epidemiology 39 (1): 9–18. doi:10.1007/s00127-004-0701-4. PMID 15022041

Simeon, D., & Abugel, J. (2006). Feeling Unreal: Depersonalization Disorder and the Loss of the Self. New York, NY: Oxford University Press.

Simeon D (2004). "Depersonalisation Disorder: A Contemporary Overview". CNS Drugs 18 (6): 343–54. doi:10.2165/00023210-200418060-00002. PMID 15089102.

Sierra, M., & Berrios, G. E. (1998). Depersonalization: neurobiological perspectives. Biological Psychiatry, 44(9), 898-908.

Sierra, M., Lopera, F., Lambert, M. V., Phillips, M. L., & David, A. S. (2002). Separating depersonalisation and derealisation: the relevance of the “lesion method”. Journal of Neurology, Neurosurgery & Psychiatry, 72(4), 530-532.

Simeon, D., Guralnik, O., Hazlett, E. A., Spiegel-Cohen, J., Hollander, E., & Buchsbaum, M. S. (2000). Feeling unreal: a PET study of depersonalization disorder. American Journal of Psychiatry, 157(11), 1782-1788.

Saks, E. R., & Behnke, S. H. (2000). Jekyll on trial: Multiple personality disorder and criminal law. NYU Press.


About the left and right side of the brain

Persons of each handedness use both hemispheres of the brain.

If you're asking specifically whether taking an action with your right hand preferentially activates motor control in the left hemisphere, the answer is yes. Motor function for the right side of your body is mapped to the left side of your brain, and vice versa. So for crossing your right leg over your left, that specific action uses your left brain to move your right leg. But that does not mean a person who crosses his or her leg right-over-left all the time is a "left-brained" person.

"Analysis is left-brain" is a pop psychology myth. A specific capability may be found in one place (e.g. speech production in Broca's area, which is often in the left hemisphere), but higher-level functionality like logical analysis or creativity have been found not to be lateralized (i.e. not fixated in one hemisphere or the other).

Nielsen, et al. 2013. "An evaluation of the left-brain vs. right-brain hypothesis with resting state functional connectivity magnetic resonance imaging." PLOS ONE


What is the causal relationship between extreme jealousy and poor mental health?

I think it can go both ways. According to Tesser's Self Evaluation Maintenance Theory, any two people in a relationship make themselves feel better by comparing themselves to each other. The key idea is that if you are closer to a person then you will tend to feel more jealous. For example, suppose your best friend got a really fancy car. You will naturally feel jealous. However, what if someone told you that Bill Gates got a really fancy car? You wouldn't feel jealous.This is similar to mental construal theory mentioned in this post.

If you tend to be jealous of someone close to you all the time I would think this would lead to depression. Depression is marked by rumination which is what happens if you are constantly jealous. Then again, if you are depressed because of some acute stress (e.g. death in a family) then you could feel jealous of other people without this particular stress.

One of the best ways of overcoming jealousy is to accept that you are jealous and empathize/congratulate the person you are jealous of. Exercises like mindfulness meditation would help promote empathetic behaviors.


How / when does neurogenesis occur while learning?

It has been discovered that neurogenesis takes place only on the hippocampus.

Quoting Leonard E. White:

  We now agree that the production of new
  neurons in the human brain is really
  limited to a special set of stem cells
  that seem to sit in the basal region of
  dentate gyrus of the hippocampus.
  So in this subgranular zone, we have a
  population of neural stem cells that can
  differentiate into interneurons that are
  found in the granule cell layer of the
  hippocampus.

Also as you said, this production could be modulated through some interventions (e.g. learning)

  This genesis of new
  neurons in the hippocampus can be
  modulated.
  By all kinds of different interventions
  including pharmacological agents such as
  antidepressant medications.
  As well as physical interventions, such
  as exercise.

Also, this has been mentioned in this ted talk:

https://www.ted.com/talks/sandrine_thuret_you_can_grow_new_brain_cells_here_s_how

In summary, the following activities impact positively on neurogenesis:

Learning
Sex
Running
Good diet

While these ones impact negatively:

Stress
Bad sleep
Ageing

pd: Concerning how memory works, my knowledge there is limited.


As pointed out in another answer of mine, therapists are not immune to psychological problems. In fact, one study shows the lifetime rate of depression in psychologists and social workers to be higher than that of the general population (Deutsch, 1985).
They hear about difficult, sometimes traumatic experiences as their clients share their issues. This can lead to problems due to the phenomenon known as Emotion Contagion. They too occasionally have personal problems and things they may find difficult work through without some assistance. See This TalkSpace article for some other examples of how therapists might need therapy.
As you indicated in your question, sometimes this may not be immediately noticed by the therapist for reasons like hidden issues. As I have pointed out in another previous answer - see for more info., there is Clinical Supervision which helps to highlight any possible psychological issues or hidden traits — e.g. prejudices or other incorrect thought patterns/conclusions) — which may need therapy (See my answer talking about Johari Windows for more on that). This is standard practice, and required in codes of practice for registered counsellors, psychotherapists, psychologists, psychiatrists, etc. and those in training.
References
Deutsch, C. J. (1985). A survey of therapists' personal problems and treatment. Professional Psychology: Research and Practice, 16(2), 305–315. https://doi.org/10.1037/0735-7028.16.2.305


Why I value celebrities opinion more than a person I have actually met?

My take on this is because there are no other options. We have no previous emotional involvement, attachment or knowledge of them on a personal level.

We trust strangers on a daily basis. We get on a bus, which is driven by  a stranger. We go out to eat food and that food is cooked by strangers. We also work for strangers (until we get to know them, better). Celebrities are paid, celebrities are smart. They build up reputation and we trust statistics more than just one example from our personal lives. Thousands of people know Leo. Millions. There are probably no public statistics on our friends or co-workers, people we work with or spend time with. We just go by our opinion.

When you meet someone and work with them, what does that relationship entail? Emotional involvement. You get to know them and form opinions. Things you like about them and things you don't like. You're listening to more than just a few conversations about a given topic.

If you're listening to a speech from a celebrity you know of and their opinion is to your liking, that's all you're hearing. You don't really know anything else about them to have any other options but to trust them.

  This is also very similar to why some people trust their therapist
  over their friend, even if what both of them say are similar. Sometimes, they aren't similar. We tend to trust what we're more objective towards. Who you're surrounded by makes a huge difference. They can be abusive, vulgar, rude. You're seeing more than just one side to them. You're only seeing one side of your therapist. The helpful, knowledgeable side.

If we spend enough time to form an emotional bond with a therapist or let's say someone we've never met, we could very well go back to square one. Not trusting them as much as another celebrity you're objective towards.

When we're listening to the opinion of someone we know, other emotional factors are involved. Our dislikes (and other opinions of them) influence our trust in them and their opinions or knowledge of a given topic.

It's about things being objective. What we don't know can't  hurt us. In your case, you don't know much about Leo's personal life. You only know the opinions he shares. There's nothing else to go by and usually documentaries give you the best parts specified information. Nothing that sounds inaccurate, immoral, wrong or questionable.

Helpful Sources

Why We Trust Strangers More Than Our Friends
We Trust Strangers, Even When It Doesn’t Make Sense to Do So
Why do some people prefer to trust what strangers say rather than those they know?


The root cause is almost certainly procreation. Our relationship tendencies developed along with our biology. Humans tend to have one child at a time, and human children mature very slowly. This suggests that during most of human history, it would be advantageous for a female to keep a male with her, helping to provide food and protection for herself and her children. The strategy for the male is either to play along, or to breed so quickly as to outweigh the devastating effect of a long maturation without sufficient protection. Others species, many of which breed in greater numbers, have different mating habits.


"High-density EEG" refers to the number of electrodes in the array.  Typically, any EEG rig with more than 64 electrodes is considered to be high-density electroencephalography.


What are the top contributions from neuroscience to AI and viceversa? How much progress has been made from the interaction between these two fields?

There is a really close correspondence between Auditory Scene Analysis and Computational Auditory Scene Analysis. If you tried to build a speech recognition system, especially for use in noisy environments, while ignoring what we know from auditory psychophysics, physiology, and anatomy, I would guess that you would not get too far. The things we have learned from CASA have lead to better hearing aids and cochlear implants, which in turn have taught us about the auditory system, which of course leads to further improvements in CASA.

Bregman has a nice summary (along with conferences) on his webpage


Difficulty of expressing thoughts verbally

This is not a direct answer to the question, but a related construct that may be useful is alexithymia.

Alexithymia is a personality construct describing relatively decreased ability to identify and express emotions. Psychometrically, the alexithymia construct has seen extensive use and undergone testing that by and large supported its validity (Bagby, Parker and Taylor, 1994a; Bagby, Parker and Taylor, 1994b). In clinical populations, the causes have been theorized to include anterior cingulate cortex and right hemispheric dysfunction, but the cognitive neuroscientific evidence is currently mixed (Zaidel, 2005).

Unfortunately, I am not aware of any direct parallel for the inability to adequately express thoughts, nor of any direct treatments, and I was not able to find anything in the literature. Hopefully, the alexithymia construct may still be of some use in finding an answer.

References

Bagby, R. M., Parker, J. D., & Taylor, G. J. (1994). The twenty-item Toronto Alexithymia Scale—I. Item selection and cross-validation of the factor structure. Journal of psychosomatic research, 38(1), 23-32.
Bagby, R. M., Taylor, G. J., & Parker, J. D. (1994). The twenty-item Toronto Alexithymia Scale—II. Convergent, discriminant, and concurrent validity. Journal of psychosomatic research, 38(1), 33-40.
Zaidel, G. T. E. (2005). Alexithymia, interhemispheric transfer, and right hemispheric specialization: a critical review. Psychother Psychosom, 74, 81-92.


What happens in my retina if I press on my eyeballs?

Short answer
Pressure phosphenes are believed to be induced by sensory neurons in the retina downstream from the photoreceptors due to stretch-mediated activation.

Background
You are referring to pressure phosphenes. They are visual perceptions induced by applying pressure to the eye ball. They are often described as a glow with arcuate or circular characteristics and are generally perceived in the visual field opposite to the area of pressure. If the object applying the pressure is small, the center of the perceived area appears light with a dark surround and a bright outer portion. However, there is substantial inter-individual variability in how pressure phosphenes are perceived (Chew et al., 2005).

Eyeball deformation leads to an activation of ON-center ganglion cells in the retina, while OFF-center ganglion cells are inhibited. It is thought that the activation of ON-center and inhibition of OFF-center ganglion cells by eyeball deformation are caused by retinal stretching, which may also lead to horizontal cell stretch. Stretching the horizontal cell membrane probably generates an increase in membrane sodium conductivity and a depolarization of the membrane potential. This depolarization of the horizontal cell membrane potential is transmitted either directly or indirectly (via receptor synapses) from the horizontal to the bipolar cells. The bipolar cells, in turn, can activate or inhibit the ganglion cells (Grüsser et al., 1989). Note that in this model, the photoreceptor cells in the retina are not involved - it occurs downstream in the secondary sensory neurons.

References
- Chew et al., Eye (2005) 19: 683–5
- Grüsser et al., Physiol Bohemoslov (1989); 38(4): 289-30


Why do dreams lose clarity quickly over time after we awaken?

Short answer: Because areas of the brain needed for remembering are turned off during dreaming.

Dream Amnesia:

The process of converting perception into a memory construct that can be stored is called encoding, and is essentially the same during both wakefulness and sleep: That is, the same factors can hamper or promote successful encoding when awake or dreaming.  During sleep, the brain undergoes cyclical changes in which activity in some parts of the brain increases (hyperactive), while other areas decrease in activity (hypoactive).  Some areas of the brain associated with memory encoding are hypoactive during dreaming, resulting in most dreams being forgotten.

Red = hyperactive; Blue = hypoactive; F = prefrontal cortex

The most prominent area implicated in memory encoding of episodic memories is the prefrontal cortex (PFC).  Activity in this region is correlated with memory in studies conducted in awake subjects, and is similarly correlated with dream amnesia: During dreaming, this area is typically hypoactive (turned off), and its level of activity is predictive of dream recall.  Activity in the PFC during sleep may be modulated by levels of acetylcholine, dopamine, and other neurotransmitters.

Vanishing Memory:

Nir & Tononi (2010) review the issue:

  Unless the dreamer wakes up, most dreams are forever lost. Upon
  awakening, memory for the dream often vanishes rapidly unless written
  down or recorded, even for intense emotional dreams. It is not clear
  why this is the case since from a neuroimaging perspective, limbic
  circuits in the medial temporal lobe that are implicated in memory
  processes, are highly active during REM sleep. Perhaps the
  hypoactivity of prefrontal cortex, also implicated in mnemonic
  processes, plays an important role in dream amnesia.

Theoretically, waking up reactivates the areas of the brain that are turned off during sleep, allowing for memories to be encoded.  This process is unreliable, as memory encoding in both awake and sleeping subjects is modulated by attention - also a function of the PFC - so how much and how well dream content is remembered also depends on how much attention is given to it during waking.  Without attention, the memory trace fades quickly.  This interpretation is consistent with the reduced dream recall in awakenings from deep (slow-wave) sleep, that are characterized by disorientation and lower PFC activity, and with higher dream recall of lucid dreaming, characterized by awareness, control, and higher PFC activity.

Note: The above is certainly an over-simplification of a complex and poorly understood system, but it does suggest that any factor affecting the processes involved in memory encoding and attention (such as certain neurotransmitters, psychoactive drugs, lesions, mood disorders, training, experience, etc) may impact dream recall.  On the other hand, NMDA, a neurotransmitter involved in long-term memory consolidation (LTP) - a different activity that is increased (hyperactive) during dreaming - is less likely to be implicated in dream amnesia.


Understanding a negative correlation between Pc and signal strength

I find that it is the signal strength of the second signal that more so determines correct detection (0,1)

The ideal unbiased observer bases the decision on $X1-X2$ while it sounds like your subjects are basing their decision on $aX1-X2$ where $a < 1$. While it is suboptimal, it is not a big deal. The fact that you know it means either report it or train the subjects out of it.

  the correlation between probability of correct detection (p) and both signals is significant and negative.

If the first stimulus is very weak, the difference between it and the second stimulus will on average be larger than if the first stimulus is of moderate strength. One would therefore expect Pc to initially decrease as the strength of the first stimulus decreases. Additionally, if the first stimulus is very strong, the difference between it and the second stimulus will again be larger on average than if the first stimulus is of moderate strength. Therefore, for an ideal observer, the dependency of Pc of the strength of the first signal should be non-monotonic. The same holds for the second stimuli.

We know from the above statement that your subjects are not ideal. If the bias depends on the strength of the first signal (i.e., $a(X2)$ increases with X2) then the non-monotonicity of Pc on the strength of the stimuli could be hidden.


Understanding the concept behind d-prime

First lets write down some math for the above figures assuming Gaussian distributions with means $\mu_{n}$ and $\mu_{s}$ both with a standard deviation of unity. In this case the probability of a detection is
$$P_D=1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x-\mu_{s})^2/2}dx$$
and the probability of a false alarm is
$$P_F=1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x-\mu_{n})^2/2}dx$$
and the normal deviates are
$$Z_D=\Phi^\prime(P_D)$$
and
$$Z_F=\Phi^\prime(P_F)$$
where $\Phi^\prime(x)$ is the inverse of $\Phi(x)$
$$\Phi(a)=1/(\sqrt{2\pi})\int_{-\infty}^{a}e^{-x^2/2}dx.$$
We also need to note that
$$1/(\sqrt{2\pi})\int_{-\infty}^{c}e^{-(x)^2/2}dx+1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x)^2/2}dx=1$$
and that
$$\Phi(-x) = 1-\Phi(x).$$
Now using integration by substitution on $P_D$ and the above equalities  gives us
$$P_D=1/(\sqrt{2\pi})\int_{c-\mu_{s}}^{\infty}e^{-(x)^2/2}dx=1-1/(\sqrt{2\pi})\int_{-\infty}^{c-\mu_{s}}e^{-(x)^2/2}dx=1-\Phi(c-\mu_{s})=\Phi(\mu_{s}-c).$$
You can play the same mathematical games and get that $P_F=\Phi(\mu_{n}-c)$ or that $Z_D=\mu_{s}-c$ and $Z_{CR}=c-\mu_{n}$ (this one is a little trickier ...).
Now on to your questions

(1) As in the plot above, d' is always depicted as the difference of the means of the two distributions (of signal and noise, for instance). Say however that I find in my data that the Hit rate (or Hit probability) is 0.8 - I would think that now, I would need to find z(Hit = 0.8), would this not be to the right of the mean:

This depends on what the means are. If the signal distribution has a mean of $-100\sigma$, then $Z_{hit}$ will likely be to the right of the mean, but if the signal distribution mean is $100\sigma$ it will likely be to the left.

In addition, I am am uncertain about the arrows associated with Z(CR) and Z(H) on panel A above.
For one, in my opinion, CR includes the entire area before the criterion. The arrow, however, associates Z(CR) with only the distance mean-criterion - why?

This is a direct result of the magic of the math above.


What do we know about schizophrenia and mathematics?

I spent times of the order of five to eight months in hospitals in New
  Jersey, always on an involuntary basis and always attempting a legal
  argument for release. And it did happen that when I had been long
  enough hospitalized that I would finally renounce my delusional
  hypotheses and revert to thinking of myself as a human of more
  conventional circumstances and return to mathematical research. In
  these interludes of, as it were, enforced rationality, I did succeed
  in doing some respectable mathematical research.

Seems like he himself is saying his research suffered while unwell and not staying in institutions.

However, the standard deficit in IQ, of it seems around 10 points, may be inconsequential in someone like Nash. Even if the executive function and memory impairments are more significant.


I think there is a significant confound in your experimental design: The anchored subjects only make 1 estimate whereas the "no anchor" subjects make 2 estimates. Note that on the first estimate the anchored subjects were much closer to the anchor than the non anchored ones, which is entirely consistent with Tversky's heuristic.

Also, "In all cases, Jelly Bean Counter 5000 provided the exact number of jelly beans in the jar." means that this isn't really a standard anchoring task. Normally, anchoring values aren't correct (in fact much of the anchoring work involves very incorrect anchors). This task confounds being close to the anchor with being close to the correct answer.

You might have an interesting finding: more anchoring after a non-anchored guess, but without correcting for the 2-guess and perfect anchor confounds your results can't be properly interpreted.


What's the difference between Confirmation Bias and the Affect Heuristic?

Confirmation bias is the tendency to search for, interpret, favour, and recall information in a way that confirms pre-existing beliefs or hypotheses (WikiPedia; Plous, 1993)

The affect heuristic is a mental shortcut that allows people to make decisions, and solve problems quickly and efficiently, in which current emotion - fear, pleasure, surprise, etc. - influences decisions.

  In other words, it is a type of heuristic in which emotional response, or "affect" in psychological terms, plays a lead role. (WikiPedia)

Or in the words of Slovic,

  As used here, ‘‘affect’’ means the specific quality of ‘‘goodness’’ or ‘‘badness’’ (Slovic, et al. 2007)

They can sound similar, and in a way they can be; but generally they are different.  With confirmation bias, I would be looking for something to back up a belief I “know” is correct, while I may or may not like this belief,

  it is the only correct answer!

This is different to the affect heuristic, where I don’t like the proposition put forward by others and so I am going to look for evidence to back the ideas I like.

--Edit for further clarification after comment--

You could say

  You can search for evidence to confirm something is right if you believe it's right, and you can search for evidence to confirm something is wrong if you believe it's wrong

and that is true.  That would be Confirmation Bias if you are searching purely for evidence to prove your belief based on what is known.  Let's look at the difference in another way.

Scenario where there are two opposing points of view ($X$ and $Y$).

$X$ has a conclusion based on plenty of evidence which is corroborated by many unbiased studies.$Y$ has a conclusion which is also based on plenty of studies which corroborates each other.However, there were flaws in some studies and others were biased due to undeclared financial interests with some participants.

When there is no bias, you are completely open minded and you would be taking an unbiased viewpoint on the evidence presented, therefore it would be fair to assume that $X$ is true and $Y$ is false.  When looking for more evidence, you are looking for evidence for and against both $X$ and $Y$.

When there is Pure Confirmation Bias, you totally accept $X$ being true, and it fits with your beliefs and way of life, and when looking for more evidence, you are looking to strengthen that truth with more evidence to back $X$ and more evidence to refute $Y$.

When there is Confirmation Bias with Affect Heuristics, this can be where you don't like viewpoint $X$ because it doesn't fit with your beliefs.  You can accept $X$ being true, but there is the counteracting wish for $Y$ to be true.

There can be affect heuristics involved when looking for any strong counteracting evidence, yet you are still accepting that $X$ is true, so whilst looking for counteracting evidence, you are also looking for evidence confirming $X$.  You could be forgiven for thinking that this is unbiased research, but it is not unbiased, because you wish for $Y$ to be true as you have a vested interest in $Y$ but you also accept $X$.

When there are pure Affect Heuristics, you cannot accept $X$ as true because of your beliefs, or because it adversely affects your way of life, and when looking for more evidence, you are looking for evidence to back $Y$ and plenty of evidence to refute $X$.

References

Plous, S. (1993). The Psychology of Judgment and Decision Making. New York: McGraw-Hill p.233

Slovic, P., Finucane, M. L., Peters, E., MacGregor, D. G. (2007). The affect heuristic. European Journal of Operational Research 177(3),1333–1352DOI: 10.1016/j.ejor.2005.04.006


Is there a good entry-level tutorial for SPM?

The best way to learn is probably not by reading, but by doing. The SPM website contains a number of useful datasets with tutorials for various tasks.

I also find PowerPoint slides from lectures and talks useful. There are a bunch of slides on the SPM website, but you can also find more on Google by limiting your results to type:pptx.


How to make diagnosis of these symptoms using Pet scan, fMRI, and EEG?

T2 weighted MRI scans can reveal white matter lesions, so that may explain the detection of demyelination.

Of course, that's not fMRI...


Is there a relation between speed of executing a task and ones intelligence?

Short answer: Processing speed is linked to executive functioning (EF) ability as well as specific, individual abilities (verbal, spatial, etc.), whereas generalized inspection time (IT) and reaction time (RT) to simple stimuli is more representative of general intelligence.

Detailed answer:
There are several factors that go into intelligence. Three specific, measurable paradigms are reaction time (RT), inspection time (IT), and speed of processing. Reaction time refers to the ability to respond to simple, familiar stimuli, and inspection time refers to the ability to identify a familiar stimulus. For example, if you are asked to press the space bar when you see a letter on the screen, your IT is being measured (time it takes to recognize the letter) as well as your RT (time it takes to press the space bar). Speed of processing is related to your ability to quickly perform familiarized or over-learned tasks, particularly when high mental efficiency is required. The difference: With RT and IT, you are asked to perform simple tasks that require little 'effort', yet they are (presumably) not tasks that are familiar to you. Speed of processing comes into play when you are asked to perform over-learned tasks that require more mental effort.

Though speed of processing has always been linked to intelligence in some form, it is now believed that RT and IT are related to general intelligence, whereas specific abilities (e.g. verbal abilities, spatial abilities) are moreso related to processing speed than to general intelligence. [1].

Speed of processing is often linked to working memory capacity. [2] This is demonstrated in those with certain learning disorders (such as ADHD), who often have working memory deficits and thus often process information slowly, regardless of IQ. Studies have also found that removing a time limit on testing removes the problems associated with dysfunctional working memory (such as lapses in attention). Thus it can be said that speed of processing is greater linked to executive functioning ability (which is a higher set of cognitive processes that working memory is a part of). [3]

So the answer to your question is that speed of processing is representative of specific abilities insofar as one's working memory capacity (and, by proxy, general executive functioning ability) is not dysfunctional, whereas the time it takes to identify and respond to a simple situation is linked to general intelligence.

In your particular instance, you were asked to answer an unfamiliar question with a non-trivial answer. Thus, it was speed of processing that was at play here, more closely linked to ability or knowledge of the topic at hand than general intelligence. The method in which the knowledge was acquired may have to do with intelligence, but there is too little context (and evidence) to support this.

Sources used:

[1] Placing inspection time, reaction time, and perceptual speed in the broader context of cognitive ability

[2] Conway AR, Kane MJ, Engle RW (December 2003). "Working memory capacity and its relation to general intelligence". Trends in Cognitive Sciences 7 (12): 547–52.

[3] "Working memory function in attention deficit hyperactivity disordered and reading disabled children". British Journal of Developmental Psychology 19 (3): 325–337.


Does a person experience release of dopamine while doing something she/he enjoys?

Like many topics in neuroscience, this is a controversial subject.  While dopamine is very popular among the public as a mechanism for pleasure, recent research challenges that view and has started to tease apart pleasure from motivation, finding a distinction in dopamine.

John Salamone's opinion:

  Low levels of dopamine make people and other animals less likely to work for things, so it has more to do with motivation and cost/benefit analyses than pleasure itself.

and his peer reviewed research:

Salamone, John D. and Correa, Merc. (2012).  The Mysterious Motivational Functions of Mesolimbic Dopamine.  Neuron, 76:3, pp.470 - 485.

It's more likely that the experience of pleasure is a distributed circuit phenomena, not down to any one neurotransmitter:

Smith, Kyle S.; Mahler, Stephen V.; Peciña, Susana; Berridge, Kent C.
Kringelbach, Morten L. (Ed); Berridge, Kent C. (Ed), (2010). Pleasures of the brain. , (pp. 27-49). New York, NY, US: Oxford University Press, viii, 343 pp.


How fast can the brain react in order for someone to pull a trigger?

Short answer
The motor response latency to a visual stimulus is approximately 210 ms.

Background
You are basically asking for the visually induced reaction time of a motor response. Reaction times have been assessed many times in various studies. In a very recent study with an impressive subject population of more than 1400 (aged 18 - 65), the motor response latency to a visual stimulus was estimated at an average of 213 ms. Reaction times increased with age, but were unaffected by sex or educational level. Old age mainly affected the motor latency, and not so much the visual processing speed.

Reference
- Woods et al., Frontiers Human Neurosci (2015); 9:131-12p


Why did DSM-5 and subsequently ICD-10 allow personality disorders to be diagnosed in children

An article on the NCBI website states

  Many clinicians are reluctant to diagnose personality disorders (PDs) during youth, viewing paediatric personality deviations instead as reflective of given developmental stages. This is so despite evidence that certain youth are indeed at risk for the eventual development of PDs as adults. Unfortunately, late identification of these disorders prevents timely treatment and potentially increases morbidity.

There are also a fair few references to articles backing the idea up


What is the extent of social grooming in humankind?

The literature on social grooming in humans mentions

  examples of grooming, most of which are unique to humans, include: running fingers through another’s hair, giving massages, washing the body or hair, shaving, removing lint or hair from another’s clothing, swatting away insects, and giving manicures or pedicures, and removing pus from blemishes or wounds. Grooming for humans can also include applying something to the skin or body as with lotion, nail polish, or make-up.

However, probably the more prominent and interesting line of research in this regard concerns language. The foundational BBS article by Dunbar (1993) argues that

  Group size covaries with relative neocortical volume in nonhuman primates. This regression equation predicts a group size for modern humans very similar to that for hunter-gatherer and traditional horticulturalist societies. Similar group sizes are found in other contemporary and historical societies. Nonhuman primates maintain group cohesion through social grooming; among the Old World monkeys and apes, social grooming time is linearly related to group size. Maintaining stability of human-sized groups by grooming alone would make intolerable time demands. It is therefore suggested (1) that the evolution of large groups in the human lineage depended on developing a more efficient method for time-sharing the processes of social bonding and (2) that language uniquely fulfills this requirement. Data on the size of conversational and other small interacting groups of humans accord with the predicted relative efficiency of conversation compared to grooming as a bonding process. In human conversations about 60% of time is spent gossiping about relationships and personal experiences. Language may accordingly have evolved to allow individuals to learn about the behavioural characteristics of other group members more rapidly than was feasible by direct observation alone.

In short, under Dunbar's proposal, because human groups are so large and complex, if we were to use the regular, manual grooming of our relatives, we would have to spend around half (e.g. 42% in Dunbar 1993) of our time grooming, which is entirely unsustainable. Language is instead used (and evolved) to more economically fulfill that role. Linguistic gestures, especially small talk, largely overtake the role of manual grooming in humans.

Make of this what you will, it's certainly an important and interesting proposal.


Reducing ceiling effect with a Likert scale measure

Here are a few thoughts:

Work out whether the construct has ceiling effects or whether it is a measurement issue: You need to consider whether people actually discriminate between the rated objects.

Multiple items per rated object: For each medical treatment you could ask participants to answer several questions. You could then take the mean of their responses for the items to get an overall rating of each treatment for each participant. This increases the number of possible scores and should also increase the reliability of measurement.

Is the aim to measure the group property or an individual property: For example, if you are aiming to get a measure of the degree to which a group considers a treatment effective, then by averaging over many individuals you should get nuanced measure. So even if people are generally answering 4,5, and 6, one treatment will have more 4s and 5s and another might have more 5s and 6s. The result is that the mean of such ratings will still be nuanced measure, and you can then say things like one treatment having a mean of 4.5 and another having a mean of 5.5, and so on. So in that sense, you can still compare group-level opinions of effectiveness.

Forced choice or ranking format: You could adopt a forced choice or ranking format where participants are asked to rank or make some form of comparative assessment of the relative effectiveness of a set of treatments. This has pros and cons. It will obviously give you a good understanding of perceptions of relative effectiveness, but you will not have information on how effective they perceive the treatments relative to a general standard of effectiveness.

Change the response scale: There are many choices for response scales. You can add more scale points (e.g., go to 7 or 10 point scale). You could even design a scale that is not balanced, so you make more distinctions of effectiveness. Personally, I think you need a principle to govern your choice of scale. A good general rule is to talk to people doing the rating and find out what words they use to describe the effectiveness of treatments. How many distinctions do they make? What is the difference between ineffective and very ineffective in their mind?


I contacted the author. He's now in University of Trento.

He says it refers to the theory of multiple levels of reality, the dynamics of each level, and the interaction among them.


Why do some people stutter only when they are nervous?

Interesting question!

Assuming you are talking about stuttering, as occurs in about 1% of the population (Sommer et al., 2003), as opposed to non-pathological stammering during stressful situations that many more people experience, my answer is as follows:

Stress and speech disruption in stutterers are undoubtedly related (e.g., Craig, 1999). In fact, they may be causally related, as stress can provoke or aggravate stuttering, which in turn may cause more stress to the stutterer due to feelings of shame or loss of control. This in turn may induce more stuttering and may thus lead to a downward spiral, or vicious circle (Schwartz, The Stuttering Child) that may grossly disrupt speech.

The underlying physiological basis of why stress provokes stuttering has been addressed by Weber & Smith, (1990). It shows that speaking increases autonomic activity (elevated blood flow, increased heart rate, sweating) and that this sympathetic arousal was correlated with increased stuttering behaviors in stutterers. Interestingly, the sympathetic arousal of stutterers was found not to be outside the range of controls. The authors bring up several hypotheses as to why sympathetic activity may deteriorate speech fluency in stutterers:

Increased autonomic activity has been associated with irregular breathing, which may affect speaking;
Release of the stress hormone adrenalin may induce muscle tremor and spasms that can affect speech production;
Sympathetic regulation of afferent control of the sensitivity of sensory receptors (muscle spindles and mechanoreceptors) in the oralmotor, laryngeal and respiratory system may affect speech motor processes;
The gain of reflex arches (feedback) involved in the musculature engaged in speech may be modulated such that speech fluency is negatively impacted.

These processes may aggravate the underlying pathology of stutterers (Büchel & Sommer) and hence lead to more pronounced stuttering under stress.

PS: Being a stutterer myself since early childhood, I support the behavioral consequences of stress mentioned in above studies by anecdotal experience :)

References
- Buchel & Sommer, PLoS Biol 2004; 2(2): e46
- Craig, J Speech Hear Disorders 1990; 55: 290-4
- Schwartz, The Stuttering Child, Coping With Stuttering
- Sommer et al., Movement Disorders 2003; 18(7): 826*30
- Weber & Smith, J Speech Hear Res 1990;33(4): 690-706


Does the meta-analytic literature overestimate the relationship between conscientiousness and job performance?

I'm posting a summary here (thanks to @DJ Sims for directing me to the paper of interest). Kepes and McDaniel (2015) re-analysed data from an existing meta-analysis. The existing meta-analysis had been examining various moderators of the relationship between big 5 personality and job performance. Kepes and McDaniel performed a range of sensitivity analyses.

They summarise their results as follows:

  Publication bias analyses
  demonstrated that the validity of conscientiousness is moderately
  overestimated (by around 30%; a correlation difference of about .06).
  The misestimation of the validity appears to be due primarily to
  suppression of small effects sizes in the journal literature.

As evidence for publication bias, they show that the average validity for conscientiousness is lower in unpublished samples:

  The results for the sub-group distributions of samples from journal
  articles (k = 67) and non-journal sources (k = 46) [indicate that] samples
  published in journal articles reported larger average
  effect size estimates (   $\bar{r}_{oRE}$   = .19) than samples from non-journal sources (
    $\bar{r}_{oRE}$ = .12.

A few critical comments:

When publishing results showing the relationship between big 5 personality and performance, there are five correlations presented. Assuming that publication bias sometimes led to a requirement to have at least one significant correlation, then the publication bias should be less.

The study does not cite or discuss other common meta-analyses on the Big 5 and job performance, which interestingly have often obtained meta-analytic estimates similar to what they say is the correct value. For example, the famous early meta-analysis by Barrick & Mount (1991) using 12,893 cases and 92 correlations obtained a mean raw correlation between conscientiousness and job proficiency of $\bar{r}$ = .13. In a meta-analysis by Hurtz and Donovan that exclusively used correlations for measures using the big 5, they obtained an overall validity for conscientiousness of $\bar{r}$ = .14. This also is very close to what might be expected.

These traditional estimates of validity from previous meta-analyses are sample weighted means. Thus, they naturally weight large samples more. So, for example, one study with 2000 participants would be weighted as much as 20 studies each with 100 participants.

There are good reasons to assume that publication bias would have less of an effect on large sample studies (e.g., n > 1000). First, when the sample size is sufficiently large, the results become intrinsically interesting. Reviewers can not argue that it was merely a lack of statistical power. Second, such studies generally have sufficient power to detect correlations in the r = .10 area. For example, assuming a population correlation .10, alpha of .05, and a two-tailed test, to have at least 90% power to detect a significant correlation you would need at least 1,046 participants.

My take away from the paper:

There is probably publication bias in the literature in relation to small sample studies. I imagine this publication bias is relative. If I were to guess, I'd say strong bias at n < 100; moderate bias n < 200, and progressively less as you move to 500+.

References

Kepes, S., & McDaniel, M. A. (2015). The Validity of Conscientiousness Is Overestimated in the Prediction of Job Performance. PloS one, 10(10), e0141468. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141468


How does recalling a specific memory decrease depression?

In a meta-anylysis, Bohlmeijer (2007) found that:

  In the last twenty years reminiscence has been applied in a large
  number of settings and with a large number of target groups. Examples
  of applications are: community-residents with a major depression,
  elderly with moderate depressive symptoms, nursing home residents,
  elderly with dementia, rural-dwelling older adults, elderly in
  assisted-living communities. ... We conducted a meta-analysis to
  assess the effects of reminiscence on depression across different
  modalities and target-groups. An over-all effect size of 0.84 (95% CI
  = 0.31 – 1.37) was found, indicating a statistically and clinically significant effect of reminiscence and life review on depressive
  symptomatology in elderly people. This effect is comparable to the
  effects commonly found for pharmacotherapy and psychological
  treatments. (p. 152f.)

To answer your first question, it seems that reminiscence and life review are an effective treatmtment of depression for a wide variety of (elderly) patients. It should be noted that a "significantly larger effect was found in studies in which life-review was the intervention (d=1.04) as compared to studies that used simple reminiscence (d=0.40)" (p. 152).

Several theories have been applied to try to explain how recalling memories decreases depression:

disengagement theory
ego-integrity theory
continuity theory
socio-emotional selectivity theory

Disengagement Theory

  The foundations for reminiscence and life-review therapy were laid by
  Butler (1963) in his famous paper The life-review: an interpretation
  of reminiscence in the aged. In this paper Butler put down his
  clinical observation of an increase of reminiscence – the act or
  process of recalling the past - in older people and postulated that
  this was due to the universal occurrence of an inner experience or
  mental process of reviewing one’s life. He conceived of life-review as
  a spontaneously or naturally occurring process that is ‘characterized
  by the progressive return to consciousness of past experiences, and,
  particularly, the resurgence of unresolved conflicts’ (Butler, 1963,
  pg 66). He hypothesized that it is caused by the ‘realization of
  approaching dissolution and death, and the inability to maintain one’s
  sense of personal invulnerability’ (Butler, 1963, pg 67). Though he
  recognized that people of all ages review their past from time to time
  and that any crisis may prompt life review, Butler stressed that
  life-review is more intensive and observed more frequently in (early)
  old age. He discerned adaptive and constructive manifestations of
  life-review from psychopathological manifestations. The adaptive
  variant is described as a reconsideration of former life-experiences
  and their meanings. It will often be accompanied by mild feelings of
  nostalgia or regret but is generally typified by expanded
  understanding and acceptance of one’s life, the experience of
  meaningfulness and declining death-anxiety. (Bohlmeijer, 2007, p.
  32)

Ego-Integrity Theory

  In its early stages reminiscence was studied mainly within the context
  of developmental stage theory (Erikson, 1963; Webster, 1999).
  Life-review was seen as a naturally occurring process which takes
  place in the last stage of the psychosocial development of human
  beings. The main hypotheses that could be deduced from this theory
  were that life-review is universal and old-age specific. These
  hypotheses were not confirmed in empirical studies. ... Based on
  studies rejecting the claim that life-review is old-age specific, it
  was suggested that reminiscence and life-review could be better
  understood within a life-span perspective (Webster & Cappeliez, 1993;
  Webster, 1999). ...

  In addition to the disengagement theory (Baum & Baum, 1980; Butler,
  1963) and the ego-integrity theory (Erikson, 1956; Taft & Nehrke,
  1990), in recent years new theories are applied to reminiscence, for
  example the continuity theory and socio-emotional selectivity theory.
  These theories fit with a contextual and life-span approach to
  reminiscence. (Bohlmeijer, 2007, p. 37f., 40)

Continuity Theory

  According to continuity theory individuals, when confronted with
  life-events or transitions, ‘attempt to preserve and maintain existing
  internal and external structures and they prefer to accomplish
  this objective by using strategies tied to their past experiences of
  themselves’ (Atchley, 1989, pg 137). This sense of continuity, with
  the aid of reminiscence, will promote adaptation (Parker, 1999).
  Continuity theory would predict that people will reminisce more
  frequently during periods of personal transition than in more stable
  periods. In testing this hypothesis, Parker (1999) found that young
  people were significantly more likely to reminisce during transitional
  periods than older adults. (Bohlmeijer, 2007, p. 40)

Socio-Emotional Selectivity Theory

  Another theory applied to reminiscence is
  the socio-emotional selectivity theory (Carstensen, 1995). This theory
  proposes that with growing age emotion regulation becomes more
  important than information gain and that the elderly arrange their
  social life in such a way (concentrating on close relationships) that
  they can have as many emotionally meaningful interactions as possible
  (Pasupathi & Carstensen, 2003). One important aspect of such
  self-regulation is known as the positivity effect (Carstensen &
  Mikels, 2005), in which it is assumed that an emo- tionally gratifying
  focus ‘...would bias attention and memory in favour of material that
  optimizes emotion regulation (i.e., positive material) even if there
  are costs to focusing only on such material’ (p. 118). This hypothesis
  has been supported by many studies (Kennedy, Mather, & Carstensen,
  2004).

  Older adults will therefore actively look for social
  interactions in which they reminisce because of the potential for
  emotion regulation and well-being (Penne- baker, 1997; Bluck & Levine,
  1998). This preference for talking about the past in social
  interactions with strangers was confirmed in several studies
  (Pasupathi & Carstensen, 2003). (Bohlmeijer, 2007, p. 41)

Note:

Bohlmeijer's dissertation gives a comprehensive overview of this area, if you want a quick introduction. It is available for free online (see link below). Serrano's article has been quoted 157 times, according to Google Scholar. Probably some of those articles will provide interesting criticism and more recent research not covered in Bohlmeijer's meta-analysis from five years ago. You can find these articles listed at Google Scholar.

Sources:

Bohlmeijer, E. (2007). Reminiscence and depression in later life (Dissertation). Am- sterdam: Faculty of Psychology and education, Vrije Universiteit. Available online at http://www.researchgate.net/publication/8958357_Effects_of_reminiscence_and_life_review_on_late-life_depression_a_meta-analysis/file/79e4151397c8674185.pdf


This statement on Wikipedia is merely intending to separate the agency of determining "What is pain?" from the nociceptors. Nociceptors can be activated by a number of stimuli that reflect possible damage (i.e., a possible threat): this could include signals released by cells that are actually damaged, it could include hot temperature, it could include certain types of pressure or touch.

The decision about whether a particular stimulus is sufficiently threatening to warrant a response (which could include things like reflexes all the way up to the perceptual and emotional experience that we refer to as pain) is made in the spinal cord and brain. At the level of the nociceptor, "possible threat" and "real threat" aren't any different: the nociceptor is just reporting the possibility of the threat. The CNS makes a 'decision' about how to respond.

This system is really no different than the other sensory systems, they all carry some information to the CNS which then interprets that information.


Will some people ever be able to make our dreams visible on a screen?

As @AaronWeinberg stated in the comments, just like many other technologies within Science Fiction, the Science Fiction of viewing dreams on screen has started to become Science Fact.

Rebecca Morelle, a science reporter for the BBC World Service wrote an article about researchers in Japan who used MRI scans to reveal the images that people were seeing as they entered into an early stage of sleep.

From the articles I have seen, it looks like the research has been led by Professor Yukiyasu Kamitani, from the ATR Computational Neuroscience Laboratories, in Kyoto.  It seems that the research started in 2005 with an article titled Decoding the visual and subjective contents of the human brain (Kamitani & Tong, 2005) followed by the article Neural Code Converter for Visual Image Representation (Yamada, et al. 2011), follwed then by Decoding visual experience from the human brain (Kamitani, 2012) and then the source of the first linked article Neural Decoding of Visual Imagery During Sleep (Horikawa, et al. 2013)

The results of the first study within the 2005 article demonstrated that

  fMRI activity patterns in early visual areas, including primary visual cortex (V1), contain detailed orientation information that can reliably predict subjective perception.

The 2011 article says

  [T]he neural code converter may provide a basis for brain-to-brain communication of visual images.

The 2012 article says

  Despite the wide-spread use of human neuroimaging, its potential to read out, or "decode", mental contents from brain activity has not been fully explored. In this talk, I present methods for decoding visual representations from fMRI activity patterns based on machine learning techniques.

and the final article in 2013 says

  Our findings demonstrate that specific visual experience during sleep is represented by brain activity patterns shared by stimulus perception, providing a means to uncover subjective contents of dreaming using objective neural measurement.

References

Horikawa, T., et al. (2013) Neural Decoding of Visual Imagery During Sleep. Science 340(6132): pp. 639—642DOI: 10.1126/science.1234330

Kamitani, Y. & Tong, F. (2005) Decoding the visual and subjective contents of the human brain. Nature Neuroscience 8(5): pp. 679—685
DOI: 10.1038/nn1444

Kamitani, Y. (2012) Decoding visual experience from the human brain. Proceeding MM '12 (Proceedings of the 20th ACM international conference on Multimedia). New York:Association for Computing Machinery pp. 5—6 DOI: 10.1145/2393347.2393353

Yamada, K., et al. (2011) Neural Code Converter for Visual Image Representation. 2011 International Workshop on Pattern Recognition in NeuroImaging: pp. 37—40DOI: 10.1109/PRNI.2011.13


Are there any significant alternatives to the theory that the mind exists?

Theory of mind doesn't really "presuppose" a mind. Theory of mind is just a name for a particular cognitive capacity: the ability to know that you have a mental state and to realize that others have a mental state, and that their mental state is not the same of yours. Calling this ability "theory of mind" might be a bit confusing because it sounds like it's a scientific theory, but it's not, it's just referring to an ability to theorize (make educated guesses) about the contents of other peoples' mental states. It could have been named something else (see Why is the theory of mind named as such? as well). Therefore, it doesn't really make any sense to think about "alternatives" to theory of mind, maybe just alternatives to the name of the ability.

Theory of mind is really important to human social interactions, and impairments in theory of mind are part of the spectrum of social difficulties in autism.

As one example of how theory of mind works day-to-day, very young children who have not yet developed theory of mind have difficulty understanding that knowledge they have is not shared by everyone. If they see you hide a candy under one of two cups, they would be confused why someone else who wasn't in the room to see where the candy was hidden doesn't know which cup the candy is under (Frith and Frith, 2005, tell a similar story to explain theory of mind).

The nature of the mental state is not actually a part of the definition of theory of mind. You might be thinking of philosophy of mind.

Frith, C., & Frith, U. (2005). Theory of mind. Current Biology, 15(17), R644-R645.


What is a good beginner's book to read to get a greater understanding of neuroscience?

You could try this one: 30-Second Brain: The 50 Most Mind-blowing Ideas in Neuroscience, Each Explained in Half a Minute. ISBN-10: 184831647X. I haven't read it myself but it covers a really wide spectrum: single neurons, neural networks, brain architecture, awareness, perception, disease, ageing, etc.
Importantly it's written by really good scientists in who are all currently doing really interesting things.


Why is the hopfield network a model of associative memory?

An Associative Memory is a synonym for Content Addressable Memory or a memory which stores the result of associative learning, wherein an input item is learned to be associated with an output item.

A Hopfield network is a type of associative memory, wherein an input item (including partial, noisy representations of the original trained/encoded item) is an associated to a the ideal representation of the trained/desired/encoded input item.

For further discussion of Hopfield networks, I recommend look at the question "What's the difference between a Hamming and Hopfield network?"


How are qualia localized in consciousness?

This question has been unanswered for a long time and I will attempt to address the issues posed not one by one, as there are a great many questions, but with an overall working of the sensory nervous system with respect to topographic mapping. Moreover, the question uses a great many "suppose ifs" that have never, and most likely will never or cannot be tested. Therefore a basic overview of topographical mapping may shed light on the matter.

The somatosensory cortex is a highly topographically organized structure. Although warped in size, it basically contains an exact topographical map of the body, referred to as a homunculus:

Source: Guardian

In other words, perceptions in the upper arm are represented very near to the lower arm representation in the somatosensory cortex. The motor cortex contains a very similar map.

Similarly, the visual cortices contain many maps representing the visual field, referred to as the retinotopic map. Likewise, the auditory system maps frequency space in a highly topographical manner (the tonotopic map).

Removing a part of the somatosensory cortex out of its context may wreck havoc on this ordered structure. For example, it has been shown by groundbreaking work from Michael Merzenich and colleagues that when the fingers of a monkey are sewn together, the finger representations in the sensory cortex also fuse, i.e., the border between the coupled fingers degrades and vanishes eventually. This experiment shows that when two separate bodily structures are repeatedly and structurally stimulated simultaneously, they fuse in the cortex. Upon separation, original mapping is restored (Allard et al., 1991). I consider this proof that adjacent structures influence each other's representations in the cortex because they often receive parallel stimulation. Coherent stimuli typically result in increased synaptic strength.

Phantom limbs are interesting indeed. For example, the groundbreaking work by Ramachandran focused on upper arm amputees. These folks would feel sensations in their (amputated) hand when their cheek was stimulated. In the homunculus it can be readily seen that facial representations are close to the hand representation. Upon deafferentation of the arm region in the cortex, surrounding bodily representations take over the 'silenced' regions, and the cheek region 'steals' the hand (which is relatively huge). However, interestingly, the cheek not only serves its own original representation, but refers now to the amputated hand as well. Hence, the memory of the hand lingers, showing once again that the bodily map is strongly imprinted in the brain and that it is not simply isolated from its context.

How then are visual and tactile stimuli fused as being correlated? This happens in the higher multi-sensory areas in the brain, the so-called association cortices such as found in the temporal lobe.

Source: Insituto Balseiro

These higher areas will link various perceptions and merge them into coherent perceptions. Limbic association areas may couple the butterflies to love.

Conclusion
In all, qualia are localized in the brain by mapping sensory information onto highly organized topographic maps in the cortex. Changes in the periphery (e.g. amputations) will affect this cortical mapping due to plasticity and hence these cortical maps are plastic (subject to change). The reverse can never be easily tested (taking a piece of brain away will have gross consequences) as said, but I think that the quote "Neurons that wire together fire together" is important here. As said, synaptic strength increases when adjacent neurons fire in coherency and when taken apart their mapping will become distorted. Lastly, emotional feelings are combined with the physical sensation of butterflies in your stomach and synthesized into a holistic feeling of love, probably by the limbic association cortices and perhaps other association areas. in general, the association areas synthesize the various sensory systems by linking them, most likely due to experience.

Reference
Allard et al., J Neurophysiol 1991;66:1048-58


Analysis of psychology/sociology of fashion?

Mair, C. (2019). Speaking of Psychology: Psychology of Fashion. Retrieved August 25, 2020, from https://www.apa.org/research/action/speaking-of-psychology/fashion


From Hubbard & Ramachandran (2005):

  [...] the estimated prevalence of synesthesia has varied dramatically, between as many as 1 in 20 (Galton, 1883) and as few as 1 in 25,000 (Cytowic, 1989). The most widely cited study to date suggests that synesthesia occurs in at least 1 in 2000 people (Baron-Cohen et al., 1996), although this is now generally regarded as an underestimate. Our own informal samples have suggested that the prevalence of grapheme-color synesthesia might be between 1 in 200 (Ramachandran and Hubbard, 2001b) and 1 in 100 (Mulvenna et al., 2004). Subsequent large-scale studies have suggested that the prevalence of synesthesia might be as high as 1 in 20 across all forms and 1 in 100 for grapheme-color synesthesia (J. Simner, personal communication). This high prevalence argues against the notion that synesthesia is merely a “benign cognitive variant” (see Ward and Mattingley, 2005) and instead suggests that it is a widespread phenomenon that may provide novel insights into the neural basis of the mind (Ramachandran and Hubbard, 2001b).

References

  Hubbard, E. M., & Ramachandran, V. S. (2005). Neurocognitive mechanisms of synesthesia. Neuron, 48(3), 509.


Is there a neurological difference between someone experiencing a "normal" trauma response, and someone with PTSD? Or are they on the same continuum?

First, your question pertains to two possible populations:

"less long-lasting" PTSD is diagnosed as acute stress disorder (ASD); PTSD cannot be diagnosed until at least one month after exposure to the inciting trauma, and ASD sometimes resolves without progression to PTSD.
"less intense" PTSD is usually diagnosed as an adjustment disorder, meaning a maladaptive response to some psychosocial stressor that somehow doesn't meet the criteria for ASD/PTSD.

Is it likely that the same neurological changes would be taking place, just to a lesser extent?

We need to define those changes:

Sherin, J. E., & Nemeroff, C. B. (2011). Post-traumatic stress disorder: the neurobiological impact of psychological trauma. Dialogues Clin Neurosci, 13(3), 263-278.

Table I. Summary of neurobiological features with identified abnormalities and functional implications in patients with post-traumatic stress disorder. CRH, corticotropin-releasing hormone; 5HT, serotonin; GABA, γ-aminobutyric acid; NPY, neuropeptide Y; ACTH, adrenocorticotropin; NE, norepinephrine; CSF, cerebrospinal fluid

Additionally, other studies have demonstrated reduced amygdala volume in PTSD patients. It should come as no surprise that ASD features many of the same neurobiological changes (especially hypocortisolism) as PTSD, although quantitative differences may not correlate with symptom burden.

Marshall, R. D., & Garakani, A. (2002). Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. Psychiatr Clin North Am, 25(2), 385-395.

Studies of the acutely traumatized have found that those individuals who are at increased risk for chronic PTSD are relatively more likely to experience a more severe acute emotional reaction. This includes not only the intensity of emotions such as fear, anxiety, and/or despair, but also dissociative experiences and cognitive disruption. This clinical picture, in turn, is associated with increased heart rate, increased skin conductance, and relatively lower levels of blood cortisol compared to those who will not develop PTSD (discussed later in this article). However, an interesting caveat to this generalization is that the presence of acute dissociative symptoms appears to mediate the intensity of the peripheral sympathetic nervous system response. Griffin et al. found that peritraumatic dissociation was associated with both greater severity of PTSD symptoms, and relatively greater suppression of autonomic physiologic responses.

Similarly, more recent research confirms the expectation that comparable neuroanatomic changes occur in ASD as with those seen in PTSD (particularly amygdala activation). In summary: ASD and PTSD share many neurobiological characteristics.
In contrast, adjustment disorder (sometimes referred to as "situational depression") is far more nebulous. It can be acute or chronic, and it can present in a variety of ways to the extent that its existence has been contested as ‘a progression threshold from normal human adaptation under conditions of stress, change, and loss, into the dark web of “mental illness.”’ In the linked article, John Daniels argues that adjustment disorder should be treated as a collection of behavioral responses to normal emotional states that can act as a precursor to better-characterized clinical pathologies like anxiety disorder, depression, and conduct disorder. This group of behaviors, Daniels contends, should be treated with counseling instead of pharmaceutical "brief therapies" that might be better served in combating the biochemical changes seen in ASD. There is an abundance of literature regarding the lack of rigorous study of adjustment disorder (a,b).

Or is it more analogous to depression, where (if I understand correctly!) research on how the brain responds to depression isn't necessarily analogous to how the brain responds to feeling "sad"...

Ultimately, your analogy here is good for differentiating between the two possibilities you identified in being "sub"-PTSD (duration [ASD] vs. intensity [adjustment disorder]). Generally speaking, ASD has a similar neurobiological profile to PTSD with respect to chemical, physiological, and anatomic changes. To use your words, adjustment disorder "isn't necessarily analogous" to PTSD and rather encompasses a broad spectrum of (possibly normal) emotional responses to both acute and chronic stressors. This tracks with our understanding of other diseases: matching symptoms of variable duration are more likely to have the same underlying etiology (e.g. a mild runny nose lasting one week might be correctly ascribed to a host of different viral causes) as compared to symptoms of varying intensity that bear a passing resemblance to each other (e.g. rhinorrhea caused by a cluster headache doesn't implicate a virus).
You may find additional pertinent information on (and in the citations of) the Wikipedia pages for PTSD, ASD, and adjustment disorder.


What is the relation of visual quality and distance from the central field of view?

Assuming you are talking about the ability of the visual system to resolve spatial detail (resolution, if you wish), then your question is on visual acuity as a function of eccentricity on the retina (Fig. 1).

Due to the densely packed cones at the fovea (corresponding to the central field of view (FOV), see Fig. 1), visual acuity (VA) is the greatest at the center of fixation. More eccentrically, VA declines markedly. E.g., at 10 minutes of arc (1/6 of a degree) from fixation, there is a 25 % loss of visual acuity (Fig. 1.) This dependence of VA on eccentricity is indeed nonlinear (cf. Fig. 1) and correlates with the cone packing density and photopic resolution in the region up to a few degrees eccentricity.

However, at larger eccentricities, visual acuity is worse than that predicted by cone spacing alone, indicating that other post-receptoral retinal elements are the limiting factor. One of these factors is the increased density of rods in eccentric regions; rods are built for speed and sensitivity. The latter is accomplished in part by funneling the inputs of multiple rods onto a single retinal ganglion cell (RGC). RGCs transmit the signals via the optic nerve to the visual centers in the brain stem, ultimately ending up in the brain. Foveal cones, on the other hand, are connected 1:1 and hence the spatial resolution and thus SA is much better in foveal regions. The foveal region contains high densities of cones (good VA), while more eccentrically more rods are present (worse VA); see Fig. 2. This is exactly the reason that we read by focusing our central foveal view on the characters.

Fig. 1. VA as a functin of eccentricity. Source: Kalloniatis & Luu (2016)

Fig. 2. Rod and cone densities as a function of eccentricity. Source: Kolb (2016)

References
- Kalloniatis & Luu. Visual acuity. In: Webvision. The Organization of the Retina and Visual System. Kolb et al. (eds). Utah University (2016)
- Kolb. Photoreceptors. In: Webvision. The Organization of the Retina and Visual System. Kolb et al. (eds). Utah University (2016)


Can we enter data at the speed of thought?

I am unfamiliar with such research. However, considering this from a User Interface design perspective, as well as from a cognitive perspective, I would add one bit of clarification to the question.

Can we enter data at the speed of organized thought?

If the limitations in user interface technology are overcome to the point where the input gate is no longer the limitation, it is quite possible that we would discover that our thought processes are so chaotic as to render the new technology virtually useless.

As support for this I would point out that sitting and typing a message, while slow, is already a method by which thoughts evolve into lucid communication.


Why do we forget what we try to remember?

What you are describing may be the tip of the tongue (TOT) phenomenon.

There are two major explanations for this: the direct-access view and the inferential view.

The direct-access view: the memory strength is just not strong enough to recall the item, but strong enough to trigger the recall
The inferential view:

  It claims that TOTs aren't completely based on inaccessible, yet activated targets; rather they arise when the rememberer tries to piece together different clues about the word. Emotional-induced retrieval often causes more TOT experiences than an emotionally neutral retrieval, such as asking where a famous icon was assassinated rather than simply asking the capital city of a state.

The second view is interesting, because frustration is an emotion by definition. So when you are frustrated for not remembering the word, your frustration by itself narrows down your ability to retrieve it. This loop goes on until you yell "fuck it. I quit".

So while emotion plays an important role in memorizing a piece of information, it also may hindrance you to recall it back. But if you can devote a lot of cognitive resource (thinking it hard) without being frustrated, then you can still retrieve it.

TOT is seemingly a very important topic in memory research.

Sources:  Tip of the tongue, Recall (memory)


What role do the ego and group unconsciousness have in Jungian "individuation"?

Short answer

The ego, the collective unconscious and the persona collectively help the person to self-actualise and reach individuation through the elements of the psyche being in harmony with each other.

Long answer

A lot of what I am providing in this answer has been put together using my knowledge of Jungian Psychology from my 3 year Psychotherapy course I am sudying at Reading University and information within Wolberg (2013).  Anything not referenced here is from the Wolberg book.

Individuation

Let's first of all define the word Individuation

  In the broadest possible way, individuation can be defined as the achievement of self-actualization through a process of integrating the conscious and the unconscious. Once again, any accurate understanding of Jung should come from [Jung]. (Source: Journal Psyche)

Self Actualisation is a term coined by Abraham Maslow with his Hierarchy of Needs, and refers to having a fulfilment and mastery of all your needs from the simplest to the more complex.

Jung, the Psyche, and the Collective and Personal Unconscious

According to Carl Gustav Jung, the psyche is compartmentalised in a different way than Freud proposed. He divided the psyche into

a superficial part, the personaa social mask assumed by the individual, made up of social interests and sanctions
a less superficial aspect, the egowhich is only to some extent conscious and reflects past-personal experiences, and
a deeply unconscious partwhich has within it the collective unconscious and contained archetypes (Creator, Caregiver, Ruler, Jester...).

Difficulties occur when there is a lack of harmony among the persona, the ego, and the collective unconscious. Jung conceived of the idea that baser elements of the soul were present in the collective unconscious, and he characterised these as “the Shadow.”

The psychic reality of the situation created by the psychic images, developed in the conscious, create complexes [e.g. Inferiority Complex] and the issues, and their connected experiences are repressed or suppressed into the "shadow lands" of the personal unconscious.

Jung also believed that the collective unconscious contained

  creative fountains of energy. Primitive fears and other untoward manifestations of the unconscious invaded the patient’s conscious mind and created tensions and various neurotic symptoms that were attempts at self-cure. The collective unconscious, unleashed, constituted a source of danger for the person.

The 2 different human characters

Jung also evolved a theory of character, whereby people are divided into two types: introverts and extroverts. The introvert’s interests centred on himself or herself; the extrovert’s interests were on the external world.

  A human being, said Jung, had an innate religious craving which powered the need for self-realization. There was, he explained, no retreat from life’s burdens other than to find refuge in spiritual strivings with “acceptance of the irrational and unbelievable.” By experiencing the collective unconscious, an individual no longer would experience personal sorrow "but the sorrow of the world, no longer a personal isolating pain, but pain without bitterness, binding all human beings together.” We are brought “back to ourselves as an existing, living something, stretched as it were between two worlds of images, from which forces proceed that are only dimly discerned but are all the more clearly felt. This something, though strange to us, is yet so near, it is altogether ourselves and yet unrecognizable, a virtual middlepoint of such a mysterious constitution that it can demand anything, relationship with animals and with gods, with crystals and with stars.” These ideas were elaborated by Jung (1961) in his last book, Memories, Dreams, Reflections, a fascinating autobiographical document that explains his relationship with Freud and gives us a broader understanding of the essence and meaning of his work.

Putting it together for psychotherapy

During Jungian psychoanalytic therapy...

  an effort is made to explore “archetypes” in order to determine how these imprints contaminate the patient’s present life and interfere with self-development and self-realization (individuation). Bringing the individual into contact with his or her collective unconscious is said to help liberate creative forces that will have a constructive effect on adjustment. Once non-conscious elements are recognized, an attempt is made to guide the patient actively into a productive relationship with the unconscious.

References

Wolberg, L. R., 2013. The Technique of Psychotherapy - Fourth Edition,Chevy Chase, MD:International Psychotherapy Institute E-BooksAvailable free from http://www.freepsychotherapybooks.org

For further in-depth information on Jungian Analytical Psychology:

Frieda Fordham (1991) An Introduction to Jung's Psychology, 3rd Revised Edition,London:Penguin Books Ltd. (ISBN-13: 978-0140135688)

Carl Gustav Jung (1969) The Archetypes and the Collective Unconscious (Collected Works of C. G. Jung)2nd edition translation in 1981 by Gerhard Adler & R.F.C. Hull. Princeton: Princeton University Press (ISBN-13: 978-0691018331)
exact same edition also printed in 1991 by London:Routledge (ISBN-13: 978-0415058445)


Do porn and other remotely perceived entertainments work because of Mirror Neurons?

I think it is likely the case. I agree that the idea of a "mirror neuron" is a bit dubious, as it implies that the function of those neurons are related to mirroring. It's probably the case that they represent the actual movement, and their activation in witnessing the action is tangential to that.

As for your question, research was done on this exact topic, with positive results. Mouras et al. found that the magnitude of erection achieved by participants watching erotic videos correlated to the activation of regions known to contain "mirror neurons".

References
http://www.sciencedirect.com/science/article/pii/S1053811908006897


Open magnetic resonance imaging datasets on psychosis?

The Australian Schizophrenia Research Bank (http://www.schizophreniaresearch.org.au/bank/research-information/information-on-datasample-availability-for-researchers/) has an 'open' database of clinical MRI (T1s and DTI) as well as healthy controls. Access isn't free though - they charge an administration fee to cover costs. It is an ongoing effort and I think there is about 500 MRIs from patients in there now, but I'm not sure what the latest numbers are exactly.