What does 'Mean Diffusivity' tell me about the connectivity of cortical areas?

Short answer
The mean diffusivity (MD) in diffusion tensor imaging is a sensitive, yet a rather non-specific measure. Changes in MD tell you that water movement is altered, yet why and how will have to be answered through additional studies.

Background
Diffusion MRI relies on the fact that water diffuses better parallel to axons than across them in the brain. Hence, in white matter that consists mainly of bundles of parallel oriented axons, water primarily moves in one direction, i.e., parallel to the fibers therein. In contrast, in the brain’s gray matter and the extracellular space, water moves freely in many directions. By taking advantage of the differences in diffusion rates, the white matter can be imaged in the brain. This technique is used diffusion tensor imaging, or DTI. DTI has been used to study disruptions in brain structure caused by trauma and white matter diseases, such as multiple sclerosis (Chi, 2014).

Now, there are several outcome measures in DTI and one of them is the mean diffusivity (MD). MD describes the magnitude of water diffusion within brain tissue and can be used to examine differences in brain structural integrity. Differences in MD may reflect variations within the intra- and extracellular space, a reduction in neuropil (basically, gray matter), and/or global increases in CSF (Clark et al., 2011). For example, increased tissue water in edema will increase the MD, whereas cell proliferation (tumor) may decrease the MD. In complex diseases like multiple sclerosis (MS), brain regions may experience an unpredictable combination of demyelination, axon loss, gliosis, and inflammation, which could result in competing influences on the diffusion tensor (Alexander et al. (2007).

MD is a sensitive but rather non-specific measure that can be affected by any disease process that affects the barriers that restrict the motion of water, such as cell membranes. (Clark et al., 2011).

In your linked article (Hughes et al., 2012), the only thing they really say about the MD is

  MD increased in both thalamo-frontal and thalamo-parietal regions with increasing age [...]. These observed changes [in] white matter tracts occur in parallel with an age related decrease in frontal cortical volume and the volume of related thalamic regions.

Indeed, I think in itself the change in MD tells you only that something has changed and that the MD may be a predictor for aging in the thalamocortical system.

References
- Alexander et al., Neurotherapeutics (2007); 4(3): 316–29
- Chi, The Scientist (2014)
- Clark et al., J Psychiatr Res (2011); 45(7): 980–8
- Hughes et al., NeuroImage (2012); 63 (3): 1134-42


Why does being in a natural environment induce some kind of "peace" state while mecha/tech ones induce the opposite?

Maybe we should ask a vietnam vet if he feels less stress in nature than inside a building.

I think the reason we feel tense inside is because we've been conditioned to expect stressful situations to happen while inside, so we're on guard for it (ie tense).  Nothing bad has ever happened to us while sitting on a park bench listening to the birds chirp.  Now, if tigers start leaping out at us on a consistent basis while at the park, this feeling may change.  We might decide the sounds of clicking keyboards and tapping shoes to be more relaxing.

Another point to consider is that the sounds of birds chirping means "things are ok".  Bird have a high viewpoint compared to terrestrial animals and when birds are singing, there probably isn't a tiger stalking us.  Also, if you notice, birds sing after storms pass.  I know when I hear the birds singing, I can go back outside and get back to work... the storm is over.  Its possible this knowledge is instinctual.

The same could be said of crickets and frogs.  When you hear crickets and frogs, things are ok.  When the crickets and frogs suddenly stop, that when you grab the flashlight and see what's lurking in the woods.

An odd one is the sound of water.  If you're a prey animal, which humans would be in the wild, you'd have a large chance of being ambushed while getting a drink.  All predators gather around the watering hole and stalk victims.  So this raises the question... why are water sounds relaxing?  This is evidence against instinct.  Water sounds would be relaxing as a result of association rather than instinct.  When I take a drink of water, I feel better.  When I go fishing, I don't have to worry about anything but fishing.  Water has always been good to me, so when I hear it, I feel better.  Also, the sounds of water tends to drown-out other sounds.  That's why spies on tv tend to have their conversations near moving water.  There is something about the randomness of water sounds that won't allow pattern recognition in other sounds.  When we hear water, its hard to be disturbed by other sounds, therefore, easier to be at peace.


Is there a way that an infection could target a specific area of the brain?

There are many variation in terms of proteins or peptides across the cortex, as well as structurally (layers etc), and how it is connected to the rest of the body (axonal projections, blood vessels, etc) but basically all areas are constituted of the same basic building blocks. So most viruses will tend to affect some areas more, but I don't think an infection could ever be targeted that accurately to a specific area (let's say affect Broca's area and cause a very specific aphasia). For example rabies travels back to the brain from muscles, so it will reach the primary motor cortex first. But then it will diffuse from there. This is even more true for bacterial infections which as far as I know don't even target neurons specifically. Usually a bacterial infection will start somewhere else like an open wound, teeth or the ears. I don't think a bacteria could jump directly to the brain (I might be wrong). For example when a syphilitic infection reach the neurosyphilis stage, it has already propagated to most of the body. The neurosyphilis tends to affect frontal and parietal lobes first but that's far from an accurate targeting. I believe fungal infections are more similar to bacterial infections and don't tend to target neurons specifically.

This is not my area of expertise so if anyone with better knowledge cares to answer I would be interested as well.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679988/

https://en.wikipedia.org/wiki/Neurosyphilis


do monkeys imitate humans sometimes just for fun?

I can break this down into three questions.

(1) Do monkeys imitate? Do they ever imitate humans?

The answer to these questions is yes, though I don't know if that includes standing on two legs.

(2) Do they do it to communicate?

Well, it is difficult to define what communication and with whom we are interested in here, but monkeys (and humans) do seem to be able to recognise when they are are being imitated. So at least the potential for communication is there.

(3) Do they do it to have fun?

There is plenty of evidence that monkeys "play", and depending on one's definition we can infer that they are having fun. Some play involves imitation.

For example this study by Byrne (2005) is an interesting source for some of the above answers, and in particular the "social mirroring" type of imitation implies some communication and theory of mind. We should also be careful here to distinguish between monkeys and apes, some of these behaviours are disputed in different species.


It's a phenomenon called déjà rêvé, the French for "already dreamed":

If you've ever felt like you predicted something in a dream, you might have felt it wise to keep that feeling to yourself so that others don't think you're as out-there as an ancient oracle. Well, good news: you don't need to be so secretive about your psychic dreams. They're actually a well-documented phenomenon called déjà rêvé — but they don't actually mean you can see the future. [...]
According to a new study that looked back on the medical reports of epileptic patients from 1958 to 2015, déjà rêvé experiences are common after electric brain stimulation, a pretty standard treatment method for epileptic symptoms. It suggests that the "already dreamed" feeling is the result of something happening physiologically in the brain, and that in turn could point to a better understanding of how dreams work.  [...]
If you experience déjà rêvé, take comfort in knowing that it's totally normal — the feeling is just a harmless quirk of your brain.

And there's is actually a 2017 paper, on the occurrence in the general population; it looks like it happens to most peple at least some times:

Deja reve ('already dreamed') has been hypothesized as a cause for various forms of déjà experience. With deja reve one has the distinct impression that the uncanny familiarity one is sensing has come from a preceding dream, but one not usually remembered until the experience is taking place. In this exploratory investigation, 2,492 respondents filled out online questionnaires in which they were queried about the incidence of their deja reve experiences, about dream frequency, and about their attitudes to dreams. The Big Five personality factors were also measured using a separate, standardized questionnaire. Nearly 80% claimed to have had such experiences and the associated frequencies are presented. Age was negatively correlated with the incidence and there was little gender dependence. The results of the Big Five personality factors are also presented.

Studies of déjà rêvé aren't very numerous however. The "new study" mentioned in that first popsci article distinguishes déjà-rêvé from déjà vu (basically déjà-rêvé elicits some specific dream/memory content, not mere impression of having seen something before) and proposes a further sub-classification:

Déjà-rêvé appears to be different from déjà-vu—the two must not be confused. By construction, all déjà-rêvé episodes we collected had content, which is not the case for déjà-vu. Furthermore, déjà-vu and déjà-rêvé never involved the same bipolar contacts in the instances when both could be induced by EBS [electric brain stimulation] in the same patient. These results are critical since they support the idea that déjà-rêvé is a true phenomenon, different from déjà-vu.
Moreover, déjà-rêvé is a generic term for distinct entities: recollection of a specific and detailed dream similar to an episodic memory, reminiscence of a vague dream or elements of dream(s) which feels familiar, and finally experiences that resemble or feel like what happens during dreams. Explicit content with mental imagery referring to a previous dream exists in the first two types, but the exactness of the details and contextual elements vary. In the third type, the content of the experience is not at the foreground, but the subject has the feeling of a known sensation or a state of consciousness similar to night dreaming. Only the first two types should be called déjà-rêvé, while the last type should be referred to as “dreamy state”.

They also discuss why  déjà-rêvé is apparently not simply a hallucination, basically because of the association of the phenomenon with electrode placement in memory- and dream-related brain regions:

It may be disputed that we cannot be sure that déjà-rêvé (episodic-like or familiarity-like) are linked to true previous dreams. EBS could simply produce a random combination of visual and auditory elements, creating phantasmagoric and unrealistic experiences similar to dreams. However, EBS-inducing déjà-rêvé were all located in the temporal lobes, although extratemporal brain areas were commonly stimulated [4]. They were also exclusively induced by medial temporal lobe EBS in our database. Thus, like other subtypes of experiential phenomena, specific locations of EBS seem to correlate with déjà-rêvé subtypes. This suggests it is improbable the déjà-rêvé we reported here are pure hallucinations, otherwise patients would have reported similar phenomena after stimulation of other brain areas. Furthermore, the brain regions implicated in déjà-rêvé include structures involved in long-term memory (especially in episodic memory and familiarity processes) [27, 28, 29], in memory formation during sleep [29], in normal dreaming [30,31] and probably in dream recall [32].


Looking for text books comparing animal and human brain

I believe what your looking for is a book on Comparative Neuroanatomy the only text book I could find in the field was:
Comparative Vertebrate Neuroanatomy: Evolution and Adaptation but you will find a number of web pages via google.

Comparative Neuroanatomy


How can consumers  obtain an image and analysis of their own brain?

The easiest way to get an fMRI (and many other brain) scan is to volunteer to be a participant at your local university, hospital, or research center. They will let you keep a picture of your brain, provide some interesting information at de-briefing, and usually even give a bit of monetary compensation for your time. Since the research group has to have an MD on board in order to do these tests, they will also notify you if they detect something abnormal or dangerous in your scan. The only caveat is that the selection criteria for being a participant are usually a little bit more involved than in a standard psychological study. Thus, you might have to volunteer for a few studies before you are selected.

If you want further analysis, you might consider companies like this. There you can submit your brainscans after you've received them for further analysis.


Does knowing a word for an emotion cause a person to feel the emotion more frequently?

The answer would be no. To go along with the comments babies feel emotions however do not know words. As they grow adults help them organize their emotions for example a baby cries with frustration and anger because they may be hungry as you get older you have learned how to deal with that experience. As it is impossible to feel any emotion without having a thought first, emotions stem from what we are thinking which would be mostly concepts we don't think in random words. Therefore if we like to be happy we will think about things or do things that make us such. We are made to feel a wide range of emotions and they come and go. Knowing a word is not going to help someone know happiness better. Learning to control thoughts would be much more helpful. Just as a baby feels all emotions it does not yet understand them. What good would a huge vocabulary be if we could not put together concepts.


Does denying climate change work similar to believing the earth is flat?

There is serious work on this, despite it being a political minefield. You're probably looking for Lewandowsky, et al. (2015).
If you want to get some distance from the issues of the day (and associated name calling) and into the mechanisms that drive this sort of phenomenon in general you might get more joy out of something like Cook & Lewandowsky (2016).
That will bring you into stuff like Hahn, et al. (2018). That's not directly political at all, but I think the relevance to your question is pretty strong. This is one of those fields that is exploding thanks to ever-better desktop computing, there's a ton of stuff that hasn't been tried yet! Hope you have some fun with it.
References
Cook, J., & Lewandowsky, S. (2016). Rational irrationality: Modeling climate change belief polarization using Bayesian networks. Topics in cognitive science, 8(1), 160-179. doi: 10.1111/tops.12186
Hahn, U., Hansen, J. U., & Olsson, E. J. (2018). Truth tracking performance of social networks: how connectivity and clustering can make groups less competent. Synthese, 1-31. doi: 10.1007/s11229-018-01936-6
Lewandowsky, S., Gignac, G. E., & Oberauer, K. (2015). The robust relationship between conspiracism and denial of (climate) science. Psychological Science, 26(5), 667-670. doi: 10.1177/0956797614568432


This is quite a broad question, and the feasibility of any answer will depend on the time and resources available for performing a demonstration, assuming the objective isn't just to present a summary of existing research. A relatively simple principle to demonstrate in a risk management context would be the framing effect, whereby the emphasis on gain or loss in a given decision can affect people's preferences.
To demonstrate this quickly and easily, you could pass out a shuffled deck of small cards to your audience, with one of two versions of a question printed on each card. The question can present a single dilemma from two perspectives: one that frames a decision in terms of how much the respondent stands to gain with one of two choices, and another that frames it in terms of the cost of each choice. If half of the audience gets one version of the question, and the other half gets the other version of the question, you may be able to demonstrate a difference in the choices people make based on which version they receive with a couple polling questions. Wikipedia cites Tversky and Kahneman's (1981) example of a dilemma framed from gain and loss perspectives:

[Text from Tversky and Kahneman, 1981:] Imagine that the U.S. is preparing for the outbreak of an unusual Asian disease, which is expected to kill 600 people. Two alternative programs to combat the disease have been proposed. Assume that the exact scientific estimate of the consequences are as follows:
$$\begin{array}{c|c|c}{\rm Framing}&{\rm Treatment A}&{\rm Treatment B}\\\hline{\rm Positive}&\text{"Saves 200 lives"}&\text{"A 33% chance of saving all 600 people,}\\&&\text{66% possibility of saving no one."}\\\hline{\rm Negative}&\text{"400 people will die"}&\text{"A 33% chance that no people will die,}\\&&\text{66% probability that all 600 will die."}\end{array}$$ [Table from Wikipedia]

Other examples are available, and the principle is general enough that you could probably expect it to work with your own variations on the theme. This particular version produced a 72% preference for Treatment A in the positively framed version, and a 22% preference for Treatment A in the negatively framed version. Tversky and Kahneman also describe several examples with risk framed in terms of financial gain and loss, but they might require a different setup for demonstration. An experimental effect of this size ought to stand a decent chance of appearing even in a fairly small audience.
Reference
Tversky, A., & Kahneman, D. (1981). The framing of decisions and the psychology of choice. Science, 211(4481), 453–458. Retrieved from http://psych.hanover.edu/classes/cognition/papers/tversky81.pdf.


Is there any good evidence that sadness causes chest pain ("heart ache")?

There is a fairly recently recognized medical condition called stress-induced cardiomyopathy, associated with chest pain and physical damage to the left ventricle:

  Because this weakening can be triggered by emotional stress, such as
  the death of a loved one, a break-up, or constant anxiety, it is also
  known as broken-heart syndrome.

Although most patients recover within a few weeks, in some extreme cases, this condition is known to be fatal.  As this diagnosis is still fairly new, prevalence is not accurately known, but it might be quite common in break ups - see Koulouris et al (2010) for a review.

Psychological distress can be a causal factor in other heart conditions as well (eg, Carey et al 2014; Graff et al, 2016; Buckley et al, 2012) that may be associated with chest pain.  However, other than these indirect effects, test subjects can generally distinguish psychological pain from physical pain, so although people may report psychosomatic symptoms such as chest pain associated with romantic rejection, it is not expected to be an indicator.

Nonetheless, across cultures and in many different languages, the same terminology is used to describe both physical and psychological pain, suggesting a similarity in experience.

"Social pain" is the mental stress resulting from rejection, bereavement, heartache, exclusion, etc.  There are quite a few studies supporting a link between social pain and physical pain - see Eisenberger (2012) for a fairly recent review.  In the typical experimental paradigm, subjects who have recently experienced social pain are reminded of their experience, eliciting the social pain response, while being monitored using physiological and/or neurological measurement tools such as fMRI.

Such studies have demonstrated that social pain experience uses many of the same neurological mechanisms as physical pain.  For example, from Kross et al (2011):

  Here we demonstrate that when rejection is powerfully elicited—by
  having people who recently experienced an unwanted break-up view a
  photograph of their ex-partner as they think about being
  rejected—areas that support the sensory components of physical pain
  (secondary somatosensory cortex; dorsal posterior insula) become
  active.

Combined with similar results from lesion studies, pain sensitivity, and changes in dopamine and cortisol, this has led to the hypothesis that humans evolved a mechanism for social pain that recycles the physical pain system (Macdonald & Leary, 2005; Eisenberger & Lieberman, 2004), eg:

  It has been suggested that, in mammalian species, the
  social-attachment system borrowed the computations of the pain system
  to prevent the potentially harmful consequences of social separation.

Overlap between the neural mechanisms for physical and non-physical pain is not complete however, presumably accounting for the differences in reported experience.


Questionnaire regarding the motivation to be physically active

David Markland's website has several related questionnaires and scales that are available for research use. The Behavioural Regulation in Exercise Questionnaire seems like a good fit:

The Behavioural Regulation in Exercise Questionnaire (BREQ) measures different forms of motivation for exercise based on Deci and Ryan's (1985, 1991) continuum conception of extrinsic and intrinsic motivation.

There are several other related instruments also available on the same website:

The Exercise Motivations Inventory-2 (EMI-2) is a measure of participation motives or reasons for exercising. The Exercise Motives and Gains Inventory (EMGI) is a recent development that complements the EMI-2 to provide scales assessing perceived gains from exercise that correspond to the EMI-2 scales.
The Perceived Environmental Supportiveness Scale measures perceptions of the extent to which exercise professionals provide individuals with support for their psychological needs (i.e., autonomy support, structure and involvement).
The Exercise Causality Orientations Scale (ECOS) measures individual differences in the tendency to be autonomous, controlled or amotivated in exercise contexts and is derived from Deci and Ryan's Causality Orientations Theory.
The Locus of Causality for Exercise Scale is a short measure of the degree to which individuals feel self-determined with respect to exercise.


You may want to read Meaidi et al (2014). They obtained dream reports from congenitally blind, late blind, and matched sighted controls.
To quote the abstract, they found:

  All blind participants had fewer visual dream impressions
  compared to sighted control participants. In late blind participants, duration of blindness
  was negatively correlated with duration, clarity, and color content of
  visual dream impressions. Congenitally blind participants reported more auditory,
  tactile, gustatory, and olfactory dream components compared to sighted control
  participants. In contrast, late blind participants only reported more tactile
  dream impressions. Blind and sighted control participants did not differ with
  respect to emotional and thematic dream content. However, congenitally blind
  participants reported more aggressive interactions and more nightmares
  compared to the other two groups.

  Our data show that blindness considerably alters the
  sensory composition of dreams and that onset and duration of blindness
  plays an important role. The increased occurrence of nightmares in congenitally blind
  participants may be related to a higher number of threatening
  experiences in daily life in this group.

In summarising previous research they note that:

  previous studies seem to suggest that individuals who
  become blind after the age of 7 years retain visual imagery in their
  dreams, though congenitally blind or early blind (onset of
  blindness before the ages of 5–7 years) individuals do not.

They cite a number of previous studies that have looked at dreams of blind people that you may want to check out:

[5] Kerr NH. Dreaming, imagery and perception. In: Kryger MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine. Philadelphia, PA: W.B. Saunders Company; 2000. p. 482–90.
[6] Amadeo J, Gomez E. Eye movements, attention, and dreaming in subjects with life-long blindness. Can Psychiatry Assoc J 1966;11:501–7.
[7] Berger R, Olley P, Oswald I. The EEG, eye movements, and dreams of the blind. Quart J Exp Psychol 1962;14:183–6.
[8] Kerr NH, Foulkes D, Schmidt M. The structure of laboratory dream reports in blind and sighted subjects. J Nerv Ment Dis 1982;170:286–94.
[9] Hurovitz CS, Dunn S, Domhoff GW, Fiss H. The dreams of blind men and women: a replication and extension of previous findings. Dreaming 1999;9:183–93.
[10] Kirtley D. The psychology of blindness. Chicago, IL: Nelson-Hall; 1975.
[11] von Schumann H. Träume der blinden. Basel: S. Karger Co.; 1959.
[12] Sabo KT, Kirtley DD. Emotions in the dreams of the blind. Int J Rehabil Res    1980;3:382–5.
[13] Cason H. The nightmare dream. Psychol Monogr 1935;46:1–51.
[14] Kirtley D, Cannistraci K. Dreams of the visually handicapped: toward a   normative approach. Am Found Blind Res Bull 1973;27:111–33.
[15] Spielberger CD, Gorsuch RL, Lushene PR, Vagg PR, Jacobs AG. Manual for the state-trait anxiety inventory (Form-Y). 2nd ed. Palo Alto, CA: Consulting    Psychologists Press, Inc.; 1983.

References

Meaidi, A., Jennum, P., Ptito, M., & Kupers, R. (2014). The sensory construction of dreams and nightmare frequency in congenitally blind and late blind individuals. Sleep medicine, 15(5), 586-595. http://dx.doi.org/10.1016/j.sleep.2013.12.008


Does smoking counterbalance the effect of Belladonna?

Disclaimer: I do not work with receptor bindings very often.

First point binding sites...
Both Atropine and Nicotine bind to Cholinergic receptors. However receptor binding is not competitive as the rector sites for each neurotransmitter is different (NT): Atropine is a direct-antagonist of Muscarine binding with AChRm (muscarinic receptors) while nicotine is a direct agonist of AchRn (nicotinic receptors).

Atropine however does inhibit the action of nicotine in mediating ion currents on cholinergic receptors in the Central Nervous System (CNS). However this depends on the concentration of each NT in the neural system, low does of Atropine are enough to block high concentrations nicotine. So while a high concentration nicotine, say from an e-lite might be enough to save your life from Belladonna poisoning, I wouldn't personally go out of my way to test the theory! However the Nicotine from a cigarette probably wouldn't be a high enough dose to counter 1um of atropine. However say you did drink some belladonna because you have evil 'friends', but then you smoked a cigarette with enough nicotine to save your life. You then encounter another problem...half-life. The half-life of atropine is 2 hours, the half-life of nicotine is 1-2 hours! Do you want to risk that last hour if it takes two hours to see a medic or if you are transported back in time to medieval england!? Incidentally if you were poisoned with belladonna being transported back to medieval England would make sense. Your only option at this point, after the first hour, is to keep smoking (nicotine metabolites have 20 hour half-life, but there action is reduced), this is one of only a few situations that smoking may prolong your life! Although you will need some pretty potent tobacco to achieve this, better make sure you land in Tudor England instead.

Moral of the story...don't time travel! I'm looking at you 'doctor' with the blue box.

If you do believe you are in medieval England or the Roman empire please ask someone to call a Neurologist or a psychiatrist! If they say "what's a neurologist/psychiatrist?" you are completely sane, congratulations you have achieved time-travel.

Specifically information about competition between atropine and nicotine concentrations...

"At the holding potential of 80 mV, 1 mM atropine inhibits 1 mM acetylcholine- induced inward currents mediated by rat a2b2, a2b4, a3b2, a3b4, a4b2, a4b4, and a7 nicotinic receptors by 12–56%. Inward currents induced with a low agonist concentration are equally inhibited (a3b2, a3b4), less inhibited (a2b4, a7), or potentiated (a4b2, a4b4) by 1 mM atropine. Effects on the more sensitive 44 nicotinic receptors were investigated in detail by systematic variation of acetylcholine and atropine concentra- tions and of membrane potential. At high agonist concentration, atropine inhibits 44 nicotinic receptor-mediated ion current in a noncompetitive, voltage-dependent way with IC50 values of 655nM at80mVandof4.5M at 40mV. At low agonist concentration, 1 M atropine potentiates 44 nicotinic recep- tor-mediated ion current. This potentiating effect is surmounted by high concentrations of acetylcholine, indicating a competitive interaction of atropine with the nicotinic receptor, and potentiation is also reversed at high atropine concentrations...The apparent affinity of atropine for the agonist recognition sites of the a4b4 nicotinic acetylcholine receptor is estimated to be 29.9 mM." Zwart and Vijverberg (1997)


Math or Physics: Which is the more relevant background to enter Cognitive Sciences and Psychology?

I would go with Physics.

Physicists study the world using mathematics, while mathematicians study mathematics itself which is a construct that does not necessarily exist in the real world (Albert Einstein once said: "as far as the laws of mathematics refer to reality, they are not certain; and as far as they are certain, they do not refer to reality."). This means that physicists encounter the interface between theory and experimentations, just like cognitive researchers, while mathematicians do not.

I think this is the reason why there are many examples of models developed in the study of Physics being applied successfully in cognitive science (e.g The famous Hopfield model (1982); Spin-Glass, Amit et al (1985); Ornstein-Uhlenbeck, Heath (2000); Diffusion, Ratcliff et al (2004) ). Obviously, all of these examples use math heavily. But while a mathematics student would study them using a theoretical approach, a physics student would probably study them emphasizing their application.

(PS. My bachelor's degree is in Math, Physics, and Computer science, so I think I can say I'm unbiased here... At least I hope so)

References

Geometry and Experience, a lecture by Einstein A. English translation HTML
Hopfield, J. J. (1982). Neural networks and physical systems with emergent collective computational abilities. Proceedings of the national academy of sciences, 79(8), 2554-2558.
Amit, D. J., Gutfreund, H., & Sompolinsky, H. (1985). Spin-glass models of neural networks. Physical Review A, 32(2), 1007.
Heath, R. A. (2000). The Ornstein-Uhlenbeck model for decision time in cognitive tasks: An example of control of nonlinear network dynamics. Psychological Research, 63(2), 183-191.
Ratcliff, R., Gomez, P., & McKoon, G. (2004). A diffusion model account of the lexical decision task. Psychological review, 111(1), 159.


Leach's hypothesis is based upon case reports of prisoners of war subject to the most severe forms of incarceration and profound deprivation.  A minority of prisoners reportedly completely withdrew and ceased any form of goal directed behaviour (eating, drinking etc.).  Presumably, the prisoner's 'giving up' was in response to their self-evaluation that survival was impossible in the circumstances.
Leach, J. (2018). ‘Give-up-itis’ revisited: Neuropathology of extremis. Medical hypotheses, 120, 14-21. https://doi.org/10.1016/j.mehy.2018.08.009


What are the best known causes and treatments for apathy?

Main causes of Apathy

There are 2 main ways that Apathy can manifest itself, and that is either through a mental health condition, or a physical medical condition. (APA, 2013 p. 682) (IDC-10 Code: F07)

I will list some mental health causes and physical causes below, but the main way of dealing with the apathy would depend on the cause.

Treatment for apathy

The way to treat apathy would be to treat the root cause, where possible, through psychotherapy, psychiatric help and/or other agency support.

I emphasised root cause because where the initial cause found may be substance abuse for example, the substance abuse can be attributed to a different cause (the root cause) which could be a parent-child relationship problem or trauma.

Where apathy persists after treatment

If apathy remains after successful treatment of the root cause(s), then the problem will most likely lie with motivation.

You could look at the question on here about Theories of Human Motivation for information, or just look at various motivational courses, exercises and activities such as these activities.

Breakdown of Main Causes of Apathy

Mental health causes

This is not a full list, but includes,

Separation Axiety Disorder

  When separated from major attachment figures, children with separation anxiety disorder may exhibit social withdrawal, apathy, sadness, or difficulty concentrating on work or play.(APA, 2013 p. 192)

Major Depressive Disorder

  In major depressive disorder, the individual may avoid leaving
  home because of apathy, loss of energy, low self-esteem, and anhedonia. (APA, 2013 p. 221)

Neurocognitive Disorders (NCDs) such as Delirium

  Delirium is often associated with a disturbance in the sleep-wake cycle....The individual with delirium may exhibit emotional disturbances, such as anxiety, fear, depression, irritability, anger, euphoria, and apathy. (APA, 2013 p. 600)

Behavioral-Variant Major or Mild Frontotemporal NCD

  present with varying degrees of apathy or disinhibition. They may lose interest in socialization, selfcare, and personal responsibilities, or display socially inappropriate behaviors. (APA, 2013 p. 615)

Physical Problems Causing Mental Health Problems

This is not a full list, but includes,

Inhalant Intoxication
This can create

  Clinically significant problematic behavioral or psychological changes (e.g., belligerence, assaultiveness, apathy, impaired judgment) (APA, 2013 p. 538)

Opioid Intoxication
This can create

  Clinically significant problematic behavioral or psychological changes (e.g., initial euphoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment) that developed during, or shortly after, opioid use. (APA, 2013 p. 546)

Other toxic, metabolic, traumatic, neoplastic, or infectious disorders that impair brain function and cognition

  Numerous neurological and other medical conditions may produce the clinically significant behavioral or psychological changes (e.g., belligerence, assaultiveness, apathy, impaired judgment) that also characterize inhalant intoxication. (APA, 2013 p. 540)

Major or Mild NCD due to Traumatic Brain Injury

  may be accompanied by disturbances in emotional function
  (e.g., irritability, easy frustration, tension and anxiety, affective lability); personality changes (e.g., disinhibition, apathy, suspiciousness, aggression); physical disturbances (e.g., headache, fatigue, sleep disorders, vertigo or dizziness, tinnitus or hyperacusis, photosensitivity, anosmia, reduced tolerance to psychotropic medications); and, particularly in more severe TBI, neurological symptoms and signs (e.g., seizures, hemiparesis, visual disturbances, cranial nerve deficits) and evidence of orthopedic injuries. (APA, 2013 p. 625)

References

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Washington, DC: American Psychiatric Publishing.


After doing some searching I believe I have found the passage you are referring to.

The passage you gave is in a dissertation called The use of emotions in the implementation of various types of learning in a cognitive agent by Usef Faghihi of University of Québec.

From what I understand of it from skim reading, the passage you gave was about operations within a particular form of Artificial Intelligence, and the passage is on page 75.

Page 43 has your answer.

  Learning  Intelligent  Distribution  Agent  (LIDA)  (Figure  3.3)  is  a  hybrid  cognitive architecture,  developed  by  Stan  Franklin  and  his  colleagues  at  the  University  of Memphis  (Franklin  and  Patterson,  2006).  LIDA  is  IDA's  successor;  IDA  was  originally conceived  to  assign  new  billets  to  sailors.  In  the  American  Navy,  at  the  end  of  each sailor's  tour  of  duty,  he/she  is  assigned  a  new  billet  (task)  by  a  detailer.  IDA  performs the  detailer's  role.  It  communicates  with  sailors  via  e-mail  and  must  understand sailors'  requirements  and  preferences,  as  weil  as  respect  ail  constraints  of  the  Navy. To  reply  to  the  sailors,  it  has  to  communicate  with  different  databases  (Franklin  et  al., 2005,  Franklin  and  Patterson,  2006).

  LIDA's  architecture  is  partly  symbolic  and  partly  connectionist  and  is  equipped with  six  artificial  intelligence  software  technologies:  a  copycat  architecture,  a  sparse distributed  memory,  a  global  workspace,  a  schema  mechanism,  a  behaviour  net,  and a  sub-sumption  architecture.

  Franklin  called  LIDA  a  "conscious  agent"  for  its  fundamental  elements  and processes  rely  on  functional  consciousness  as  described  by  Baars  (Baars,  1997). LIDA  is  constructed  with  simple  agents  called  "codelets"  (which  reproduce  Baars' "simple  processors").  The  central  point  of  the  system  is  the  "access  consciousness", which  allows  all  resources  to  access  centrally  selected  information  that  is  "broadcast" to  unconscious  processes  (which  guides  the  agent  to  be  stimulated  only  with  the most  relevant  information).


Non coitus sexual activity and the brain

The first question is, what is normal human sexual behavior. The answer to this changes over time. For example, a hundred years ago masturbation was thought to cause physical degeneration and be a sin, today it is perceived as healthy, even recommended. Research shows that adolescent girls who masturbate have more and stronger orgasms as adults.

So, if anal sex is normal, then there should not be any basic difference in how the brain processes this from vaginal coitus. The difference between different normal sexual practices should be like that between different words that you hear (as compared to non-verbal sound, which should be processed differently). Maybe anal and oral sex where processed differently a hundred years ago or in different cultures. I don't know of any research into this, but maybe there is.

Paraphilias like fetishes, pedophilia, incest, voyeurism and other "deviant" sexual behavior have not been well researched. There are many psychodynamic and cognitive theories of paraphilias, but since you ask for the brain, I'll focus on biological theories here. The following is taken from the chapter on paraphilias in Davison & Neale, Abnormal Psychology.

Since most paraphiliacs are men, it has been theorized that androgen plays a role in the etiology of paraphilias. Research into hormonal differences between paraphiliacs and normal people have had ambiguous results.
Sadism and exhibitionism appear to be caused by malfunctions of the temporal lobe (Mason 1997; Murphy, 1997).
Life experiences (like childhood abuse) are seen as the most important factor in a complex net of causes.

Besides psychological therapies of paraphilias (that will obviously influence the brain), there are biological therapies:

castration: results were highly ambiguous, so this therapy has been largely abandoned
medroxyprogesterone acetate lowers the testosterone level in men, cyproterone acetate lowers the androgene level, both reduce sexual appetency: this works in many paraphiliacs, but when they stop taking the medication the symptoms return; also, the substances can cause infertility and diabetes

As you can see, that's not much, and only two articles deal with the difference in brains. There may be more in recent articles.

The sources for the temporal lobe malfunction:

Mason, F. L. (1997). Fetishism: Psychopathology and theoriy. In D. R. Laws & W. O'Donohue (Eds.), Sexual Deviance (pp. 75-91). New York: Guilford.

Murphy, W. D. (1997). Exhibitionism:  Psychopathology and theoriy. In D. R. Laws & W. O'Donohue (Eds.), Sexual Deviance (pp. 22-39). New York: Guilford.


Your question made me think of JAWS, a screen reader for the blind. I have worked with visually impaired people for a while and I have always wondered how on earth they can understand the speech produced by JAWS given the sheer high speech rates they apply on their gadgets.

Indeed, people with peripheral vision loss may learn to understand spoken language at rates of up to about 22 syllables per seconds, while the rate in normal listeners is about 8 syllables per sec (Dietrich et al., 2013). These numbers are based on speech understanding, as opposed to simply hearing it.

Hence in answer to your question

  Is speed listening detrimental to listening comprehension?

I would say no, at least not in above study, as speech understanding there was tested in a speech comprehension test, which is different than just hearing the speech.

Then your questions

  What occurs in the brain when a person speed listens?
  a. Why does the
  podcast feel "normal" at such fast speeds?
  b. Is there a
  fundamental/biological difference between those who can speed listen
  and those who can't, or is it a learned ability?

In case of blind people it has been shown that they activate their visual cortex when speed reading. This, because the deafferented area is recruited for other modalities, such as touch and hearing. This is probably not what you are after in your question though. In effect, I doubt gross effects on brain activity occurs in trained, normally sighted subjects and indeed a study where both sighted and blind individuals were trained on fast-speech understanding does not report on gross effects in the sighted group (Hertrich et al., 2006).

It feels normal because it is a learned ability; to continue with the example of these blind folks - they haven't been able to read for a long time and the only way they communicate through written materials is via screen readers. The spoken word is slower than reading so they crank up the speeds whenever possible, so they are slowly increasing their speech understanding skills.

References
- Dietrich et al., Front Hum Neurosci (2013); 7: 701
- Hertrich et al. Brain and Language (2006); 124(1): 9-21


Stiffing the tip as groups get larger ... like the prisoner's dilemma but ...?

Bystander Effect

The Bystander Effect could be your answer. The more people, the less personal responsibility.

Person gets assaulted and mugged on a crowded street in broad daylight, nobody calls the cops.
Software bugs slow company productivity almost to a halt, many employees, nobody reports the problem.

Tragedy of the Commons

The tragedy of the commons has been studied from many perspectives. You can use that commons dilemma link as a jumping off point to hopefully happen across something relevant. But I would start by looking at the psychology behind the bystander effect.


How does the brain generate answers to questions?

The task you're referring to is called the Verbal Fluency Test. In "A Biologically Constrained Model of Semantic Memory Search" by Kajic et al. wherein a neural model of this task is described.

The model assumes words were previously encoded with relations between them according to lived experience. Consequently, the words are represented as N-dimensional vectors with relations between vectors constructed into a neural associative memory. As each word is selected from the question, a memory saves the words retrieved and uses those retrieved words to inhibit the memory so it doesn't repeat itself. This control flow is shown in the diagram below:

As shown in the paper, this approach matches human data pretty well, but only if you use word-associations taken from Free Association Norms.

Open research questions include where the word encodings came from in the first place and how to make this model match human data better.


Has the inverted spectrum thought experiment ever been conducted (and if not, why)?

I don't think inverted prism goggles would be a satisfactory way to empirically test the thought experiment. A key axiom of the argument is that there are no physical changes to our brains or bodies; only the qualia have changed. In a goggles design, there would be a clear physical locus of the change (and we might reasonably call this part of your body for the duration of the experiment), so the shift in qualia would have a clear physical basis.


What does it mean to "accept my shortcomings"?

I suppose the word "accept" you hear comes from the acceptance and commitment therapy, or ACT. According to the link, the healthy attitudes towards the problem (e.g. obesity) are:

Accept your reactions and be present
Choose a valued direction
Take action

So to answer your question, it is about accepting your reactions, your emotions about the problem, not the problem itself. An obese person can be shame, guilt or embarrass about their obseity, and they want to avoid such emotions. This, according to my understanding about the approach, means that they want to avoid facing the truth that they are obese, and thus the action to change cannot be followed. By accepting such emotions, they can dissipate them.

Therefore, it's not about you want to change nothing, nor finding the problematic situation satisfactory, nor believing you don't have such problem, but about accepting the negative emotions when facing the reality.


Reduction of the hippocampus due to childhood neglect/abuse

In many studies scientists claim that the early exposure to stress can cause a hippocampal remodeling (or atrophy) (Andersen & Teicher, 2004). The atrophy is a disbalance in the brainpart were one part is bigger than the other. The decreased hippocampus is also associated with a decrease in dendritic branching and neurogenesis. Neurogenesis is the development and growth of neurons (in short) and these neurons are important for functioning.

In a study done by Teichera et al. (2003) they come with two explanations for the reduced volume of the hippocampus. One explanation is that the reduced hippocampus volume is associated with adolescence alcohol abuse due to the child abuse. The other explanation they have is that it is not the childhood abuse causing the reduced volume, but a risk factor for the persistence of Post Traumatic Stress Disorder in adulthood. So they are already born with a slightly decreased hippocampus volume, but this gets more when child abuse is involved.

Andersen, S. L. & Teicher, M. H. (2004). Delayed Effects of Early Stress on Hippocampal Development. Neuropsychopharmacology 29,1988–1993
Teichera, M. H., Andersena, S. L., Polcarib, A., Andersona, C. M., Navaltaa, C. P. & Kim, D. K. (2003). The neurobiological consequences of early stress and childhood
maltreatment. Neuroscience and Biobehavioral Reviews 27, 33-44


Is it possible to objectively measure the amount of pleasure a person is experiencing?

This is a very general answer to your question. And let me say upfront that I don't know about any measurement instruments for pleasure. However, I would like to emphasize that pleasure, just as about any psychological phenomenon, has to be considered a latent construct. What this means is that it cannot be measured directly, but only indirectly and imperfectly through a bunch of indicators. It is actually important to have more than one indicator in order to estimate how reliable the measurement is. Since you asked wether it is possible to measure pleasure or not, my answer is yes.

The question then becomes what the indicators are, that allow one to measure the amount of pleasure someone is experienceing. They should be derived from a theory about what pleasure is. In the reference that @GregMcNulty gives in the comments, for instance, the amount of pleasure is measured predominantly by activity in the prefrontal cortex. But it is also stated that "From a biological perspective, pleasure is not a unitary experience in the brain. It’s not just one region that is activated when we find pleasure in something or someone." That's speaking to the notion of having more than one indicator.

Whatever way you do it, though, you will have to come up with a good theory on what pleasure is and then find indicators. And with a construct as complex as pleasure, it is important to keep in mind that you will always have measurement error.


Are there researched approaches to learning a subject more quickly?

This question is pretty vague and broad, but the most researched techniques, according to a reasonably recent (and highly cited) review, Dunlosky et al. (2013):

It looks like distributive practice (spreading out activities over time, the opposite of cramming, I guess) and practice testing (i.e. trying to apply what you've learned) get the highest generalizability ranking. The techniques that get a moderate rating are somewhat related to these two (interleaved practice: alternating the types of activities involved), self-explanation (being aware of the steps during problem solving) and elaborative interrogation (somewhat related to the previous one: explaining [oneself] why some statements are true based on the previously learned concepts). Mnemonics, mental imagery, summarization, highlighting or re-reading were ranked low in overall utility.

But even for the high utility techniques some questions remain (that's why they're tagged with P-I for instance):

  For instance, self-explanation
  received a P-I rating for criterion tasks because the
  available evidence is positive on one dimension (generalizability
  across a range of criterion tasks) but is insufficient on
  another key dimension (whether the benefit of self-explanation
  generalizes across longer retention intervals). As another
  example, rereading received a Q-I rating for criterion tasks
  because evidence for the effectiveness of this technique over
  long retention intervals is qualified (i.e., under some learning
  conditions, it does not produce an effect for longer retention
  intervals), and insufficient evidence is available that is relevant
  to its effectiveness across different kinds of criterion
  tasks (e.g., rereading does boost performance on recall tasks,
  but little is known as to its benefits for comprehension).

You'll have to read the full for details as it's too much material to summarize here.

Also, I can't say if the findings still hold for special groups like ADHD.


What are proper EEG frequency bands and electrode placements for imagined speech?

A study by D’Zmura et al. (2009) in which two syllables were spoken in imagination showed that imagined speech information was present in EEG alpha, beta and theta bands. The beta band (13-18 Hz) proved most informative. The most informative electrodes were located mainly near the top of the head (vertex) where electromyographic artifacts had least influence.

They used various signal processing steps (standard low-pass filtering to remove 60 Hz line artifact, DC filtering, signal enveloping etc.) to clean up their signal. Please refer to the reference list for specific signal processing details.

References
 - D’Zmura et al. Lecture notes in computer science 2009;40-8. HCI International
 - Brigham & Kumar, iCBBE 2010


Is there a link between brain injuries (TBI) and PTSD?

It is reported that mild traumatic brain injury does not produce Post-Traumatic Stress Disorder however, according to this report in the American Journal of Psychiatry, severe TBI could possibly lead to PTSD in approximately 27% of cases.  In this study of 96 patients  (77 men and 19 women), after 6 months following hospital discharge for severe traumatic brain injury, 27% of them suffered PTSD.  Out of these patients:

19% reported having intrusive memories,
23% reported having nightmares,
31% reported having a sense of reliving the trauma,
65% reported avoidance of thoughts,
65% reported avoidance of places; and
73% had signs of hypervigilance.

However one point of note that the report detailed was that

  First, our patients were not selected consecutively, and their
  responses may not be representative of populations with severe
  traumatic brain injury. Second, we did not obtain neuropsychological
  information on each patient.

I must admit that when I was looking at the report, due to the high number reliving the trauma and avoiding certain places, I wondered whether the trauma leading to PTSD was actually the brain injury or if it was the traumatic effect of the event which led to the brain injury.

Another point of note is that it was also reported in a committee hearing in the U. S. House of Representatives, that people with TBI are more likely to develop PTSD than those who have not incurred a brain injury

Personally, from looking at these reports, I think the jury may be still out on this one.


Are emotions a function of muscle contractions? If so, how does the map look like?

Your brain mentally represents afferent bodily input as affect, or feelings of pleasantness/unpleasantness and arousal (Craig, 2002).  In certain theories (e.g., Barrett, 2017), your emotions are cognitive interpretations (conceptualizations) of your affect in a context.

In general, there is very weak evidence that discrete emotions correspond to specific and reliable bodily responses (for the most up-to-date meta-analysis, see Siegel et al., in press).

There is also indeterminate evidence for specific and reliable correspondences with facial movements.  This has not been studied well enough to be known, although there is compelling evidence to suggest that there are no specific/reliable links on average (see Hillel Aviezer's work).

In general, emotion research is converging on the view that emotional events are highly variable, both within and across emotion categories, as well as within and across individuals and cultures. We see this variability in neural activity, physiology, behavior, hormones, vocalizations, facial movements, and so on.  From this perspective, there are no unique emotion signatures.


Have there been any scientific experiments attempting to communicate with one's unconscious mind?

In order to find such studies, it's a good idea to start off with mapping out what kind of situations would be relevant - that is, in what cases would it even be possible to communicate with someone's unconsciousnes?
Then you need to define what kind of communication you are interested in.
Here are some ways to find some kind of unconscious communication: Sleepwalkers, hypnosis(highly controversial), vegetative states and the like, subliminal messages, facial expressions, etc.
As such, the short answer to your question is "yes". The long answer is that your question is too wide.

Here's an article on using unconscious communication as a way of identifying narcissism:

  In this paper I suggest that analytical material implicitly carries in it a message proceeding from the unconscious and which is transmitted through representations. The message is expressed only when the object is recognized as such by the subject. In the narcissistic situation the unconscious message is not emitted.
  http://europepmc.org/abstract/MED/3667086

An article on communicating with patients suffering from trauma:

  The interface among trauma, dissociation, and regression is discussed in the context of unconscious communication as a transferential enactment of unsymbolized experience.The view is offered that for certain patients in particular, past experience is not so much unconscious as “frozen in time” and that a key element of the psychoanalytic relationship is bridging dissociated aspects of self through the creation of a dyadic experiential field that is both “inside” and “outside.”
  http://www.tandfonline.com/doi/abs/10.1080/10481889109538911?journalCode=hpsd20#.VIAkl8mZGkU

Research on facial expressions:

  Studies reveal that when people are exposed to emotional facial expressions, they spontaneously react with distinct facial electromyographic (EMG) reactions in emotion-relevant facial muscles. These reactions reflect, in part, a tendency to mimic the facial stimuli. We investigated whether corresponding facial reactions can be elicited when people are unconsciously exposed to happy and angry facial expressions. Through use of the backward-masking technique, the subjects were prevented from consciously perceiving 30-ms exposures of happy, neutral, and angry target faces, which immediately were followed and masked by neutral faces. Despite the fact that exposure to happy and angry faces was unconscious, the subjects reacted with distinct facial muscle reactions that corresponded to the happy and angry stimulus faces. Our results show that both positive and negative emotional reactions can be unconsciously evoked, and particularly that important aspects of emotional face-to-face communication can occur on an unconscious level.
  http://pss.sagepub.com/content/11/1/86.short


Cognitive bias with trial and error problem solving

This sort of experience is probably better termed a heuristic rather than a bias.  The two can be related in some cases (as heuristics can cause bias when the underlying model does not fit the real situation).

From the Wikipedia page linked above, a heuristic is:

  any approach to problem solving or self-discovery that employs a practical method that is not guaranteed to be optimal, perfect or rational, but which is nevertheless sufficient for reaching an immediate, short-term goal

Choosing to manipulate the easiest variables to manipulate first is an example this. It is practical, but may not be optimal. Since there is a low cost to manipulating the easiest variables, you might save some time and effort if one of those manipulations does happen to work, even if it was improbable. Not only do you avoid trying to more complex solutions, but you also avoid expending the mental effort of determining which one to invest in trying.

A well-known and often-lamented example of this sort of heuristic is in tech support decision trees that often start with steps like "Is the power on?" and "Have you tried turning it on and off again?" These steps seem a bit silly, and often have nothing to do with the symptoms of the problem, but if they happen to work it saves the support representative a lot of further time and effort investigating the problem.

Of course, this heuristic will fail if you manipulate a lot of "easy" variables - in that case, the sum time to try all the easy steps might be more effort than it would have taken to use some mental effort in the first place.


Is there any scientific data showing one can learn while sleeping?

I don't think that it is possible to learn new facts while sleeping, but it is certainly possible to reactivate certain memories during sleep and thereby affect the probability of those memories being retained.

In one study, participants learned a visuospatial task while smelling an odour. They were better at remembering how to perform the task if they were subsequently exposed to the same odour during sleep.

  Reactivating Memories during Sleep by Odors: Odor Specificity and
  Associated Changes in Sleep Oscillations, Julia S. Rihm,  Susanne
  Diekelmann,  Jan Born and  Björn Rasch
  https://www.mitpressjournals.org/doi/abs/10.1162/jocn_a_

In another study, participants had to learn spatial locations for some objects and a sound associated with each object. The sounds associated with some of these objects were played back to them during sleep. Upon awakening, they were better at recalling the locations of objects whose sounds they had heard during sleep.

  Strengthening Individual Memories by Reactivating Them During Sleep,
  John D. Rudoy, Joel L. Voss, Carmen E. Westerberg, Ken A. Paller
  https://science.sciencemag.org/content/326/5956/1079

In another study, participants remembered melodies better if they later heard those melodies during sleep.

  Cued memory reactivation during sleep influences skill learning James
  W Antony, Eric W Gobel, Justin K O'Hare,  Paul J Reber& Ken A Paller
  https://www.nature.com/articles/nn.3152


The computational level is about available information and in-principle what can be derived from that information. For catching a ball, this would be, for example, an analysis of what information is available to a fielder using a particular perceptual device, and what possible inferences could be drawn from that information. From the flux of light projected on a stationary 2D retina, is it possible to derive where the ball will be when? What if the 2D retina can move in response to the light, then is it possible? What if there are two eyes (i.e., stereo vision)? Your description of the procedure for catching a ball assumes that the information used by procedure is sufficient, but does not explicitly analyze and prove it, so your description is probably not best thought of as the computational level.

The algorithmic level is about the particular representation and process for computing an inference and making a response. There are usually many different ways to compute an answer. For example, adding two numbers can be done with Roman numerals and a difficult process, or with binary numerals using a power-of-2 place system and a simple process. Your description of a procedure for catching the ball seems closest to the algorithmic level, but the description would have to specify more details to be a fully fleshed-out algorithm.

The implementational level is about "hardware". How do the optical tracts of the brain encode and process the signal, and how does the body implement the motions requested by the brain? Your description of a process for catching the ball does not rely upon or mention these details, so is probably not best thought of as the implementational level.

(At least, that's my take on it. I think that the levels were intended as a useful framework for organizing and thinking about theories and how they interconnect. Marr suggested --if I recall correctly-- that it was valuable to do a computational analysis before diving into algorithmic particulars. But discussants sometimes devolve into heated philosophical debates about the "correct" interpretation of this or that. I hope this answer does not generate too much heat.)


What form might Jungian archetypes take in the brain?

As you mentioned in your question, Jung was less than perfectly consistent in his definition of archetype throughout his career. This ambiguity reflects the continuing debate about semantic representation in the brain.

His early work stressed the emergence of archetypes as fundamental dichotomies of self experience- whose Enantiodromaic character was the origin of their emergence in the psyche. Thoughts are either expressed or not expressed, whence the self is divided into Persona and Anima; thoughts (at least if one takes Jung at his word in his characterisation of thought as Libido) provide desire or fear, whence Ego and Shadow. This presents a potential picture of Jungian archetypes in the brain as primarily distributed phenomena-a set of pairwise partitions of the conscious brain.

His later writings, however, while still shewing their enantiodromia in their dialectical function, are more liberal concerning their origin. Concerning the Senex archetype for example; is a thought either that of a young or old man? -I would doubt it. The archetypes of these later writings are much more amenable to so-called 'sparse' representation.

Sparse representation is the (to borrow a term!) enatiodromaic opposite of distributed, in which small populations of neurons, or even single neurons can code for a given semantic character. Under assumptions of sparse representation, hypothetical 'Grandmother cells' could code for whole semantic classes, and so archetypes themselves.

Evidence for sparse representation has been found implicating the Medial Temporal Lobe in representing semantic classes across sensory modalities in single neurons (Quiroga  et al., 2005). This is however hotly contested, and experimental limitations abound (there's a nice microcosm of the debate at the wiki page for Grandmother Cell, which also features a potted summary of the linked experiment).

References

Quiroga RQ, Reddy L, Kreiman G, Koch C, Fried I. (2005) Invariant visual representation by single neurons in the human brain. Nature 435, 1102-1107. http://www.nature.com/nature/journal/v435/n7045/full/nature03687.html


What is the difference between behaviorism and cognitivism?

Short answer:  Behaviorism treats the human brain/mind like a black box whose internal processes cannot be known.  As such, behaviorists claim that it only makes sense to study the association between a given stimulus and the behavioral output it produces.

Cognitivists, on the other hand, examine internal mental processes (attention, executive control, predictive coding, etc) and are just as interested in what behavior a stimulus elicits as how it elicits it.


What are the effects of negative self image on cognition and brain function?

Some information that partly answers your questions.

There have been some studies based on these questions, a significant article related to this type of study is Self-esteem, locus of control, hippocampal volume, and cortisol
regulation in young and old adulthood (Pruessner et al. 2005).

This article makes the link between self image and the individual's 'locus of control', they found that:

  our results clearly demonstrate that self-esteem and
  locus of control are significantly linked to the volume of the
  hippocampus in healthy young and elderly subjects. Further, we
  found evidence that these two factors are also related to the acute
  and chronic regulation of the major stress hormone in humans,
  cortisol.

(Note: the authors of the article acknowledge that their data does not allow them to make firm conclusions).

Cortisol affects, amongst other things, memory, learning and concentration.  A specific study about this is in the article "Cortisol differentially affects memory in young and elderly men." (Wolf et al. 2001) and "Impaired memory retrieval correlates with individual differences in cortisol response but not autonomic response" (Buchanan et al. 2006).  From the second article/study:

  [This study] suggest that individual differences in cortisol reactivity affect memory retrieval performance, and help to explain the differential effects of stress on memory.

I will say that this is not the complete picture, but the link between self image and cortisol levels seem to be a major factor about how self image affects cognitive abilities such as learning, memory etc.


If you create an (free) account at: https://db.humanconnectome.org , I believe you should be able to find connectomes through here.
It seems like a bit of a hassle to download the files though (and they only seem to come in very large packs).
Another perhaps easier method, if you just want some simple and easily accessible files to work with right away is:
https://neurodata.io/project/connectomes/
which you can read more about in this article.
There you can just download some graphs directly in .graphml format. Then you can use them in e.g. python with networkx. For example, to construct a graph object from a graphml file, plotting it and getting the adjacency matrix, you'd simply write:
import networkx as nx

G = nx.read_graphml("/rhesus_brain_2.graphml")
M = nx.adjacency_matrix(G)
nx.draw(G, node_size = 10, width = 0.1, arrowsize = 2, pos = nx.spring_layout(G))

This is just a simple example, but I hope it helps. It sounded as if that was perhaps just what you needed: something raw and simple to get you started; and those datasets are sometimes the hardest to find.
(I am myself on the lookout for more specific types of connectomes; see my question here. If you happen to come across anything more, I'd be really grateful if you'd let me know.)


Unable to run AxoGraph v1.7.6 on macOS 10.15 Catalina

Response from AxoGraph Support

I received an answer from John of AxoGraph suggesting to follow the steps outlined in this tutorial to set up a virtual machine (VM) on my computer with an earlier version of macOS using the Parallels software ($79.99/year).

He also discouraged using VirtualBox, the free VM manager, as "there's more work involved, and it’s not so smoothly integrated with Catalina." In his reply, John also promised "to finish the new completely re-written 64-bit version of AxoGraph," which "is not far from completion," first releasing a new data-acquisition-only version, subsequently followed by an update with data analysis features. It sounded like all of this would take at least several months, though.

My Solution

After some digging, setting up a virtual machine (VM) with an earlier version of macOS indeed did seem to be the best option for me at this point. What I was after, however, was a free solution - and eventually, I managed to get a Mojave VM to work on my Catalina using VirtualBox. Getting through the whole process was a patchwork of several different sources (mostly following this tutorial and its comments), so I decided to re-write the detailed steps I took below (some steps may be adjustable but I used these specific settings with success):

1. Download macOS Mojave Installer:

Go to this link: https://support.apple.com/en-us/HT210190
Click on Get macOS Mojave in step 4, and open in App Store.
Click on GET - that will open the updater, which will download the installer (if you already have Catalina installed, the "update" will stall after the download automatically)
Find it in your Applications folder as Install macOS Mojave.app

2. Create an ISO installation media using Terminal:

Create a temporary disk image from the install file & make a bootable installer using Terminal:

hdiutil create -o /tmp/Mojave.cdr -size 7000m -layout SPUD -fs HFS+J

Attach that file, with Terminal command:

hdiutil attach /tmp/Mojave.cdr.dmg -noverify -mountpoint /Volumes/install_build

Build it, with command:

sudo /Applications/Install\ macOS\ Mojave.app/Contents/Resources/createinstallmedia --volume /Volumes/install_build

Move it to your mac’s Desktop:

mv /tmp/Mojave.cdr.dmg ~/Desktop/InstallSystem.dmg

Unmount the file:

hdiutil detach /Volumes/Install\ macOS\ Mojave

Convert it to ISO:

hdiutil convert ~/Desktop/InstallSystem.dmg -format UDTO -o ~/Desktop/Mojave.iso

Rename it to remove the CDR extension:

mv ~/Desktop/Mojave.iso.cdr ~/Desktop/Mojave.iso

Exit Terminal via Terminal command:

exit

3. Create a new virtual machine (VM) in VirtualBox:

Download Oracle's VM VirtualBox Manager (https://www.virtualbox.org) & install it on your Mac
Open VirtualBox
Click on New
Select Type: Mac OS X and Version: Mac OS X (64-bit)
Memory size: 8192 MB (at least 3 GB)
Hard disk: Create a virtual hard disk now
Hard disk file type: VDI
Storage on physical hard disk: Fixed size
File location and size: 32.00 GB

4. Tweak the VM before installation:

With your newly created VM selected in VirtualBox, go to Settings → Storage:

Click on Empty → Remove [square with a red cross at the bottom]
Click on Controller: SATA → Add optical drive [CD with a green plus sign] → Add → Find the .iso file you created and click Choose

Settings → Display: Video Memory - at least 128 MB
Settings → System: Processor(s) - at least 2

5. Install the macOS on your VM:

With your VM selected in VirtualBox, click Start
Wait until the Language selection appears; select your preferred language and continue
macOS Utilities: Disk Utility → Continue
Select VBOX HARDDISK Media → click on Erase in the toolbar
Name the drive as you wish and keep the default selections: Format: Mac OS Extended (Journaled) and Scheme: GUID Partition Map; click Erase
Quit Disk Utility when done
Select Install macOS, Continue, and Agree to the license
Select the hard drive you just erased and Install
MacOS starts installing; wait and be patient! (It took about half an hour for me. The VM may restart at least once in the process.)
Go through the MacOS setup (select your Country, keyboard, etc.)

It is recommended that you do not log in with your Apple ID at this time and click Set up later instead
I also did not allow Location Services, nor data collection from Apple
Once installed, you can eject the installation disc from within the VM
It also might be a good idea to go to System Preferences... → Software Update → Advanced... → uncheck Check for updates

6. Install the latest version of AxoGraph on your VM:

Open Safari within your VM
Go to https://axograph.com/download
Click on Mac OS X 10.4 and up*
Install AxoGraph

  Voilà!

  Now you can run AxoGraph, as well as other 32-bit applications, on your MacOS Catalina!

You should be able to turn off the VM from within, as you usually would shut down your Mac
It is booted again by selecting your VM in VirtualBox and clicking Start


What is acquaintance and how can it help a person?

Short answer
Acquaintance at the start of a new study can help to build a network of friends. Friends can offer mental support in difficult times, they can stimulate you in your studies, you can discuss homework with them and you can just spend your free time with them to (re-)charge before the new semester. Friends are not only fun to have, they are a necessity for a social animal species like Homo sapiens. On the the other hand, friends can also lure you into skipping classes, not doing your homework and focus on the 'wrong' things in life such as doing drugs. It goes both ways.

Background
Social networks can impact our health, happiness, wealth, emotions, and even physical well-being. College students spend a lot of time with their friends. One estimate suggests that the average college student spends only 15 hours a week in class but 86 hours a week with his or her friends.

Freshmen no longer have their parents constantly guiding them or checking in. That’s one reason why supportive friends are an important part of one’s social life during this period. These friends actually turn into students’ families during college. During this period, friends are everything; they are often the closest bonds students will ever make and sometimes the entire support system (source: Weisman).

It has been shown that different people generate different kind of networks. McCabe showed, in a relatively small sample of students, that there are roughly three types (McCabe, 2016):

"Tight-knitters" have a single cluster of close friends.
"Compartmentalizers" have a bunch of unrelated clusters of friends (e.g. a group of friends at university, the other at a sports club).
"Samplers" have one-on-one friendships with individuals who didn't necessarily know one another.

Now, why is this important? Every tight-knitter reporting to have friends that provided academic motivation and support eventually graduated. Among the ones who said they lacked this support and their friends distracted them from schoolwork, only half managed to graduate within six years.

Compartmentalizers and samplers both risked to be 'torn' between social contacts groups and could experience social isolation (source: NPR).

Reference
- McGabe, Connecting in College. How friendship networks matter for academic and social success. University Chicago Press (2016)


Elaboration likelihood model: would attractiveness be a peripheral or central route?

Unless the advertisement is actually advertising the person's attractiveness directly, this should be a peripheral issue. Consider Wikipedia's description of the central route:

  Central-route processes involve scrutiny of persuasive communication (e.g., a speech or an advertisement) to determine the arguments' merits. Under these conditions, a person's cognitive response to the message determines its persuasive outcome. If they evaluate a message as reliable, well-constructed and convincing, it may be received favorably even if it contrasts with the receiver’s original position on the message.

Thus the only circumstance in which a person's attractiveness should be a central route is one in which the advertisement's argument is about the person's attractiveness per se...I'm not sure I can even think of a good example of such an advertisement. Even beauty product advertisements (which are about the product, not the person) routinely appeal through peripheral routes by using supermodels with immaculately styled hair, wearing much more makeup than the object of the advertisement – not to mention expensive clothes and other fashion accessories – in idealized, studio-lighted environments. If anything, factors like these obscure the real efficacy of the given beauty product, because most observers will just be overwhelmed by the model's beauty and by the desire to emulate it, regardless of how little the product in question has to do with it. Again, see Wikipedia on the peripheral route:

  Peripheral-route processes do not involve elaboration of the message through cognitive processing of an argument's merits. They rely on a message's environmental characteristics: the perceived credibility of the source, message presentation quality, the source's attractiveness or a catchy slogan, and is frequently used when the argument is weak or lacks evidence. The peripheral route is a mental shortcut which accepts (or rejects) a message based on external cues, rather than thought. It is used when the audience is unable to process the message due to the message's complexity or the audience's immaturity. The commonest influences are rewards such as food, sex or money, which create rapid changes in mind and action. Celebrity status, likability, humor and expertise are other factors governing the peripheral process. Appearance can gain an individual's attention; while it can create interest in a topic, it will not effect strong change. The goal of the peripheral process is to create change which can be weak (or temporary) compared with the strong, lasting change of the central route.


Are sensations of turbulence after flights proprioceptive hallucinations?

As there is no sensory input from reality which could cause these sensations, are they technically proprioceptive hallucinations?

Not really, although I think it wouldn't be completely inaccurate to think of them that way. A hallucination has no basis in reality (e.g. auditory hallucinations); what you're describing has a physical basis in reality. It is based on a physical disconnect between your previous reality (a mildly turbulent flight of significant hours duration) and the removal of such stimuli (your disembarkation) while your sensitized vestibulo-occular mechanism continues to function as if you were on board.  First noticed on ships, but expanded to flights and other stimuli, it's been called landsickness [1] when of short duration, and Mal de Debarquement if it lasts longer much longer than 1-2 days.[2]

To understand this, a bit of basic physiology is in order. First, there are three semicircular canals located in little pockets of bone called the inner ear, one on each side. The three canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).[3]  Because the connections are excitatory, increased firing from a canal afferent leads to contralateral movement of the eyes (which is how spinning ice skaters can keep track of / focus on where they are visually). Normally all this occurs without our notice.

The latency of action of the rotational vestibulo-ocular reflex (r-VOR) is 7-15 milliseconds, which is the time required for the eyes to respond in an equal, but opposite, manner to the motion of the head. This time is remarkably fast compared with the latency for visually mediated eye movements, which is longer than 75 milliseconds.[4]

What happens is that with excitation (say, spinning in one plane), the cilia of the hair cells (see @Chuck Sherrington's diagram here) are displaced, and remain displaced as long as one is spinning with the same velocity and direction. Once the spinning suddenly stops, the cilia proceed to move to their default position, tricking the VOR into moving the eyes in the opposite direction repeatedly until the cilia come to a complete stop.[3] You can observe this phenomenon by looking into the person's eyes immediately after they stop spinning (make sure they are safe from falling.) Once things settle down in the inner ear, the vertigo (perception of spinning) stops shortly thereafter as well.

Flying or being on a ship causes multiple VOR inputs and adjustments (by our brains) to this movement. As the flight continues and you experience choppy motions, your VOR "adjusts" to these frequent shifts and you don't feel them as much. When you disembark, however, there is an adjustment period to go through; we are still receiving mixed signals until we are completely sensitized to the new "normal". It is of varying intensity and duration, and can appear suddenly (maybe on head movement or rapid eye movement) and be persistent or transient.

If you can relax, you can enjoy these tricks the brain is playing on your mind, and marvel at how well we are adaptable. I had my first truly noticeable episodes of this phenomenon while traveling on the vaporetti in Venice for a few days. If you feel it's worse that what I describe, I would start my search with sea legs, landsickness, and MDDS (though the latter is highly unlikely).

[1] landsickness
[2] Mal de Debarquement Syndrome
[3] Anatomy and Physiology of the Vestibular System Gizzi, et. al.
[4] Vestibuloocular Reflex Testing - Amin, et. al.
[5] Baloh and Honrubia's Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Kevin Kerber, MD


This is an interesting question, which may or may not garner more than one useful answer. There will be a small element of opinion in the answer which must be very limited for an answer to be a good one for this site, and therefore I will try and formulate my answer with as little opinion as possible.
Your question on whether psychology is an art or work depends much on the differences within your definitions of each.  I will base the difference on the first statement you made:

Some are born psychologists and they have passion towards it unlike some people who just work to earn money on it.

In other words, it is an art if you only need to have a passion for psychology, rather than it being work because you just need to be able to analyse effectively.
This then leads on to the question of whether you can analyse human psychology effectively if you don't have a passion for it or a high interest in it.
@sfxedit cited an interesting study (Gollwitzer & Bargh, 2018), which points out that:

some lay individuals can reliably judge established social psychological phenomena without any experience in social psychology.

with social psychological phenomena meaning

predicting how human beings in general feel, think, and behave in social contexts and situations

You can predict how human beings in general feel, think, and behave in social contexts and situations without actually empathising with the people in question.  A problem with that if you work directly with clients is the fact that clients can detect whether the therapist is empathic or not (Xiao et al. 2015) so can those who are only providing therapy for the money going to be that effective?
That is open to opinion, so I will leave that for you to decide, however, the founder of Person Centered Therapy (Carl Rogers) believes that one of the core conditions for effective therapy is empathy. Plus, from my own personal experience as a client facing therapist, in order for a strong rapport to be built, you need to be able to empathise with your client's situation.

We believe that the most useful definition of empathy would emphasize the ability to detect accurately the emotional information being transmitted by another person. This entity has been termed empathic accuracy by others (see Ickes et al., 1990, for a brief review)   — Levenson & Ruef 1992

So my answer to your question depends on the kind of psychologist you are wanting to be.  If you are a Research Psychologist who is not client facing, then all you need is to be able to analyse the data effectively. Whether the effectiveness will depend on your passion for the subject or not is open to opinion, as is whether the work of a non-client-facing Research Psychologist is work or just an art.
If you are a Clinical Psychologist, or other Clinical Therapist who is client facing, you need to be able to empathise.  For this reason, and the fact that empathising in harrowing client situations can be emotionally draining, it is work in the definition and context put forward. There is however, an art involved in effectively dealing with the emotions internalised through empathy.
So in summary, Psychology and related fields can be seen as an art or hard work.  The decision on that definition is yours.
References
Gollwitzer, A., & Bargh, J. A. (2018). Social psychological skill and its correlates. Social Psychology, 49(2), 88. doi: 10.1027/1864-9335/a000332
Ickes, W., Stinson, L., Bissonnette, V., & Garcia, S. (1990). Naturalistic social cognition: Empathic accuracy in mixed-sex dyads. Journal of personality and social psychology, 59(4), 730. doi: 10.1037/0022-3514.59.4.730
Levenson, R. W., & Ruef, A. M. (1992). Empathy: a physiological substrate. Journal of personality and social psychology, 63(2), 234. doi: 10.1037/0022-3514.63.2.234
Xiao, B., Imel, Z. E., Georgiou, P. G., Atkins, D. C., & Narayanan, S. S. (2015). " Rate My Therapist": Automated Detection of Empathy in Drug and Alcohol Counseling via Speech and Language Processing. PloS one, 10(12), e0143055. doi: 10.1371/journal.pone.0143055


Giovanni Sala was concerned by this same question, so he did a meta-analysis of 24 studies in "Beyond the 64 Squares: Does Chess Instruction Enhance Children’s Academic and Cognitive Skills? A Meta-Analysis" and found that there was still a lot of doubt in the results. Specifically, in all the papers, he never found the control group was reasonable. Of course children who played chess rather than doing nothing performed better at various tasks, as can be seen in "Enhancing Creativity in Children by Imparting Chess Training". But what about regular instruction or playing other games?

Consequently, he followed his meta-analysis up with a randomized plucebo controlled trial focused in mathematical cognitive skills in "Does Chess Instruction Enhance Mathematical Ability in Children? A Three-Group Design to Control for Placebo Effects" and found that the effect of chess, when compared to actual mathematics instruction (Control), was meaningless as shown in the tables below. However, it did surpass the game Go in transfer learning outcomes.

As he concluded at his talk at the CogSci 2016 conference (where all the papers I cited come from) which I attended, far transfer-learning is really hard. To improve skills in certain domains, it is better to study that domain than to hope a marginally related activity will grant insight. To make studying that domain easier, new materials need to be developed rather than searching for new related activities.

Note: This area is still under active research, as discussed in "The Effects of Chess Instruction on Pupils' Cognitive and Academic Skills: State of the Art and Theoretical Challenges"