Are there recent theories on physiognomy?

Facial shape

Aggression relates to facial width-to-height ratio (Carré, McCormick, & Mondloch, 2009; Carré & McCormick, 2008). The width-to-height ratio is the distance between the left and right zygion (the outside of the cheek bone) divided by the distance between the top of the upper lip and the mid-brow. Here's a useful image displaying the meaning of this ratio from the 2009 article:

Carré et al. found that the lower the width-to-height ratio, i.e. the shorter the distance between lip and brow in relation to the distance from cheekbone to cheekbone, the more aggressive the person is (as measured through a well-validated laboratory task) and is perceived by strangers.

Also, the Big Five differ in observability (Penton-Voak, Pound, Little, & Perrett, 2006). Participants were asked to rate the Big 5 aspects of the personality of strangers. There was a strong agreement between these ratings and the results of a personality test the depicted persons had filled in (reliability calculated as Cronbach's $\alpha=.70\text{–}.89$ for all dimensions, only male conscientiousness was $.63)$. Similar results were found with composite images.

Here are some composite facial images from that article:

Differences are subtle, but perceptible! BTW, I think I came across this from The Personality Puzzle (Funder, 1997) originally, but I'm not 100% certain.

Some of these facial differences may relate to testosterone. Dominance and masculinity relate to perceptible differences in male facial shape due to the prenatal influence of testosterone, but fortunately for the scope of this answer, these differences do not affect attractiveness to females (Neave, Laing, Fink, & Manning, 2003; Swaddle & Reierson, 2002).

Body shape

Body mass index

There is some evidence that body mass index (BMI) relates to higher extraversion and psychoticism and lower neuroticism in middle-aged Japanese people (Kakizaki et al., 2008), impulsivity (Murphy, Stojek, & MacKillop, 2014; first citation of the new year!), hypomania (Valenti, Omizo, & Mehl-Madrona, 2011), and worse cognitive executive functioning (Gunstad et al., 2007). However, one study did not find a relationship between BMI and personality psychopathology (Picot & Lilenfeld, 2003). Another study found a positive relationship between neuroticism and BMI in middle-aged American women only (the opposite of the relationship in the Japanese population according to Kakizaki et al., who did not mention prominent sex differences) and extraversion among men only (same direction as in Kakizaki et al., but again, more sex differences), as well as negative relationships with openness, agreeableness, and conscientiousness (Brummett et al., 2006). Low conscientiousness related more strongly to BMI in women, and predicted BMI increases over time.

Testosterone

Another set of correlations between personality and body shape are mediated by testosterone, which affects several, readily observable, physical characteristics, including muscle mass, bone length, vocal pitch and tone, hair growth patterns, body odor, dermal oil secretion and acne, subcutaneous facial fat and facial bone contours, and prominence of the Adam's apple. Testosterone relates to many behavioral patterns in romantic relations, the general trend being toward more competitive promiscuity and less long-term fidelity with increasing testosterone (e.g., Burnham et al., 2003). Testosterone increases in men anticipating competition, but may decrease in women (Mazur, Susman, & Edelbrock, 1997). This effect may be moderated by implicit power motivation (Schultheiss, Campbell, & McClelland, 1999); if so, it's conceivable that personality could affect appearance over time by altering testosterone levels. Power motivation interacts in complex ways with sex and the outcome of social contexts in affecting testosterone (Schultheiss et al., 2005; Schultheiss, Wirth, & Stanton, 2004).

One of the underlying personality differences associated with testosterone appears to be in sexual motivation, which manifests in non-human animals as well. Testosterone also relates to sensation-seeking (Roberti, 2004; Gerra et al., 1999; Daitzman & Zuckerman, 1980; Zuckerman, Buchsbaum, & Murphy, 1980) and risk tolerance (Sapienza, Zingales, & Maestripieri, 2009; Stanton et al., 2011; Stanton, Liening, & Schultheiss, 2011), though the relationship exhibits some complexities across domains of risk (Stenstrom, Saad, Nepomuceno, & Mendenhall, 2011). The relationship between testosterone and risk aversion may be mediated by abstract reasoning ability (Brañas-Garza & Rustichini, 2011).

Testosterone also relates to dominance (Mazur & Booth, 1998), aggression (Archer, 2006; Birger et al., 2003; Ehrenkranz, Bliss, & Sheard, 1974; Archer, Birring, & Wu, 1998), and lack of empathy, the last of which appears to be an empirically established effect of testosterone (Chapman et al., 2006; Knickmeyer, Baron-Cohen, Raggatt, Taylor, & Hackett, 2006; van Honk et al., 2011; Ronay & Carney, 2013; see also Auyeung & Baron-Cohen, 2013). Testosterone may even explain deficits in social development (Knickmeyer & Baron-Cohen, 2006) and autistic traits in general (Auyeung et al., 2009; Ingudomnukul, Baron-Cohen, Wheelwright, & Knickmeyer, 2007), according to a theory that conceptualizes autism as extreme cognitive maleness (Baron-Cohen, 2002; Baron-Cohen, Knickmeyer, & Belmonte, 2005; Chakrabarti et al., 2009).

Testosterone relates positively to emotional arousal and anger, but also relates positively to attentiveness to angry facial expressions in others (van Honk et al., 1999). This latter result demonstrates that testosterone doesn't unilaterally decrease awareness of others' emotional states, especially to whatever extent they pose immediate threat. The relationship between testosterone and antisocial behavior is also moderated by socioeconomic status (Dabbs & Morris, 1990). These complexities may limit the otherwise impressive relationships between personality and testosterone.

In women, estradiol may instead play a similar role to testosterone in men, modifying dominance motivation (Stanton & Schultheiss, 2009). Wikipedia lists some observable physiological effects of estradiol, but these claims currently lack supporting citations.

References (there's a ton; I recommend zooming in with Ctrl++ or copy-pasting into a word processor)

· Archer, J. (2006). Testosterone and human aggression: An evaluation of the challenge hypothesis. Neuroscience & Biobehavioral Reviews, 30(3), 319–345. Retrieved from http://aggroreview.googlecode.com/svn-history/r31/sources/downloaded/testosterone/Archer_2004.pdf.
· Archer, J., Birring, S. S., & Wu, F. C. (1998). The association between testosterone and aggression among young men: Empirical findings and a meta‐analysis. Aggressive Behavior, 24(6), 411–420.
· Auyeung, B., Baron‐Cohen, S., Ashwin, E., Knickmeyer, R., Taylor, K., & Hackett, G. (2009). Fetal testosterone and autistic traits. British Journal of Psychology, 100(1), 1–22. Retrieved from http://www.personal.rdg.ac.uk/~sxs02dtf/auyeung2009.pdf.
· Auyeung, B., & Baron‐Cohen, S. (2013). Prenatal and postnatal testosterone effects on human social and emotional behavior. In S. Baron-Cohen, M. Lombardo, H. Tager-Flusberg, & D. Cohen (Eds.), Understanding Other Minds: Perspectives from developmental social neuroscience. Oxford University Press.
· Baron-Cohen, S. (2002). The extreme male brain theory of autism. Trends in Cognitive Sciences, 6(6), 248–254. Retrieved from http://cogsci.bme.hu/~ivady/bscs/read/bc.pdf.
· Baron-Cohen, S., Knickmeyer, R. C., & Belmonte, M. K. (2005). Sex differences in the brain: implications for explaining autism. Science, 310(5749), 819–823. Retrieved from http://docentes.cs.urjc.es/~odeluis/Docencia/ABP/Articulos/baroncohen.pdf.
· Birger, M., Swartz, M., Cohen, D., Alesh, Y. A., Grishpan, C., & Kotelr, M. (2003). Aggression: The testosterone-serotonin link. IMAJ-RAMAT GAN-, 5(9), 653–658. Retrieved from http://www.ima.org.il/FilesUpload/IMAJ/0/54/27288.pdf.
· Brañas-Garza, P., & Rustichini, A. (2011). Organizing effects of testosterone and economic behavior: Not just risk taking. PLoS ONE, 6(12), e29842. Retrieved from http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0029842#pone-0029842-g001.
· Brummett, B. H., Babyak, M. A., Williams, R. B., Barefoot, J. C., Costa, P. T., & Siegler, I. C. (2006). NEO personality domains and gender predict levels and trends in body mass index over 14 years during midlife. Journal of Research in Personality, 40(3), 222–236. Retrieved from ResearchGate.
· Burnham, T. C., Chapman, J. F., Gray, P. B., McIntyre, M. H., Lipson, S. F., & Ellison, P. T. (2003). Men in committed, romantic relationships have lower testosterone. Hormones and Behavior, 44(2), 119–122. Retrieved from http://www.bec.ucla.edu/papers/Gray_10-20-03.pdf.
· Carré, J. M., & McCormick, C. M. (2008). In your face: Facial metrics predict aggressive behaviour in the laboratory and in varsity and professional hockey players. Proceedings of the Royal Society B: Biological Sciences, 275(1651), 2651–2656. Retrieved from http://rspb.royalsocietypublishing.org/content/275/1651/2651.full.pdf%20html.
· Carré, J. M., McCormick, C. M., & Mondloch, C. J. (2009). Facial structure is a reliable cue of aggressive behavior. Psychological Science, 20(10), 1194–1198. Retrieved from http://carrelab.com/Carre_et_al_2009_Psyc_Sci.pdf.
· Chakrabarti, B., Dudbridge, F., Kent, L., Wheelwright, S., Hill‐Cawthorne, G., Allison, C., ... & Baron‐Cohen, S. (2009). Genes related to sex steroids, neural growth, and social–emotional behavior are associated with autistic traits, empathy, and Asperger syndrome. Autism Research, 2(3), 157–177. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/aur.80/full.
· Chapman, E., Baron-Cohen, S., Auyeung, B., Knickmeyer, R., Taylor, K., & Hackett, G. (2006). Fetal testosterone and empathy: Evidence from the empathy quotient (EQ) and the “reading the mind in the eyes” test. Social Neuroscience, 1(2), 135–148. Retrieved from http://docs.autismresearchcentre.com/papers/2006_Chapman_etal.pdf.
· Daitzman, R. J., & Zuckerman, M. (1980). Disinhibitory sensation seeking and gonadal hormones. Personality and Individual Differences, 1, 103–110.
· Dabbs, J. M., & Morris, R. (1990). Testosterone, social class, and antisocial behavior in a sample of 4,462 men. Psychological Science, 1(3), 209–211. Retrieved from http://connect.issaquah.wednet.edu/cfs-file.ashx/__key/telligent-evolution-components-attachments/13-8431-00-00-00-04-77-28/Testosterone-and-Antisocial-behavior.pdf
· Ehrenkranz, J., Bliss, E., & Sheard, M. H. (1974). Plasma testosterone: Correlation with aggressive behavior and social dominance in man. Psychosomatic Medicine, 36(6), 469–475.
· Funder, D. C. (1997). The personality puzzle. W. W. Norton & Co.
· Gerra, G., Avanzini, P., Zaimovic, A., Sartori, R., Bocchi, C., Timpano, M., Zambelli, U., Delsignore, R., Gardini, F., Talarico, E., & Brambilla, F. (1999). Neurotransmitters, neuroendocrine correlates of sensation-seeking temperament in normal humans. Neuropsychobiology, 39, 207–213.
· Gunstad, J., Paul, R. H., Cohen, R. A., Tate, D. F., Spitznagel, M. B., & Gordon, E. (2007). Elevated body mass index is associated with executive dysfunction in otherwise healthy adults. Comprehensive Psychiatry, 48(1), 57–61. Retrieved from http://postcog.ucd.ie/files/Gunsted.pdf.
· Ingudomnukul, E., Baron-Cohen, S., Wheelwright, S., & Knickmeyer, R. (2007). Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Hormones and Behavior, 51(5), 597–604. Retrieved from http://beyond-belief.org.uk/sites/beyond-belief.org.uk/files/Baron-Cohen%20hormonesandbehavior.pdf.
· Kakizaki, M., Kuriyama, S., Sato, Y., Shimazu, T., Matsuda-Ohmori, K., Nakaya, N., ... & Tsuji, I. (2008). Personality and body mass index: A cross-sectional analysis from the Miyagi Cohort Study. Journal of Psychosomatic Research, 64(1), 71–80.
· Knickmeyer, R. C., & Baron-Cohen, S. (2006). Fetal testosterone and sex differences. Early Human Development, 82(12), 755–760.
· Knickmeyer, R., Baron-Cohen, S., Raggatt, P., Taylor, K., & Hackett, G. (2006). Fetal testosterone and empathy. Hormones and Behavior, 49(3), 282–292. Retrieved from http://www.researchgate.net/publication/7540638_Fetal_testosterone_and_empathy/file/50463515da285cea18.pdf.
· Mazur, A., & Booth, A. (1998). Testosterone and dominance in men. Behavioral and Brain Sciences, 21(3), 353–363. Retrieved from http://cogprints.org/663/1/bbs_mazur.html.
· Mazur, A., Susman, E. J., & Edelbrock, S. (1997). Sex difference in testosterone response to a video game contest. Evolution and Human Behavior, 18(5), 317–326. Retrieved from http://cogprints.org/630/1/Pong.html.
· Murphy, C. M., Stojek, M. K., & MacKillop, J. (2014). Interrelationships among impulsive personality traits, food addiction, and Body Mass Index. Appetite, 73, 45–50.
· Neave, N., Laing, S., Fink, B., & Manning, J. T. (2003). Second to fourth digit ratio, testosterone and perceived male dominance. Proceedings of the Royal Society of London. Series B: Biological Sciences, 270(1529), 2167–2172. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691489/pdf/14561281.pdf.
· Penton-Voak, I. S., Pound, N., Little, A. C., & Perrett, D. I. (2006). Personality judgments from natural and composite facial images: More evidence for a “kernel of truth” in social perception. Social Cognition, 24(5), 607–640. Retrieved from http://www.alittlelab.stir.ac.uk/pubs/Penton-Voak_06_kernaloftruth_SocCog.pdf.
· Picot, A. K., & Lilenfeld, L. R. (2003). The relationship among binge severity, personality psychopathology, and body mass index. International Journal of Eating Disorders, 34(1), 98–107.
· Roberti, J. W. (2004). A review of behavioral and biological correlates of sensation seeking. Journal of Research in Personality, 38(3), 256–279. Retrieved from ftp://psyftp.psychology.mcmaster.ca/dalywilson/Papers/DawnPatrol/Roberti2004.pdf.
· Ronay, R., & Carney, D. R. (2013). Testosterone’s negative relationship with empathic accuracy and perceived leadership ability. Social Psychological and Personality Science, 4(1), 92–99. Retrieved from http://faculty.haas.berkeley.edu/dana_carney/published.Ronay%26Carney.2012.SPPS.pdf.
· Sapienza, P., Zingales, L., & Maestripieri, D. (2009). Gender differences in financial risk aversion and career choices are affected by testosterone. Proceedings of the National Academy of Sciences, 106(36), 15268–15273. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741240/.
· Schultheiss, O. C., Campbell, K. L., & McClelland, D. C. (1999). Implicit power motivation moderates men's testosterone responses to imagined and real dominance success. Hormones and Behavior, 36(3), 234–241. Retrieved from http://www.psych2.phil.fau.de/~oschult/humanlab/publications/scm1999.pdf.
· Schultheiss, O. C., Wirth, M. M., & Stanton, S. J. (2004). Effects of affiliation and power motivation arousal on salivary progesterone and testosterone. Hormones and Behavior, 46(5), 592–599. Retrieved from http://www.psych2.phil.uni-erlangen.de/~oschult/humanlab/publications/sws2004hb.pdf.
· Schultheiss, O. C., Wirth, M. M., Torges, C. M., Pang, J. S., Villacorta, M. A., & Welsh, K. M. (2005). Effects of implicit power motivation on men's and women's implicit learning and testosterone changes after social victory or defeat. Journal of Personality and Social Psychology, 88(1), 174–188. Retrieved from http://www.psych2.phil.uni-erlangen.de/~oschult/humanlab/publications/s2005jpsp.pdf.
· Stanton, S. J., Liening, S. H., & Schultheiss, O. C. (2011). Testosterone is positively associated with risk taking in the Iowa Gambling Task. Hormones and Behavior, 59(2), 252–256. Retrieved from http://www.scottliening.com/research/publications/StantonLieningSchultheiss_HB.pdf.
· Stanton, S. J., O’Dhaniel, A., McLaurin, R. E., Kuhn, C. M., LaBar, K. S., Platt, M. L., & Huettel, S. A. (2011). Low-and high-testosterone individuals exhibit decreased aversion to economic risk. Psychological Science, 22(4), 447–453. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653580/.
· Stanton, S. J., & Schultheiss, O. C. (2009). The hormonal correlates of implicit power motivation. Journal of Research in Personality, 43(5), 942–949. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818294/.
· Stenstrom, E., Saad, G., Nepomuceno, M. V., & Mendenhall, Z. (2011). Testosterone and domain-specific risk: Digit ratios (2D: 4D and rel2) as predictors of recreational, financial, and social risk-taking behaviors. Personality and Individual Differences, 51(4), 412–416.
· Swaddle, J. P., & Reierson, G. W. (2002). Testosterone increases perceived dominance but not attractiveness in human males. Proceedings of the Royal Society of London. Series B: Biological Sciences, 269(1507), 2285–2289. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691166/pdf/12495494.pdf.
· Valenti, M. P., Omizo, M. M., & Mehl-Madrona, L. (2011). Personality and obese Body Mass Index. The New School Psychology Bulletin, 9(1), 34–38. Retrieved from http://www.nspb.net/index.php/nspb/article/viewFile/204/294.
· van Honk, J., Schutter, D. J., Bos, P. A., Kruijt, A. W., Lentjes, E. G., & Baron-Cohen, S. (2011). Testosterone administration impairs cognitive empathy in women depending on second-to-fourth digit ratio. Proceedings of the National Academy of Sciences, 108(8), 3448–3452. Retrieved from http://www.researchgate.net/publication/49817064_Testosterone_administration_impairs_cognitive_empathy_in_women_depending_on_second-to-fourth_digit_ratio/file/d912f50b5d773ca9e0.pdf.
· van Honk, J., Tuiten, A., Verbaten, R., van den Hout, M., Koppeschaar, H., Thijssen, J., & de Haan, E. (1999). Correlations among salivary testosterone, mood, and selective attention to threat in humans. Hormones and Behavior, 36(1), 17–24.
· Zuckerman, M., Buchsbaum, M. S., & Murphy, D. L. (1980). Sensation seeking and its biological correlates. Psychological Bulletin, 88(1), 187–214.


Rationale behind an “all-or-nothing” design for a test for the purposes of diagnosis and epidemology

Many construct scales are developed with relatively little attention to the content.  Researchers may start with a large set of candidate questions, versions, formats, and phrasings, and then through a validation process, narrow them down to a subset that correlates well with the construct that they are trying to measure.  The goal is a balance between keeping the test short while also retaining its predictive value.  In Baron-Cohen et al's (2001) introduction, they note:

  The AQ as shown in the Appendix is the outcome of piloting multiple
  versions, over several years.

In many cases, researchers care less about why the questions work, and more just that they work.

Having said that, the decision to go with a forced-choice format vs. say, a Likert-type rating scale with more granularity and a neutral option, can be political:

  Ipsative measures may be more useful for evaluating traits within an
  individual, whereas Likert-type scales are more useful for evaluating
  traits across individuals.

This can make forced-choice measures desirable for stigmatized labels to discourage comparing individuals to one another:

  Encouraging pupils to beat their previous scores can take peer
  pressure out of situations and eliminates the competitive element
  associated with norm-based referencing.

Note also that the original study confirms that mathematicians score significantly higher on this scale, as is to be expected:

  ... scientists score higher than nonscientists; and within the
  sciences, mathematics, physical scientists, computer scientists, and
  engineers score higher than the more human or life-centered sciences
  of medicine (including veterinary science) and biology. This latter
  finding replicates our earlier studies finding a link between autism
  spectrum conditions and occupations/skills in maths, physics, and
  engineering.

This suggests that the authors thought it perfectly valid for mathematicians to score higher on their autism scale (ie, this scale is not designed to differentiate the autistic tendencies of mathematicians from those of individuals diagnosed with autism).


How many diagnosable mental disorders are included in the DSM?

I have not come up with a definitive answer myself as there is a wide range of figures online.

Michael Noll-Hussong states on ResearchGate

  The total number of specific diagnoses was reduced from 172 in DSM-IV to 157 in DSM-5.
  see, e.g., McCarron RM. The DSM-5 and the art of medicine: certainly uncertain. Annals of internal medicine. 2013;159(5):360-1.

I have recently managed to access this referenced article (DOI: 10.7326/0003-4819-159-7-201310010-00688) and it states

  The number of psychiatric disorders decreased from 172 (DSM-IV) to 152 (DSM-5). (This does not include disorders that are “Not otherwise specified” or “Other specified/unspecified.”)

The Huffington Post states that there are over 300 in DSM-5

Because of discrepancies in the information available I have seen, I have therefore, painstakingly gone through my copy of DSM-5 and pages 877—896 provide a

  Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)

ICD-10 codes are provided for cross-referencing, and I have counted roughly 742 of them by saying that a full page has 45 and there are 20 pages with some listings taking more than 1 line.  The problem with the approximate figure of 742 is that in the list are items such as obesity which are not mental disorders.


What's the best way to calculate an index score based on reaction time, variance and accuracy?

This overlaps a lot with these two questions: So check them out

How to measure group differences incorporating reaction time / accuracy trade-off?
How to analyze reaction times and accuracy together?

Regarding some specifics of your question, reaction time variance will often be strongly correlated with reaction time mean. So in routine measures of individual differences where speed is the main focus, it may be sufficient to focus on mean reaction time and accuracy. E.g., mean reaction time possibly with some sort of penalty for errors (see the above answers).

If you are wanting to get very precise, then there are a range of modelling approaches that may be relevant (e.g., this question on LBA and diffusion models).

With regards to go-no-go, I believe there are fairly standardised procedures for scoring such tests.


Does sitting idle for one month without work leads to depression?

Two answers:
The first, and most important one: do not ask any online forum whether you are getting depressed, since usually there will be many opinions about your situation from people who are not qualified in the field, be it psychiatry or psychotherapy. Please: if you do not feel well, and if your current situation is worrying you, seek help from your general physician or better if accessible to you a psychotherapist/ a psychiatrist with whom you can talk personally. There is no shame in seeking help from these persons, and in case you find out together with them that you truly need some kind of help, they will know ways of help that are based on evidence from empirical research and likely better and better fitting to your individual situation than suggestions on the internet.

Second: Your question's title implicitly asks whether sitting one month without work in front of a computer always leads to depression. It might and it might not depending on many factors (such as coping strategies with gratification crises, previous episodes of depressive disorders, social support, and many more, which differ from person to person). The danger of answers to a question stated like this is that yes-answers might lead you to think you are depressed, even though you are not, or no-answers lead you to think you aren't depressed even though you might need help. This is to say, the danger is to mistake such an answer for a diagnosis, which are two completely different things. A diagnosis needs to be done by a person qualified to do this, such as psychotherapists or psyhiatrists. They, too, will know further steps in case a diagnosis is given.


Are chatbots based on deceased loved ones healthy?

In my opinion, it depends on whether they would like the AI to synthesize novel thoughts/opinions or to merely contextually quote a history of that individual's textual recordings.

Making a value judgement here, I would say than an AI saying "I forgive you." (from beyond the grave) is not healthy.

But if the chatbot acted as a way of indexing into the individual's actual history, then all potential errors become ones of context (and not content).
(This level of reproduction may not be totally necessary depending on the users' sensitivity to cognitive dissonance, but I would personally feel slimy if I tried to pass off a markov chain of scripts and data as my friend.)

If you're open to alternatives to chatbots, I would suggest that you frame the project as a tribute to your friend's life; even a simple collection of stories from your time together could have a powerful (healthy) impact on the grieving parents.


Why isn't high functioning autism recognized by the DSM-5 or the ICD-10?

Asperger's being "subsumed" in DSM-5 is not the whole story. There's indeed a new DSM-5 coding for the severity of the disorder. But applying the DSM-5 actual clinical criteria results in fewer people being diagnosed with autistic spectrum disorders, and the reduction is more significant for the mild versions (such as Asperger's):

A 2014 mini-review looking at 12 papers concluded:

  The application of DSM-5 diagnostic criteria resulted in an approximately one third reduction in Autism Spectrum Disorders. The reduction was approximately two thirds for mild forms of Autism.

So yeah, the DSM-5 take (intentional or not) is that a lot of "Aspies" don't have a level of dysfunction that raises to the (DSM-5) bar of a mental *disorder *.

However in an astute form of politicking, people with an existing Asperger's diagnosis were "grandfathered in" by the DSM-5. From the same review:

  The American Psychiatric Association partially acknowledged
  the exclusion of mild forms of ASD when the added
  rider to the diagnostic criteria was that “Individuals with a
  well-established DSM-IV diagnosis of autistic disorder,
  Asperger’s disorder, or pervasive developmental disorder not
  otherwise specified should be given the diagnosis of autism
  spectrum disorder”, but this approach to diagnosis of autismis
  strange. It enables individuals who previously were diagnosed
  with ASD to continue to be eligible for services, but results in
  two odd consequences. First, consider two individuals with
  identical symptoms who meet DSM-IV criteria for ASD, one
  of whom was diagnosed before the publication of DSM5 and
  one diagnosed after: The first will be diagnosed with ASD and
  eligible for services, but the second will not. The second
  consequence is that the meaning of the DSM5 term ASD is
  obfuscated as it refers to different entities using the same term.

And a 2016 meta-analysis confirms the effect of stricter criteria (using twice as many studies as the 2014 review):

  Our meta-analysis measured the percentage of people with an ASD diagnosis from the DSM-IV or DSM-IV-TR obtaining an ASD diagnosis from the DSM-5. All 24 studies identified indicated a reduction in the number of people with a DSM-IV or DSM-IV-TR ASD diagnosis being eligible for a DSM-5 ASD diagnosis, a 35 and 37 % reduction respectfully. Our meta-analysis also showed that those with a DSM-IV-TR or DSM-IV diagnosis of PDD-NOS were the least likely to qualify for a DSM-5 ASD diagnosis at 26 and 47 % followed by 55 and 19 %, respectfully of people with Asperger syndrome, and 80 and 87 %, respectfully of people with an autism diagnosis.

A more recent (2017) study on Australian children (where the use of DSM is mandated by certain government programs) found that DSM-5 did seem to stop to the previously increasing trend in rising autism diagnoses:

  De-identified data for 32,199 children aged under 7 years between 2010 and 2015 was utilised. [...] The incidence of autism increased from 2010 to 2013, and then plateaued to 2015. A significant trend-relative reduction in the number of children registered to receive autism-specific funding was evident post 2013, suggesting the more stringent DSM-5 criteria may have curbed the trend of increasing diagnoses over time.

As for why the DSM-5 removed the separate criteria (including Asperger's), quoting from the last paper:

  These previously distinct diagnostic
  categories were removed in light of empirical data
  that questioned the reliability and validity of these subtypes
  (Daniels et al. 2011; Lord 2012; Macintosh and Dissanayake
  2004; Mahjouri and Lord 2012).

Whether this was the right thing to do or not... it depends who you ask. Asperger's diagnosis definitely has its supporters, at least one of whom even predicted its return in the next version of the DSM.


Is there any formal understanding of how humans perceive humanity/vitality in other entities?

Yes, there's a lot of work on this! Still a ton of open questions though, and plenty of smart people working in quite disconnected paradigms.

A classic study in this space is Heider F. & Simmel M. (1944). An Experimental Study of Apparent Behavior, The American Journal of Psychology, 57 (2) 243. DOI: 10.2307/1416950

But note the date! 1944! I think what you're really looking for is the community that is still citing this today.

One recent example might be people interested in Bayesian Theory of mind, eg:
Baker CL, Jara-Ettinger J, Saxe R, & Tenenbaum JB (2017). Rational quantitative attribution of beliefs, desires and percepts in human mentalizing. Nature Human Behaviour

Also, 'agency' is one of the areas identified/investigated as part of core developmental knowledge by Spelke and collaborators, see for example
Spelke, E. S., & Kinzler, K. D. (2007). Core knowledge. Developmental science, 10(1), 89-96.

This answer doesn't really do justice to the breadth of this literature, there's a lot of it! But hopefully the citations and cited-by links from these will throw up the kind of thing you're looking for.


How can the mind be trained to accept ongoing mental or emotional
  suffering?

Experiential avoidance: avoiding what we don't like

From the lens of Acceptance and Commitment Therapy (ACT), the process of regressing to a favourable past experience of escapism would be a maladaptive response to experiential avoidance. We avert our attention and stray away from the very things that cause us distress, e.g. we shift our attention to favourable past experiences with previous relationships when we are fighting with our loved ones in the present. We avoid the very things we need to deal with by distracting ourselves with other behaviours.

Experiential avoidance is defined as (EA; Hayes, Strohsahl, Wilson et al., 2004):

  ... [an] unwillingness to experience feelings, thoughts and sensations as
  well as attempts to alter them.

For example, to avoid feeling loathe and resentment for their partner, a person resorts to seemingly pleasurable activities like gambling and drinking.

Mindfulness and psychological flexibility: seeing things the way they are

How do we then train the mind to address behaviours that arise from experiential avoidance?

The model of psychological flexibility is a good starting point in understand how to address ongoing distress, both physical and mental. The theory of psychological flexibility is around cultivating a sustained capability to observe experiences non-judgmentally while committing to value-driven activities (Masuda et al., 2011):

  it is an overall behavior pattern of experiencing whatever one is
  experiencing as it is fully and non-judgmentally without excessive
  defense (i.e., mindfulness), while engaging in value-directed
  activities at the same time (i.e., commitment to actions).

Firstly, in the context of a loveless marriage, the mental training involved would be around cultivating mindfulness to observe the experiences that cause the craving for 'mental and physical pleasures'. To see things clearly is paramount. The descriptor 'loveless' is not an indicator of factual evidence that a relationship is slowly dissolving. Recognising how one uses language and how it affects cognition is important in practicing mindfulness.

Secondly, values are the key catalyst for behavioural change. By systematically seeing things as they are through non-judgmental awareness, one can train their mind in focusing on acting in-line with 'what truly matters to them'. This has eudaemonic roots but has practical implications for psychological flexibility. Consider this very simple hypothetical example:

  X believes that he or she is in a 'loveless' marriage. This causes X a
  lot of  psychological distress, e.g. X feels anxious and hopeless
  about the future with Y (partner). This anxiety manifests in thoughts
  such as 'I don't love Y. Why am I with Y?'. This is the language
  component that considerably causes a high amount of distress for X. X
  recognises the distress he/she feels and learns to become
  non-judgmentally aware and accepts that these thoughts and emotions
  for what they are. X identifies the values in his life that holds
  dear. As a result, X finds that he has greater clarity around how he
  should behave - he wants to be in a committed and flourishing
  relationship and does not want to resort to seemingly pleasurable
  activites, e.g. excessive alcohol, cheating etc.

Freedom in experiencing and choosing

So the key to accepting ongoing mental or emotional suffering is to acknowledge them non-judgmentally and recognise any avoidant behaviours that are arising. Regarding the loveless marriage, the same concept applies: be aware of the thoughts and feelings causing the avoidant behaviours, tap into your values (i.e. for a better marriage, better relationship) and act accordingly to those values. Thus, rather than consumed in mental and physical pleasures - one has the freedom to take a step back and respond to their needs rather than react to ongoing emotional turmoil. This is by no means passive resignation.

Additional: Simple explanation on mindfulness and values

As humans, our thoughts and feelings seem like the only source of truth in understanding ourselves and the world. However, we can get caught up in thoughts and feelings believing that they are true when they are not. This is where mindfulness and values are important.

Mindfulness refers to non-judgmental awareness of our thoughts, feelings and experiences. In some ways, we become observers of our thoughts and feelings and we "take a step back" rather than act on them instantly. Some of these thoughts can cause behaviours where we avoid addressing how we feel rather than sort them out. For example, assume that X has a thought - "She/He never wants to have sex. I'm so frustrated about this." Because of this, X might go and cheat on his/her partner. This is the avoidant behaviour: X behaves in a way that he/she does not address how he/she feels or is thinking. Therefore, practicising mindfulness may help us recognise how we feel and think and not act so quickly.

What next? Well, clear values help us know how we want to behave. X may realise that his/her value is to have loving, intimate and sexual relationship with someone he/she cares about. He/she may then decide to communicate with his/her partner about the problem or decide to move on. Either way, X behaves according to his/her values and not simply how he/she feels.

References

Hayes, S.C., Strohsahl, K., Wilson, K.G., et al. (2004). Measuring
experiential avoidance. A preliminary test of a working model.
Psychological Record, 54, 553–578.
Masuda, A., Anderson, P.L., Wendell, J.W., Choi, Y.Y., Price, M. & Feinstein, A.B. (2011). Psychological flexibility mediates the relations between self-concealment and negative psychological outcomes. Personality and Individual Differences, 50(2), 243-247.


Is Orwellian Double-think Psychologically Possible?

When double-think is explained to mean

the power of holding two contradictory beliefs in one's mind simultaneously, and accepting both of them.

It can be seen to be the same as repression in a sense, whereby one version of events is known, but repressed in favour of an alternative version of events, but it isn't repression in the true sense of the word when referring to the Freudian theory of ego-defence mechanisms.
When you look at my other answer today regarding the defence mechanisms, I pointed out that they can involve both unconscious and conscious thought processes and actions.
As for repression, it is a powerful ego defence mechanism whereby it can prevent a thought or memory which can be psychologically damaging from reaching the conscious.
When mentioning the interaction between O'Brien and Winston in your question, where O'Brien was trying to instil in Winton that some people didn't really exist when they did, I can see where the confusion lies when linking that to repression. The knowledge of these people's existence is trying to be altered by O'Brien and Winston was wanting to have nothing to do with it.
The key to the whole idea of repression is that it is a completely unconscious defence mechanism. When we deliberately and consciously try to push away thoughts, this is suppression.
Although some claim that suppression is a psychoanalytical myth with no scientific support, fMRI data suggest otherwise. For more on that, you can read Defense Mechanisms: Neuroscience Meets Psychoanalysis in Scientific American
Also:
Anderson, M. C., Ochsner, K. N., Kuhl, B., Cooper, J., Robertson, E., Gabrieli, S. W., ... & Gabrieli, J. D. (2004). Neural systems underlying the suppression of unwanted memories. Science, 303(5655), 232-235. https://doi.org/10.1126/science.1089504
and
Bailey R, Pico J. (2020) Defense Mechanisms. In: StatPearls. Treasure Island, FL: StatPearls Publishing. Available free from: https://www.ncbi.nlm.nih.gov/books/NBK559106/


Difference Between Schema and Mental Model

At a high level, schemas and mental models are of a kind in cognitive science. You can think of both as cognitive or representational structures that aid in the storage and retrieval of information. Schemas were introduces earlier (Bartlett, 1932), and were followed by concepts such as scripts and frames (Schank & Abelson, 1975; Rumelhart, 1972). All of these, in general, describe the way that information can be structured in the mind such that we can easily navigate complex yet familiar situations, as well as adapt to and learn how to navigate novel situations.

I usually attribute the introduction of mental models to Johnson-Laird (1980, 1983). A lot of this work was based on evidence of spatial representational structures in peoples' minds when they do things like read a story, and (since I'm a language guy), these ideas were further extended to situation models of text, which suggest we hold mental representations outside of the realm of space and time, and into causality and goals (e.g., Kintsch & van Dijk, 1983; Zwaan & Radvansky, 1998; and others such as Glenberg, Morrow, ...). I kind of think of this work as extending more abstract notions such as schemas into people's actual memories and experiences.


Which area of the brain was first correctly associated with a specific function?

Broca is generally considered the first person to localise structure to function, however, there are some earlier individuals to consider:

EDIT: i recommend the chapter Neurolinguistics from the Middle Ages to the Pre-Modern Era: Historical Vignettes in: Stemmer, B. & Whittaker, H.A. (1998). Handbook of Neurolinguistics. Academic Press: London.
it has a very thorough look at this topic as it relates to language localisation and cites a number of case studies published well before broca. there are some departures from what i have written below and whittaker seems to give more significance to bouillaud's work. of note, bouillaud identified the significance of the double-dissociation paradigm in demonstrating the localisation of function:

Bouillaud  claims  first  to  be  able  to  demonstrate that  speech  movements  may  be  compromised  separately  from  limb  movements  and
second  to  demonstrate  which  part  of  the  hemispheres  is  involved  in  the  control  of  speech  movements.  To  prove  his  first  claim  he  states  that  two  actions  are  functionally  separate  if  they  can  be  disrupted  in  isolation  from  each  other,  which  is  evident  for three  cases  in  which  a  severe  speech  disorder  was  not  accompanied  by  any  impairment  of  limb  movement  or  by  any  defect  of  nonspeech  tongue  movements.  Thus,  speech has  its  own  motor  control  center.

wittaker notes that broca wasn't the first to localise language to the frontal lobe, but the political and scientific climate was such that he was essentially credited for this. in 1859, for example, he had founded the French Anthropological Society, which by the early 1860s had already commenced debating the cerebral localisation of mental functions.

Franz Joseph Gall (1758-1828)
Known as the father of phrenology. Most will generally mock gall for this theory, but you need to appreciate his ideas in context: he was the first to propose that the brain is the organ of an individual's faculties, tendencies and feelings. Of relevance to relating structure to function:

Gall did not study patients with acquired loss of speech but instead, studied the bumps and protrusions on the skill of highly musical persons... Gall localised the music faculty (Tonsinn) in a specific location of the brain, which was in close proximity to the area for language.

Kennaway, J. Music and the Nerves, 1700-1900.

Jean-Baptiste bouillaud (1796-1881)
Another alternative. In 1825 he wrote:

Finger, S. (2001). Origins of Neuroscience: A History of Explorations Into Brain Function.

Marie-Jean-Pierre Flourens (1794-1867)
But perhaps the most compelling of the three is flourens:

... in 1825 Flourens carried out localised lesions of the brain in living pigeons and rabbits, observing the effects on motricity, sensility and behaviour. These experiences demonstrated convincingly for the first time that the main division of the brain were indeed responsible for largely different functions. When the cerebral hemispheres were removed, for example, all perceptions, motricity, and judgement ended. When the cerebellum was removed, the animal's equilibrium and motor coordination suffered. When the brainsteam was removed, the result was death. Thus [he] concluded that the cerebral hemispheres are responsible for higher cognitive functions, the cerebellum for regulating and integrating movements, and the medulla for vital functions, such as circulation, respiration and general bodily stability.

Eiss, H. (2014). Insanity and Genius: Masks of Madness and the Mapping of Meaning and Value.


How does PRIMs solve the binding problem?

PRIMs doesn't claim to solve to binding problem. It just passes on the responsibility of representing the symbols and combining them accordingly. In this way the binding problem "is no longer an issue" of PRIMs, however it is a problem of whatever representational system it's working on top of. Whether it be symbolic like ACT-R or more neural, such as the NEF.


Here are the ones I know about; there's much more about neuroscience than, say, theoretical or computational cognitive science, but a lot of the neuroscience podcasts cover cognitive science indirectly or partially.

All in the Mind--it's also neuroscience and mental health stuff (a lot of mental health stuff)

Brain Science Podcast--books about and interviews with researchers in neuroscience

Neuropod--Nature's neuroscience podcast

Neuroscene--"the future of neuroscience", mostly interviews or topical explorations

Naked Neuroscience--the neuroscience offshoot of Cambridge University's Naked Scientists


Measuring changes in hemispheric dominance over time

I would first like to discuss the concept of lateralization and clear up a common misconception about hemispheric dominance.

  "A brain is considered to be asymmetrical (or lateralized) if one side (hemisphere or other brain region) is structurally different from the other and/or performs a different set of functions." (Bisazza et al., 1998).

A good example is the lateralization of language which relates to handedness. It has been widely accepted that a majority of people are left dominant for language, although right dominance increases with the degree of left handedness (Knecht et al., 2000).

Lateralization and behavioural asymmetries are neither restricted to language or humans (Bisazza et al., 1998). In the scientific community, hemispheric dominance is usually discussed in the context of a specific function. However, there is a common misconception by those who have an incomplete understanding of brain lateralization, particularly worsened by the spread of popular science articles and pseudoscientific tests (such as the one linked to in the comments) that wrongly assumes there is an overall dominance of one side of the brain (with left corresponding to logical and analytical thinking and right corresponding to emotional and creative thinking), that determines your personality trends. This is an incorrect oversimplification that is explained in a good article by RationalWiki.

Thus, your question is misguided in focusing on changes in hemispheric dominance. Even if you focused on change of lateralization for a specific function, this is unlikely as it requires substantial reorganization of the brain that is really only observed during development and to a much smaller extent following brain injury. However it is still good to question what changes there may be due to using a non-dominant hand more often! In fact (Teixeira and Teixeira, 2007) looks at how practice with the non-preferred hand alters manual preference for a specific task, and suggests this generalizes to other related motor tasks (Teixeria and Okazaki, 2007). The task used in their 2007 study involves sequentially touching the thumb with (in order) the ring, middle, little, and index fingers. The goal is to complete 5 cycles without interruption in the shortest time possible. They assess this before, after, and 30 days following practice, observing a noticeable shift in those that are allowed to practice compared to controls. You can choose a similar task and/or something different (for example, score in a quick video game that requires pointing with the trackball) and measure how you improve in comparison to a friend who doesn't practice with the left hand.

Ironically, they discuss how the left premotor cortex is dominant for learning sequential tasks (whether performed with right or left hand) and so might limit the observable shifts. For this reason it might be good to try their task to compare with that study and also your own task for personal interest.  If you are really interested in how performance and practice (especially long term) can affect the brain, there is lots of existing literature and imaging studies on the differences in brains of musicians compared to non-musicians or amateurs. Due to years of practice, professional musicians often have differences in and sometimes larger motor areas (Schlaug, 2006), increased cerebellar volume (Hutchinson et al., 2003), increased auditory cortical representation (Pantev et al., 1998) and increased assymetries such as in the planum temporale (Schlaug et al., 1995).


There is enough evidence to tackle the issue of exercise and depression. I am not sure about the rest of the psychiatric spectrum and disorders. A 2013 review by Cooney et al found differences in the methodological rigor of the trials.

  For the 35 trials (1356 participants) comparing exercise with no treatment or a control intervention, the pooled SMD for the primary outcome of depression at the end of treatment was ‐0.62 (95% confidence interval (CI) ‐0.81 to ‐0.42), indicating a moderate clinical effect.

However, when they examined a smaller more methodologically rigorous group, the effect size lessened but was still significant.

  6 trials (464 participants) with adequate allocation concealment, intention‐to‐treat analysis and blinded outcome assessment, the pooled SMD for this outcome was not statistically significant (‐0.18, 95% CI ‐0.47 to 0.11). Pooled data from the eight trials (377 participants) providing long‐term follow‐up data on mood found a small effect in favour of exercise (SMD ‐0.33, 95% CI ‐0.63 to ‐0.03).

So yes, definitely exercise is very helpful for depression with meaningful improvements.

Reference:

Cooney  GM, Dwan  K, Greig  CA, Lawlor  DA, Rimer  J, Waugh  FR, McMurdo  M, Mead  GE. Exercise for depression. Cochrane Database of Systematic Reviews 2013, Issue 9. Art. No.: CD004366. DOI: 10.1002/14651858.CD004366.pub6.


Can curiosity be described as an emotion?

The currently accepted model of curiosity is that of Litman. It describes curiosity as a sort of motivating factor:

  Curiosity as a feeling of deprivation (CFD) reflects feelings of uncertainty and tension that motivate information-seeking and problem-solving behavior.

Now we only need to establish a link between motivation and emotional intelligence. In this study, scientists found a link between the two, but came to conclusion that:

  Structural
  equation modeling indicates that motivation is not a factor of emotional  ntelligence but that it is related to the construct particularly through the regulation of emotion and the appraisal of others’ emotions

Edit based on more updated study:

Before we proceed further, I tried to find further proof that curiosity is indeed a motivation. I found confirmation of that here, which categorises curiosity as an intrinsic motivation.

Back on topic, Here is an invaluable resource that I found thanks to mrt: The Psychological Construction of Emotion - Edited by Barrett and Russell

The entire chapter 11 is relevant. It contains lots of relevant citations too (Specially the works of Panksepp). I can't quote all of it because fair use has a limit. I will just post a glimpse:

  In view of the clear evidence linking DA transmission to aspects of
  motivation, what does this say about dopaminergic involvement in emotion? Is DA irrelevant as an ingredient in emotional states? Not necessarily.
  Burgdorf and Panksepp (2006) suggested that ventral striatal mechanisms
  are not related to “pleasure” or “consummatory reward” in the traditional sense, but instead are involved in anticipatory or appetitive energizing effects of stimuli.

The book establishes a difference between hedonic "liking" and dopamine-induced "wanting". [ Dopamine has been linked to pleasurable simulations as well as aversive stimulations ] Depressed people do not lose their appreciation of pleasurable things like tasty food (quoting the book here), but find no energy in their pursuit of motivational stimuli, exertion of effort, and motivational anticipation.

In conclusion: I would like to propose that being curious is similar to being a foodie, or adventurous. Not sure about lexical term, but there seems to be a need to differentiate between core emotions and their drive.


What is the difference between affect and feeling?

According to constructionists (e.g., Russell & Barrett, 1999), affect (or "core affect") is a composite of valence and arousal, which underlies all emotional experience.  So when I feel good and highly aroused, that's affect.  When I categorize my affect (good, high arousal) as excitement, that's an emotion.

According to those who consider emotions to be multi-componential reactions to the environment (e.g., Gross, 1998), affect is an umbrella word to describe anything related to emotions or mood.  It's definition isn't as specific as the one above.

On the other hand, "feelings" has no specific definition.  It's a vague term that most emotion theorists don't use because it could refer to almost anything (e.g., interoception, nociception, exteroception like touch).  To specify that feelings are specific to the affective domain, we often use the phrase affective feelings, but it's not a word that's central to any modern emotion theory that I know of.

So when in doubt, don't use the word feelings. But do use affect, emotion, or mood, as long as you explicitly define them using whatever theory you subscribe to.


What models/mechanisms exist for the brain to chain movements together?

In the paper "Control of automated behavior: insights from the discrete sequence production task" a task similar to piano playing is discussed. The task, shown in the figure below, involves a user pressing a key corresponding to visual input.

One of the most interesting results from the paper is, as shown below, after learning, the response times of certain series of movements have lower reaction times. They also seem to be organised in specifically sized chunks.

The model of how this works is called the Dual Processor Model (DMP), which claims that two processors, one cognitive and one motor, race each other to execute a task. It is only described at a high level and never built into a model.


For what kind of concepts do we really need an analogy?

Loosely defined, analogy is the process by which "novel situations and problems can be understood in terms of familiar ones". By this definition, a number of cognitive scientists would and do say that analogy plays a role in acquiring just about any new concept - they would say that especially examples and learning by doing are means of refining one's ability to map from the known to the unknown and uncover the latter's structure/properties. In addition to the linked book, which offers a collection of papers/essays in cognitive science on analogy, you could check out Douglas Hofstadter's Surfaces and Essences: "Analogy-making, far from happening at rare intervals, occurs at all moments, defining thinking from top to toe, from the tiniest and most fleeting thoughts to the most creative scientific insights." In the appendix there is a very long list of scientific publications supporting his assertions.


What is the term for the rhetorical, "How hard could it be?"

I believe the closest match is the illusion of control:

  ... the tendency for people to overestimate their ability to control
  events; for example, it occurs when someone feels a sense of control
  over outcomes that they demonstrably do not influence. ... people base
  their judgments of control on "skill cues". ... When more of these
  skill cues are present, the illusion is stronger.

This bias only operates when a plausible case can be made for one's skill or intent influencing outcomes - such as a programming task given to a programmer.  In such instances, how well the task or problem is understood, its actual level of difficulty, and the actual level of control over outcomes are overestimated or ignored.

Positive illusions - biases that describe how people overestimate their own abilities, success, and control - are the broader category that contains the illusion of control, and the planning fallacy, among others.  These biases typically go away when estimating the success of others instead of one's self.

There is another bias worth noting here, called the hard-easy effect:

  ... a tendency to overestimate the probability of one's success at a
  task perceived as hard, and to underestimate the likelihood of one's
  success at a task perceived as easy. ... "Hard tasks tend to produce
  overconfidence but worse-than-average perceptions," ...

This bias also ignores how well understood a problem is, but it suggests that a problem perceived as hard (whether or not it actually is) is more likely to result in overestimating success.  This bias is not as robust or widely accepted as the former.


Name of cognitive bias when you diminish one's competency based on someone else's for the same function?

The broad topic is norm theory. Kahnemann & Miller (1986) give a nice overview of the topic. The specific effect is a contrast effect.

Higgins & Lurie (1983) have an experiment which matches the situation nicely. In their experiment, subjects read a series of short stories describing the sentences handed out by various judges for similar crimes. Some judges were harsher or more lenient than others. As you might expect, a specific sentence (e.g. Judge Wilson sentenced the guilty person to 3 years of prison) was judged as being more harsh if the other judges tended to give shorter sentences, and more lenient if the other judges tended to give harsher sentences.

Their result also suggests that your memory of the first manager's competency (the really good manager) will be affected by the exposure to the new manager. They brought the subjects back to the lab a few days after reading the original stories. When subjects came back, they were given a new set of sentencing decisions to read. Then they were asked to recall how long the sentence was of a specific judge (e.g. Judge Wilson) from the first session. The memory for the original sentence was skewed by the new stories that they read. If the new stories all tended to be lenient, then subjects underestimated Judge Wilson's original sentence. If the new stories were all harsh, then subjects overestimated Judge Wilson's original sentence. They call this a change-of-standard effect.


What is the rationale behind filler words?

What is the rationale behind those constructs from a neurolinguistic point of view?

A simple conversation engages multiple areas of the brain, there are temporal areas for recognizing, planning & generating speech, motor areas for executing it,Frontal & PreFrontal areas for making sense of it,defining social context, and memory subsystems for holding both to small sound bites and longer conversational threads.

In my view,filler words are the speech equivalent of learned reflexes for movement or conditioned responses in the context of a conversation. Additionally, since we are also capable of overriding and co-opting such mechanisms, they can also be thrown in consciously (when stalling for time as you note) or avoided when public speaking by breaking cadence with silence.

From a neurolinguistics point of view, they most likely involve wernicke's area which is involved in the planning and selecting of words for speech ( along with recognition) and might involve PF-Temporal Areas trying to catch up in word and ideas selection or comprehension while maintaining cadence.

Source: Cognitive Neuroscience: The Biology of the Mind, ( The language chapter)


Kelly Criterion Observed to Be Adhered by Psychopaths?

I do not know about psychopaths adhering to the Kelly criterion or not. Technically, for a perfectly informed agent seeking to take advantage reccuringly from an objectified winning yet risky position, the Kelly criterion sets the maximum bet amount over which betting would be irrational. In the sense that betting more than the Kelly criterion would deplete your finances by exposing yourself to too much risk.

Imagine that you know that a tossed coin ends up 49% of the time on heads and 51% of the time on tails. For 1 buck you bet, you earn 0 or 2 bucks depending on the outcome of the coin toss.

Betting on heads is irrational. So you bet on tails. The question is "what proportion of your total assets" are you willing to bet? If you bet 0% of your assets, you never earn anything. If you bet 100% of your assets, you've got 49% chances of being broke the next round and having nothing left to bet again, which is kind of stupid since you've got a rational structural advantage on the bookmaker.

The question therefore becomes "what fraction of my assets should I bet to maximise the gain with respect to the risk"? The answer depends on your so called "utility function". In the case where each buck gained increases your utility linearly, (i.e. you're as eager to gain a buck whether you're broke or a bilionaire, to put it simply... a buck is a buck no matter what), the Kelly criterion applies:

You bet the the fraction that maximises the probabilistic expectation of the logarithm of the ratio of assets after the bet to assets before the bet. If I recall things well off the top of my head.

Betting less than Kelly is not greedy enough. Betting more than Kelly is self-destructive. That's the theory.

In the financial stock broking business, the Kelly criterion has been used in the past... almost. They divided the Kelly criterion by 2 to be on the safe side. The reason is simple: no matter how rational Kelly is, draw up a chart of the typical fluctuation of your assets using the Kelly criterion under perfect circumstances (even correcting for your utility function). Take a close look at it. Then you'll realise that you'll be in for such a bumpy ride for your assets that russian mountains on cocaine will feel like zen meditation. Technically, betting using Kelly is exactly being on the verge of self-destructiveness...

No one, ever ever ever ever would "reasonably" bet their assets using Kelly. Unless you have the self-denegation of a number theorist on ketamine. Not joking.

Not even a psychopath.

The closer you can get to the question would be: (1) are psychopaths inherently rational machines (2) are psychopaths greedy to the extreme that a buck is a buck whether they're broke or a billionaire, and (3) are they able to endure the cognitive dissonance by reconciling (1) and (2) assertively and agressively without fear of any sort.

I doubt this to be the case. They may well score higher than neurotypics, but it's quite a stretch to imagine a psychopath would spontaneously follow Kelly criterion when the greediest stock brokers would not dare to. According to your study, they may well score higher on points (2) and (3).

In this study, Kelly does not apply and does not determine a stop loss criterion. It simply shows psychopaths are either less emotional or have a more linear utility function than neurotypics. A fearful neurotypic may stop playing if he has had repeated bad luck. A rational and fearful neurotypic would have laid out beforehand his stop losses depending on which turn he's in and would have played all turns up to the point where he would have stopped playing definitely: he knows there's no point in postponing his luck. And he must be rather fearful to decide to stop playing, meaning that his utility function must be very concave near ruin to trigger a stop loss and very insensitive to wealth if he decides to trigger a stop loss early in the game. In a nutshell, rationality in the game is defined by playing all turns in the game up to a point where you stop playing. If the player plays, then stops, then resumes playing, he's irrational. But the more he plays, the less he's anxious. From what I've read of the article, psychopaths are not more rational, they are less fearful. Kelly has little to do here.

Another question you may ask is whether or not neurotypics and psychopaths end up behaving the same way as cohorts the longer they play at the betting game. How desensitised to the irrationality of the human conditioning to the game do neurotypics and psychopaths become the more they're exposed to it, and at what pace. To me that's perhaps the real question.

Moreover ruin theory such as developped in actuarial science is NOT Kelly criterion. It's standard stochastic calculus with ruin constraints. Kelly criterion is the poor man's naive implementation of stochastic calculus. Very much the same way that mysticism is the poor man's naive first attempt at science.

By the way, Kelly strategy cannot go to ruin, not because it's Kelly, but because it's a self-funded strategy, which in itself is a broad class of strategies, that includes very very stupid ones.

I hope that clarifies the scope of the question.


What is a scientifically plausible method by which people might in the future be able to read minds?

If you don't need the mind readers to actually know the exact "words" of the person's thoughts, you could have people who are extremely well versed in "reading" another person's facial expressions, body posture, tone of voice etc. It is a fact that those outward behaviors reflect your internal state, and in fact we all read these signs with more or less accuracy, but there are a few people (and maybe you can train that) who are better than others to deduce how you feel and what you might be thinking from these. (see "cold reading")

If you need actual mind readers, we are currently arriving at a point where we begin to be able to interpret fMRI images. There are some experiments where researchers were able to tell which images a test subject was looking at or which body parts they were moving from looking at their brain activity alone. I'm sure that our understanding of what goes on in the brain will progress and the technology to measure brain activity will get smaller and more exact, so you could have people use a device that reads minds. It is quite likely that such a device will exist in the not too far future.

If, finally, you want real telepathy (which, just to cause no misunderstanding, cognitive scientists believe does not exist) you might base it on:

an organ in human beings sensitive to magnetic or electric fields, sensing (like EEG) the brain states of another human being; there are animals who can sense electricity or magnetism, but the problem with this is that magnetism surrounding us is stronger than that coming out of the brain and will make it impossible to "feel" a brain from farther than a few centimetres away
this organ might be in the skin (actually not one organ but many receptors) so the reader could cover the head of the person to be read with his hands, much like an EEG cap
the reader would need to be trained with people telling them what they think while he "feels" their brain, so that he can learn which "sensations" in his hands correspond to which thoughts and cognitions
maybe its possible to clone human beings with specific animal genes so that humans grow electrically or magnetically sensitive receptors, e.g. in their hands (research animals with electric and magnetic senses and how their receptors work)

I'm just trying to extrapolate (my understanding of) current research, here. I cannot foresee future discoveries either technological or psychological, so I'm keeping this within the realm of the possible as much as seems plausible to me. Again: We don't think telepathy in the traditional sense (concentrating your mental powers and knowing what someone thinks) exists. If you want that, I don't see how it could be possible.

There seems to be some evidence of magnetoperception in humans:

http://en.wikipedia.org/wiki/Magnetoception#In_humans
http://www2.pe.tu-clausthal.de/agbalck/biosensor/magnetsinn.htm

It is easy to imagine that this sensitivity to the earth's magnetic field might develop to discern even the much weaker magnetic fields of the brain. After all, the other senses show a huge variety between species, too. For example, the silk moth can detect single molecules of a female's pheromones. The current sensory ability of humans is not a fixed limit for how sensitive a sense can be. If the magnetism of the brain can be measured by an artificial detector, then it can potentially be measured by a biological detector.


Role of declarative memory in learning skill

My understanding of the difference between the two is that you cannot declare what is procedural. For example, you can't tell a person how to balance on a bicycle or how to ice skate backward. You can show them different movements, and that is declarative in nature, but ultimately is not the same thing.

Whether or not declarative memory is "faster" has probably not been tested (and if it has, I would question the results). I'm not even sure it would make sense to evaluate given there are fundamentally different learning processes taking place.

Declarative knowledge can definitely be important in building skills. In almost every manual procedure exists a set of instructions which can be written and transmitted. These procedures can function as a scaffold and help the learner figure out how to do the tasks whose performance can only be demonstrated. An example of this could be a work instruction for how to ride a surfboard. They can tell you how far out from the shore to go, where to place your feet, how to get on the board, etc. but cannot actually tell you how to ride the wave. That is something you'll have to figure out on your own after doing everything you can to follow the instructions


About the possibility of 'Robot Psychology'

Depending on the definition of "psychology" and "psychological problems" sure. The APA defines psychology as "the scientific study of the behavior of individuals and their mental processes." If we take this to only apply to biological systems (as I am sure many researchers do) then no, because the robot is not a biological system and therefore we can not study it under the heading of psychology and we would probably study it under something more akin to "engineering". However, if one is happy applying the same to robots, as I assuming you are, then yes.

Assuming the latter, and if you think that a being's "'ability' to 'do' 'undirected' or 'semi-undirected' introspection and 'form' all sorts of 'thought' structures about any subject matter" is a cause of psychological problems, and we are further assuming that a robot could do this, then yes, the robot will have psychological problems by definition. (Is there direct evidence suggesting these are causes though?)


The function of pumps in forming the resting potential

Apparently the resting potential of -65mV is reached when the two forces, diffusion and electrical gradient are in equilibrium.

That is not true. You are confusing a neuron's resting potential with what is actually a type of ion's equilibrium potential.

An equilibrium potential for a particular type of ion--such as Na+ or K+--is the exact voltage across the membrane that exactly opposes the diffusional force for that ion, and thereby prevents a net flow of that ion across the membrane. So, for example, in the case of Na+ (sodium ion), in mammalian neurons, a typical value given in textbooks is something like +55 mV. In other words, the interior of the neuron needs to be 55 mV (relative to the outside of the neuron) in order to prevent all the Na+ ions from rushing into the neuron. There are equilibrium potentials for all the ions that are used in neurons to influence the voltage across the membrane: Na+, K+, Cl-, Ca++. If a fictional neuron were to be at the equilibrium potential for Na+, and there were no other ions at play, there would be no need for pumps to maintain any concentration gradient of Na+., because, by definition, there would be no net flow of charge, and so the situation would be stable.

However, the resting potential refers to the voltage of the neuron when it is at rest--not having an action potential--but that voltage is going to be some "weighted average" of the equilibrium potentials of all of the types of ions: Na+, K+, Cl-, and Ca++. Of these, K+ (potassium ion) dominates, and so we find that typical values for the resting potential of neurons is around -65mV, which is closer to the equilibrium potential for K+ (-90mV), than for Na+ (+55mV) or Ca++ (+155mV!).

But since the typical resting potential of the neuron actually is not equal to any of the equilibrium potentials for any type of ion, that means by definition all of the ions are going to have net movement across the membrane. If ion channels are left open and ions are therefore allowed to flow across the membrane, Na+ is going to flow in, K+ is going to flow out, Ca++ is going to flow in, etc. (I'm leaving Cl- out for simplicity).

Since these ions are flowing with a net direction (either into or out of the neuron), that means concentrations are changing; e.g., K+'s large concentration gradient is getting smaller as it flows out of the neuron. Over time, these ion flows move the concentrations of ions towards equality on both sides of the membrane, and therefore move the neuron's resting membrane potential toward 0 mV. In some sense, the "battery is running down". This would render the neuron incapable of having an action potential, and thus acting as a signaling machine, and therefore must be prevented.

In order to prevent that rundown of concentration gradients, ion pumps actively maintain the concentration gradients of the ions. One of the relevant ones here is the Na+/K+ exchanger, which uses ATP to power its action of pumping in two Na+ ions for every three K+ ions it pumps out. Using ATP requires producing ATP, which requires glucose, and so just maintaining "ready to go neurons" is metabolically demanding.


What exactly is meant when it is said that only you can make yourself happy?

It's mostly a fairly vapid truism (see the rhetorical sense). Here's a diagram from a popular theory from a positive psychologist at my doctoral alma mater of [what really makes people happy (or not):

(source: edbatista.com)  (Lyubomirsky, 2008)
Thus the truer truism would be, "You can make yourself happier, to some extent..." but it's tricky enough to justify the existence of very many books, studies, even the entire field of positive-psychology, due to catches like the hedonic treadmill (essentially the process by which our pleasures "get old").

As for the need for others, it's something of a personality variable, or two (McAdams & Constantian, 1983), or maybe three by a different theory's construction (i.e., relatedness, not all three here). That is to say it's not universal, much less invariant. In reading @huseyintugrulbuyukisik's answer, consider the following question: https://cogsci.stackexchange.com/q/169/4086 You'll find an answer from me based on a recent evolutionary psychological review there as well. It largely supports your assumption that people will want a significant other sooner or later, and surely this is true for most people.

However, there are certainly exceptions to the false "rule":

Asexuality may best describe as much as 1.1% of the general population (Bogaert, 2004, 2006).

A great documentary on an asexuality awareness advocate is available on Netflix. He strikes this personality psychologist right here as quite happy, healthy, and generative. He seems to suffer most from the transience of adult relationships where they lack romantic commitment. I would argue that this is our cultural problem, not his personal problem.

Asociality is a commonly familiar amotivational characteristic that relates to several other traits, states, and disorders, including:

Introversion, a "Big Five" trait dating back to Carl Jung
Depression, which is a broader state of amotivation and negative affect
Avoidant, schizoid, and schizotypal personality, social anxiety, and autism spectrum disorders

The generally undesirable tone of these exceptions belies the social nature of humanity, as does reflection on the benefits of family and social engagement for longevity...but as it is also the nature of humanity to differ individually, almost no statement of human nature is absolute. See health-relevant Wikipedia pages on solitude, social isolation, and hikikomori.

Several cultural references may serve to flesh out the variation in human experience of solitude:

The history of hermitude, non-cenobitic (eremitic) monasticism, anchorites, stylites, poustiniks, self-sufficiency enthusiasts, loners, and misanthropes
An investigative report on solitarily confined inmates
A nonfiction book and a movie based on it with a particularly poignant ending (mind the spoilers in the preceding links!)
An excellent, recent album by the Australian band Tame Impala, Lonerism, that partly celebrates self-awareness:

  "This album is like...someone growing up and discovering other people and just realising their place is not involved with the rest of the world kind of thing. Like discovering that you're a loner."[27]..."It's about the persona of someone who is really isolated – but not necessarily deliberately. Most of the songs are really about other people, being amongst other people. It's really just the idea of being someone who doesn't feel part of the rest of the world, someone trying to figure out where their place amongst everyone else is, and having a really confusing time with it and then slowly accepting that it's in their blood just to be a solitary wanderer. It's meant to put it in a positive light but also a negative light, as the album progresses."[10][13]
  Parker revealed that the album title and general themes of isolation and introspection were selected when "We were touring so much and doing all these gigs and going to places with people. It reminded me of when I was a kid trying to be social and trying to be a people person and realising that I'm not. The last years of touring and me being a people person is just something that's not in my blood. All these cool parties just make me realise I'm just a total outcast. I just can't really talk to anyone without feeling stupid." and "sometimes I just want to run home and never come out of my bedroom again".[27]

References

- Bogaert, A. F. (2004). Asexuality: Prevalence and associated factors in a national probability sample. Journal of Sex Research, 41(3), 279–287.
- Bogaert, A. F. (2006). Toward a conceptual understanding of asexuality. Review of General Psychology, 10(3), 241–250.
- Lyubomirsky, S. (2008). The how of happiness: A scientific approach to getting the life you want. Penguin.
- McAdams, D. P., & Constantian, C. A. (1983). Intimacy and affiliation motives in daily living: An experience sampling analysis. Journal of Personality and Social Psychology, 45(4), 851–861.


How should I report results of a likelihood ratio test?

General reporting recommendations such as that of APA Manual apply. One should report exact p-value and an effect size along with its confidence interval. In the case of likelihood ratio test one should report the test's p-value and how much more likely the data is under model A than under model B.

Example: The data is 7.3, 95% CI [6.8,8.1] times more likely under Model A than under Model B. The hypothesis that the data is equally likely under the two models was rejected with p=0.006.

The above statements already indicate that likelihood ratio test does not tell you which

  model is a better description of my data

as the likelihood is $p(\mathrm{Data}|\mathrm{Model})$ and to learn which model is a better description of the data you need to compute $p(\mathrm{Model}|\mathrm{Data})$.


Why don't people listen to smart people?

David Dunning and Justin Kruger have observed that, related to skill competency, individuals which are incompetent in a certain skill can exhibit a cognitive bias, called the Dunning-Kruger effect, which leads them to:

fail to recognize their own lack of skill
fail to recognize genuine skill in others
fail to recognize the extremity of their inadequacy
recognize and acknowledge their own lack of skill, but only after they are exposed to training for that skill

While the study focuses exclusively on why people can or cannot measure their strenghts and weaknesses correctly, there was an interesting subsequent study where the authors were lead by the fascination that certain incompetent poor performers fail to ever improve. They have concluded that such individuals have an apparent lack of self-insight, which leads to exhibit incorrect logic and defensive mechanisms which fixate their views even against continuous feedback and encouragement to improve.

This certainly remains a complex phenomena which we could, from experience,  observe in different forms. Based on the suggestions from the last study, it seems that this becomes an issue with individuals that have not conceived intelligence as being malleable. Apparently, they may not have been instilled to value intelligence and encouraged to approach learning and the refinement of it's processes for the betterment of one's own intelligence as an endeavor which is to be considered as rewarding.

Effectively, being that they consider intelligence as something that is fixated, failing to generate excitement when they engage others that attempt to challenge and broaden it seems to lead to the difficulties at hand, such as: I do not understand you and I am certain I never will, so I choose to continuously ignore you because I do not want to feel this discomfort that arises from knowing that I am invariably incompetent, which you and I both know is not a good thing.


Q: How do we know brain Is not involved in knee reflex?

A: The brain is involved in the knee reflex in the control of how fast/slow and strong/weak the reflex occurs, but it's not essential in the occurrence of the knee reflex. The knee reflex is still present even when the spinal cord is cut or destroyed at any level above L2 [1], which is above the reflex arc pathway (L2-4) and which cuts off the connection between the brain and the reflex arc. This is usually evident clinically. The only exception that the knee reflex may be absent after the incident is that the condition called “spinal shock” occurs [3]. However, this condition is temporary, and the knee reflex will return, usually even brisker than before the incident (due to the absence of inhibitory control from the brain). This confirms that the brain is not essential in the knee reflex and only has regulatory roles.

Q: How do we know that compressing the knee generates a feedback signal that makes the leg extend even before the signal reach the brain?

A: Electrophysiologic studies show that the latency of the knee reflex is normally about 46 msec [1] while the evoked potential (P37) recorded at the scalp over the leg area after electrical stimulation of the posterior tibial nerve is about 37 msec.[4] So, comparing data from these comparable but not identical experiments, it can be estimated that the knee reflex occurs, indeed, after the signal reaches the brain, as you asked. But don’t forget that the former latency is the time of the complete loop while the latter latency is of only halfway. It will take longer than 37 msec for the signal to complete the loop of leg-brain-leg and move the knee.

References

Xu D, Guo X, Yang CY, Zhang LQ. Assessment of Hyperactive Reflexes in Patients with Spinal Cord Injury. BioMed Research International. Vol 2015, Article ID 149875. http://dx.doi.org/10.1155/2015/149875
Wikipedia. Patella reflex.
Atkinson PP, Atkinson JLD. Spinal Shock. Mayo Clinic Proceedings. 1996 Apr; 71(4): 384–389.
Walsh P, Kane N, Butler S. The clinical role of evoked potentials. Journal of Neurology, Neurosurgery & Psychiatry 2005;76:ii16-ii22. http://dx.doi.org/10.1136/jnnp.2005.068130


Q: Are normal external stimuli still processed by the brain during a hallucination?

A: Yes, normal stimuli are still processed during a hallucination, but some of them may be distorted or obliterated. This is evident clinically. For example,

When a schizophrenia patient has an auditory hallucination (such as voices talking to him/her) [Ref 1] while he/she is doing something in the public, the patient still hears sounds in the surroundings and what other people are talking normally.
When a migraine or epileptic patient has a visual aura (a kind of visual hallucination, which usually occurs as flashing lights [scintillation], zigzag patterns [fortification spectra], or blind spots [scotomas]) [Ref 2] or a drug addict has a visual hallucination (such as insects crawling on the floor, a pink elephant coming into the room, or a stranger coming to attack him/her) from psychedelic drugs, he/she still can see the visual image of the surrounding place.[Ref 3] But, the part of visual field that the visual aura/hallucination is occurring may be normal, distorted, or obliterated, as in the figures below.

Figure 1.Visual aura of migraine. [Ref 4]

Figure 2. This is what an aura is like to one migraine sufferer. [Ref 5]

Some patients with a tumor, abscess, cyst, or other lesions at the parietal somatosensory area have sensory seizure (a kind of somatic sensory or tactile hallucinations) and some schizophrenics have tactile hallucinations, which can occur as insects crawling on the skin, the skin over the head being stretched, the patient being cuddled or kissed, etc. [Ref 6]. These patients still have intact sensory perception while they have these tactile hallucinations because they can feel touch, pain, hot, cold, proprioception, etc. as usual while they're having the hallucinations. But, although these sensations are still normal in the unaffected areas, they may be altered, diminished, or absent in the affected areas.

So, normal stimuli are still processed by the brain during a hallucination, but they may not be processed normally, especially in the affected area, and the resulting perceptual experience is the experience of a mixture of normal perception and hallucination.

References:

Larøi F, Sommer IE, Blom JD, Fernyhough C, H. ffytche D, Hugdahl K, et al. The Characteristic Features of Auditory Verbal Hallucinations in Clinical and Nonclinical Groups: State-of-the-Art Overview and Future Directions Schizophrenia Bulletin. 2012 Jun; 38 (4): 724–733. https://doi.org/10.1093/schbul/sbs061
Schott GD. Exploring the visual hallucinations of migraine aura: the tacit contribution of illustration. Brain. 2007 Jun; 130(6):1690–1703.
Teeple RC, Caplan JP, Stern TA.Visual Hallucinations: Differential Diagnosis and Treatment Care Companion J Clin Psychiatry.2009; 1(1): 26–32.
Falardeau J. Visual aura of migraine. American Academy of Ophthalmology.
Bekkie’s Wonderland. Migraine and migraine art drawn by patients.
Wikipedia. Tactile hallucination


Assuming your mask is in NIfTI format (nii or nii.gz extension), you can use the fslstats command line tool for that. Just type fslstats on the command line to see the help text for command syntax and arguments. For your specific case, you can use:

fslstats <input> -V

where <input> is the path to your mask NIfTI file. The returned numbers will be the mask volume in voxels and mm^3.

FSL install

Since you said you used FSLeyes to draw your mask, I'm assuming you have the full install of the FSL package as well. If not, see their wiki for instructions.


How long does it takes for the feeling of vengeance to fade away by time?

It depends on the individual (and possibly the trauma). Stockholm Syndrome, where captives develop a psychological alliance with their captors as a survival strategy during captivity can onset very quickly (in the original case 6 days). There are also cases where people are actively trying to escape and do not feel a bond with individuals.


What science-based strategies can slow down dementia?

It depends on the disease that causes dementia. Dementia is a syndrome that has many causes. Some of them are treatable, such as metabolic/infectious diseases. Some are primary degenerative diseases of the nervous system, such as Alzheimer disease, Pick disease, and Huntington disease. Most diseases in the first category are treatable, many are curable. But most diseases in the second category are usually not amenable to treatment. They progress slowly but relentlessly despite any treatment.

Regarding non-pharmacologic treatments, including cognitive training or cognitive rehabilitation, they seem to have some roles in the management of dementia (H C Kales)   but not have spectacular effects and still be inconclusive in improving or maintaining cognitive and functional performance of people with dementia (Diagnosis and Treatment of Dementia).


Is there a formal definition for the difficulty of learning something?

First, let me start by saying your topic is extremely broad.  There are many reasons why something may be difficult to learn.  However, the exact "difficulty associated with learning something" is known by many different terms in the scientific literature, and in particular, I have found cognitive load theory to be a particularly useful description of this.  According to Sweller, Cognitive Load falls into three distinct domains:

Intrinsic cognitive load is that difficulty that is associated with the material itself, independent of the learner.
Extraneous cognitive load is associated with the instructional methods or materials (poor instructional techniques increase this load).
Germane cognitive load is load that the learner requires to create associations and connections among the concepts, and depends on the learner's knowledge base.

The basic premise is that subjects are difficult to learn if they require a great number of connections to be formed (a mental model or schema).  The greater the connections required, the greater the difficulty.  Complicating this, certain topics are inherently difficult, such as mathematical computation and critical thinking, and learners bring their own pre-conceived mental notions to the table.  Cognitive Load theory attempts to provide a framework for thinking about the interactions between these variables.

I have studied the difficulty with teaching/learning engineering subjects, such as statistics, variability, critical thinking, etc. using controlled experiments that attempt to hone in on the second and third aspects of CLT. Here is a link to a conference proceeding that I published on the subject; I have another paper in-work that I can't share until it is published- but so far, my results very much support CLT.

Interest can be a factor, because attention given to a learning subject will take away from the students' ability to process other cognitive loads. Likewise, anxiety can also be a factor.  Lots of research left to do in this field if you ask me, though - so expect these theories to develop substantially in the next 10-20 years.


How to learn about children using hitting affectionately

The search term "children hitting for fun" seems to yield the results you may want although the results seem to come from sites such as mumsnet.

An aspect to this phenomenon is that this behaviour may lead to bullying behaviour later on in life if the right responses are not given when this occurs.  The child needs to learn the cause and effect of hitting.

Typing the same term in Google Scholar gives research articles on dealing with bullying.


Is there an open-source / free official Myers-Briggs assessment I can adopt?

The IPIP may provide what you are looking for.

  This IPIP Website is intended to provide rapid access to measures of
  individual differences, all in the public domain, to be developed
  conjointly among scientists worldwide.

In general, the scientific literature tends to focus more on a dimensional approach based on the Big 5 model of personality than the type approach. There are strong correlations between MBTI and Big 5 measures.

The IPIP website provides measures of the Big 5. The following table from Furnham (1996) summarises some correlations across a few studies between the NEO Big 5 and the MBTI.

You can find a listing of some of the multi-construct measures including Big 5 measures on the ipip website.

References

Furnham, A. (1996). The big five versus the big four: the relationship between the Myers-Briggs Type Indicator (MBTI) and NEO-PI five factor model of personality. Personality and Individual Differences, 21, 303-307.


Are studies included in most meta-analyses based on a narrow range of participants?

Hunter and Schmidt offer a a set of procedures to correct range restriction, these are included in many packages based on their meta-analytic methodology, here are some relevant references:

https://pdfs.semanticscholar.org/75e8/97a797dc876b785042dfd8ac4023a5fc85df.pdf
http://onlinelibrary.wiley.com/doi/10.1111/peps.12122/abstract
https://www.researchgate.net/publication/6644262_Correcting_for_indirect_range_restriction_in_meta-analysis_Testing_a_new_meta-analytic_procedure
mypages.iit.edu/~morriss/siop2009/Le09.ppt
mypages.iit.edu/~morriss/siop2005/Oswald05.doc
https://www.corwin.com/sites/default/files/upm-binaries/5063_Hunter_Chapter_3.pdf
https://utsa.influuent.utsystem.edu/en/publications/implications-of-direct-and-indirect-range-restriction-for-meta-an

hth,

larry


What is the underlying genetic basis for ADHD?

I hope the few sources below answer your question. I strongly recommend you read actual sources as opposed to the parts I have quoted. I don't know much about this topic so I did not attempt to translate anything in laymen terms, since I might have distorted or misinterpreted information in the process. However, the three sources below are one of the best-known studies on the genetic basis of ADHD. I have quoted the two sources in direct response to your question about the proposed role of dopamine and serotonin transporter genes.

Percentage due to variation attributed to heritability

  Twin, family and adoption studies have suggested that there is a strong genetic contribution to ADHD, with a mean heritability estimate of 76 % However, it has been difficult to implicate any specific gene in ADHD beyond reasonable doubt. The difficulties encountered in identifying genetic variants increasing the risk for ADHD could be at least in part owing to the heterogeneity and complexity of this clinical syndrome.Consequently, it has been proposed that the use of intermediate phenotypes (or endophenotypes) relevant to ADHD are likely to be more informative than the DSM-IV1 diagnoses, allowing for increased detection of genetic effects.

Genome-wide linkage scans

  To date, seven genome-wide ADHD linkage scans have been published and
  some chromosome regions such as 5p13, 14q12, and 17p11 have been
  indicated in multiple studies [Fisher et al., 2002; Bakker et al.,
  2003; Arcos-Burgos et al., 2004; Hebebrand et al., 2006; Ogdie et al.,
  2006; Faraone et al., 2007; Asherson et al., 2008; Romanos et al.,
  2008]. However, no chromosome region has been consistently identified
  across the scans and the majority of the findings were unique to each
  study. This is not unexpected because the power of individual scans is
  likely to be low for a complex trait such as ADHD which may only have
  genes of small to moderate effects [Risch and Merikangas, 1996;
  Waldman and Gizer, 2006].

Dopamine transporter (DAT1)

  The DA transporter (DAT1) gene harbours a 40-bp repeat sequence
  variable number tandem repeat polymorphism located in the
  3′-untranslated region. The most common alleles are the 10- (480-bp,
  71.9%) and 9-repeat (440-bp, 23.4%) alleles, although these frequencies are variable from one population to the next.
  Homozygosity for the 10-repeat allele was reported to be associated
  with higher DA transporter protein in the striatum, a region
  where it is heavily expressed56 and where it serves as the primary
  means of DA reuptake. Several studies have suggested a relation
  between ADHD and the DAT1 variable number tandem repeat, the 10-repeat
  allele being the risk allele; however, a roughly equal number of
  studies have failed to detect such a relation. In a review by Faraone
  and colleagues, the pooled OR associated with the 10-repeat allele in
  family-based association studies was estimated to be 1.13 (95% CI
  1.03–1.24).

  Loo and colleagues40 reported that children carrying 2 copies of the
  10-repeat allele exhibit higher commission errors, impulsive responses
  (β score) and reaction time variability compared with carriers of the
  9-repeat allele. Bellgrove and colleagues, who used a CPT–like task
  (the sustained attention to response task), found higher reaction time
  variability in children who were homozygous for the 10-repeat allele.
  However, in this study, the 2 groups did not differ in omission and
  commission errors.

Trypotphan hydroxylase 2 (TPH2)

  The TPH2 gene encodes the rate-limiting enzyme in the synthesis of
  serotonin in humans and was shown to be associated with completed
  suicide and major depression. Four studies have shown an
  association between multiple SNPs in this gene and ADHD.
  Recently, a significant association was observed between total errors
  of omission in the test of variables of attention and 2 SNPs
  (rs1386488, rs6582072). Similarly, a significant association was
  observed between rs1386488 and another SNP (rs1386497) and total
  reaction time scores as well as total reaction time variability
  scores. These intronic SNPs are part of 8 markers found to have strong
  linkage disequilibrium with each other and that compose a single
  haplotype block associated with ADHD in the tested sample. A second
  study tested IQ level and 4 SNPs previously reported to be associated
  with ADHD, but analyses were negative.

Sources:

Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies.
Oussama Kebir, Karim Tabbane, Sarojini Sengupta, Ridha Joober
J Psychiatry Neurosci. March 2009; 34(2): 88–101.

Molecular Genetics of Attention Deficit Hyperactivity Disorder
Stephen V. Faraone, Eric Mick
Psychiatr Clin North Am. 2010 March; 33(1): 159–180.

Meta-Analysis of Genome-Wide Linkage Scans of Attention Deficit Hyperactivity Disorder
Karin Zhou et. al.
Am J Med Genet B Neuropsychiatr Genet. 5th December 2008; 147B(8): 1392–1398.


Judgments of similarity between samples of writing

It sounds like you're talking about Latent Semantic Analysis. Here's their rundown of what it is.

  However, LSA as currently practiced has some additional limitations. It makes no use of word order, thus of syntactic relations or logic, or of morphology. Remarkably, it manages to extract correct reflections of passage and word meanings quite well without these aids, but it must still be suspected of incompleteness or likely error on some occasions.

It's used in a lot of automated grading programs, or systems designed to give a score to paper based on some criteria. However, because order doesn't matter, it makes syntactic and grammatical coherence much harder to measure, so quantifying 'style' might be a little hard, unless by 'style' you mean something like word choice, phrase choice, etc.

Here's a gscholar search. The first three should give a good overview.