I just came across the same section you referenced above in Kahneman's fascinating book. Like you, I was curious how to actually perform it. You are absolutely right, Add-1 (and Add-3 for that matter) seems relatively trivial if you can see the digits while performing the arithmetic.

So I searched for the author's actual study and found a more detailed description of it summarized in another book of his, Attention and Effort (1973). See page 20, which reveals that the experiment was actually harder than described in Thinking, Fast and Slow because the digits were spoken one at time (as opposed to visually seeing all 4 together), thus each digit had to remembered for several seconds until the arithmetic was required.

  The primary task involved the transformation of a digit string: the subject heard a series of four digits (e.g., 3916) at a rate of one digit/second, and he was instructed to pause for a second, then to respond with a transform of that series (4027), adding 1 to each digit of the original set.

I believe a more accurate way to recreate the original experiment with index cards would be to write only 1 digit on each card.


A plausible candidate for that is interneurons subnetwork.

Lets say some entity may be green and cold. It also may be yellow and hot, but not cold and hot. So, we can say that for this type of entities there are 2 independant variables, describing its state. If right now the variable 'color' is set to the value "red" - that means the negation of all other values of that variable (not green, not blue, ... infinity of them). The question is only how to store the construct "variable" in the neural tissue?

One can gather all possible values of the variable and wire them all with dense lateral inhibition circuit. Activation of one neuron inside that ensemble will kill the activations of the others.

And look - we've got a good instrument for detection of mistakes in our model of the world now! If the network has wired some entities' representations by lateral inhibition - it means that the network has stated a hypothesis that these entities (in some context) are just different values of the same driving factor. If in the next moment strong feedforward signal has activated 2 principal neurons inside the circle - the hypothesis was not correct. The network has detected "paradox".

This explanation is plausible because of 3 facts:

There is a famous pinwheel pattern in the visual cortex:

The figure above depicts reconstructed map of different values of the variable "spatial orienation" in the visual cortex. They are arranged in non-random order.

Superimposition of inhibitory neurons onto that map shows that one interneuron can work with different "values" of spatial orienation.

There is a scientific proposition, that underlaying algorithm is the same in all parts of the cortex (i.e. differences are more likely in hyperparameters, than in essence). We dont know the algorythm (and I dont pretend that my aswer is correct), but scientists do not see dramatical differences in the microbiology of tissue in different cortex regions. So.. if some "variable - value" relation appears in the most good studied part of the cortex (primary one) than we, probably, have some ground to expect such tendensies in other parts.

source of pictures - Neurobiology: Turning a corner in vision research,1999,Nature


Are there "awareness" related mirror neurons or processes in the brain that get activated by awareness?

Mirror neurons are actually quite a contentious area in cogsci. The debate is most certainly not settled as to what role they play, and whether they even exist, in humans. In short though, my argument would be that there are no specific awareness related mirror neurons in the brain because mirror neurons themselves are awareness. Again, this is an extremely contentious issue in cogsci, and there is no one answer widely accepted at the moment -- I'll just try to explain and justify my thoughts.

It's important in anything that's being discussed to have a working definition of the matter at hand. Personally, I would disagree with your definition of naming them "emotion infectors", instead opting to assume that mirror neurons are very specialised cells allowing for the reenactment of sensory-motor information (Rizzolatti et al.).

Gibson gave us a pretty neat applied example of this in the form of affordances. These are action possibilities possessed by items, but perceived by an agent (see Norman's review for a neat explanation as to why this changed) -- in short, a rock doesn't want us to throw it, but a human might want to throw a rock. Additionally, a mouse might see the same rock and, being unable to lift it and throw it, decide instead to hide behind it from predators. At the same time, a savvy cat may suss out what's actually going on... What does this mean for mirror neurons? Specifically that this network of cells allow us to understand actions, and create new ones, by parasitizing upon motoric and sensory systems. Essentially, our experience of the world is bound by our bodily constraints.

So what does this mean for our experience of abstract concepts? Domains like love, time, depression, and even awareness aren't physical entities, but metaphysical ones. These are conceptually understood (Lakoff). Time flies, we are down in the dumps when depressed and -- the most cheesy of all -- love hurts. Time doesn't actually fly, we don't shrink when we're depressed and love doesn't actually physically hurt, but we scaffold what is concrete (i.e. sensory-motor information) to the abstract in order to understand it (Veale & Keane).

So, I don't believe that a mirror neuron network would exist for a process like awareness, because the mirror neuron network itself is awareness. It's what provides us with a specific ability to understand the environment, to understand actions and, perhaps most importantly, understand ourselves.


What does the literature suggest about the optimal strategy for quickly memorizing various types of content?

The first and most obvious answer would be that repetition cements new information into memory. The second technique is that an event that involves a strong emotion will be more easily remembered then an event where little or no emotion is felt. If you are learning foreign languages, you could practice sentences or paragraphs in a dramatic way, like learning the lines of a play. This could be done verbally or non-verbally, but verbally would be preferred for the auditory feedback. Flashcards, mind maps, and similar tools would help with visual feedback, helpful as this article suggests. Handwriting and typing would help with tactile feedback.


Spike-timing-dependent plasticity versus Homeostatic plasticity

Homoestatic plasticity can be used with spike-dependent plasticity given they have two different goals and aren't applied uniformly across neural population. To support this argument, I'm going to use a computation model taken from "Simultaneous unsupervised and supervised learning of cognitive functions in biologically plausible spiking neural networks" by Bekolay et al.

In the model, an ensemble of neurons with input and output weights [1], is trying to learn how to change their output weights to approximate a given function. PES (STDP rule) changes the output weights of the neurons to approximate. The BCM (homeostatic rule) increases the sparsity of the input weights. When used together as hPES, they allow for less parameter sensitivity of the ensemble and a lower overall spiking rate, allowing the group of neurons to conserve energy.

[1] For a visual explanation of what this means, see this blog post.


Why isn't psychotherapy more direct with patients?

One therapeutic issue with being confrontational – a problem that does not arise unless one is direct in a bad way – is reactance. I've described this issue in a separate answer to a question you commented on five days ago, "How to change someone's beliefs?" Telling someone who doesn't believe he or she has a problem that s/he does have a problem implies that s/he should change. If the person is inclined to deny the premise of this implied suggestion, the person may also resent the suggestion itself. Thus resistance and defensiveness may arise in reaction to the suggestion that s/he is not free to simply continue behaving "normally" without further consequence.

Another potential problem with directness in a bad way  may arise by carelessly assigning diagnoses. Diagnosis of psychopathology is a very difficult process; despite my PhD, I am not qualified to perform it. Even those who are qualified (officially, at least) do not perform it with satisfactory accuracy by my (high) standards. Part of the problem is directness in the context of careless inattention or inexperience (see also schema modification). I.e., directness is not the real problem here, but it provides a channel for these problems to cause other problems via communication of misinformation, especially in the context of professional authority. Non- psychologists tend to defer to the authority of psychologists even on topics beyond the expertise of both parties. This makes restraint on the part of the more authoritative party very important. Failure to withhold first impressions and unexamined opinions about possible diagnoses can result in psychologically harmful labeling. This can impose anxiety-exacerbating pathological characteristics on the identity of the person so labeled, especially if s/he does not possess the wherewithal to question these labels or is predisposed toward anxiety or self-loathing, as often apply to psychotherapy patients.

In the opposite contexts of psychotherapy that is not pejorative or otherwise invalidating (e.g., Rogerian and other humanistic modalities) practiced by therapists with appropriate restraint and excellent breadth of experience, directness is probably desirable and helpful. Methods such as motivational interviewing benefit from their direct focus on clients' own ambivalence toward positive changes, which is often the root problem, especially with ego-syntonic disorders. Conversely, ego-dystonic disorders may benefit from treatment via methods such as cognitive behavioral therapy that directly address problematic, derogatory aspects of clients' identities, such as the inflexible conviction: "Something is wrong with me." Thus directness itself is not the problem, but more a moderator of the consequentiality of a therapist's choice of approach to the problem a client presents. If the approach chosen is bad, harm may be reduced by self-restraint. If the approach is good, benefit may be enhanced by directness.


Psychological research on memorability of passwords?

It looks like there is some empirical evidence that passphrases are easier to remember than either random passwords (not surprising) or user-selected short passwords after standard advice to use mix of upper and lower and avoid words.

http://homepages.cs.ncl.ac.uk/jeff.yan/#exp

Thanks Jeff for the pointer in a comment (same Jeff?).

  J. Yan, A. Blackwell, R. Anderson and A. Grant. The memorability and
  security of passwords -- some empirical results. University of
  Cambridge, Computer Laboratory Technical Report No. 500, 2000. (see
  also Hungarian translation). PDF

  J. Yan, A. Blackwell, R. Anderson and A. Grant. Password Memorability
  and Security: Empirical Results. IEEE Security & Privacy, Vol. 2 No.
  5, 2004. PDF

the above is reprinted as:

  J. Yan, A. Blackwell, R. Anderson and A. Grant. The Memorability and
  Security of Passwords. Refereed book chapter in Security and
  Usability: Designing Secure Systems that People Can Use (ed. by Lorrie
  Cranor and Simson Garfinkel), OReilly & Associates, USA, 2005.


How can one find out if he/she is brainwashed?

As Schroedinger's Cat pointed out, there's no clear dividing line between "brainwashing" and the normal processes of growing up in or assimilating into a culture or social group. Even in the case of deliberate, forced procedures, it can be unclear -- for example, the US military has recruits do drills and engage in synchronized practices that we know to affect thoughts, feelings, and beliefs, but most people wouldn't call that brainwashing. However, you could look into military training practices, as well as techniques used by abusive cults, and see if you've been subjected to those at any point in your life. That might answer your question.

Another way would be to think about the criteria you would use to describe a thoroughly un-brainwashed person, and work from there. For example, do you believe that you should be able to cite a preponderance of evidence for all of your beliefs? That you should have a clear and volitional explanation for your life choices? You can then work toward those goals, questioning or changing your beliefs as necessary. Be aware that hardly anyone really meets these criteria! We all absorb cultural values and prejudices, use unconscious heuristics to make decisions, and make choices that we rationalize later. But you could certainly work on moving in a more rationalist direction if you want to.


Pupillometry: how long needs the pupil to respond towards an cognitive stimuli?

What are you trying to do?  If you're trying to leverage pupil-dilation data from an eye-tracker, there are ways to deconvolute the timeseries if you can make a strong inference as to exactly when the stimulus of interest took place.

I think you'll find everything you're looking for here.


How is the g-factor of intelligence calculated?

PCA or EFA: A standard approach to calculating a g factor would be to use principal components analysis (PCA) or exploratory factor analysis (EFA). Basically, you administer a broad battery of cognitive ability measures. Then you use these tests as variables in a PCA or EFA. This will partition the variance in the tests into a set of uncorrelated factors. The first factor will be the factor that explains the most variance in the tests. It is this first factor that represents "g". Typically, each test will "load" (or correlate) with this first factor, some tests more than others. The first factor will capture something that is common across most or all of the tests. I.e., it is g, for general factor, that measures cognitive ability.

An empirical finding is that almost all tests of specific cognitive abilities correlate with the general factor. And typically, the loadings are fairly substantial. I.e., the first factor is quite substantial relative to second and subsequent factors.

Confirmatory factor analysis: It seems that what you present is a confirmatory factor analysis. This is a variant on exploratory factor analysis. Basically, you specify which observed variables load on latent factors and all other possible loadings are constrained to zero. More specifically, this is a higher-order confirmatory factor analysis (CFA). It is higher-order because, there are two-levels of latent factors. I.e., tests load on domain-specific latent factors (e.g., reasoning, spatial ability), and these domain specific latent factors load on g.

The CFA estimation procedures will find the parameter estimates that best model the data (i.e., the covariance/correlation structure of the tests).

So in this case, we see that all the tests load fairly well on their domains (i.e., > .70) and all the domains load on g (> .65), although reasoning and spatial ability load a little stronger.

In general, multivariate statistics training in psychology (typically presented at postgraduate level and sometimes latter undergraduate-level) will cover these statistical techniques. Here's Bill Revelle's notes that cover some psyhometric theory: http://www.personality-project.org/r/book/

Wouldn't this imply that all of the factors are multicollinear and make it difficult to distinguish which factors are most significant?
That's why researchers often focus more on g (i.e., the general factor). But yes, you are in a sense correct. Of course, you can still do multiple regression and such with correlated predictors; you can then look at things like semi-partial correlations to look at the unique prediction of any one domain.


Is there a cognitive bias for ascribing agency to inanimate objects?

Fortunately, some psychologists have looked into it, and in accordance to your observations, people do tend to attribute intentional agency to inanimate objects.

In the seminal work by Heider and Simmel (1944), participants were shown shapes of a triangle and disc moving around a two-dimentional landscape. They were not moving in random directions, but in ways that convinced the participants they were acting, fighting, playing or helping each other. When objects move in a purposeful manner, and not just fall to the ground aimlessly, we naturally tend to think they have intentions, belonging to the kind of beings with some kind of intelligence. See also Barrett and Johnson (2003): The Role of Control in Attributing Intentional Agency to Inanimate Objects.

Further more, this tendency is used by the camp of the skeptics, like Dan Dennet or Steven Pinker, to explain why people recognize many events around them as the actions of of gods or super-natural beings. By coincidence, they see some random event or movement, which has no obvious or natural explanation. The witness of such event looks for the agent behind it, and when one can't be found, it is attributed to a hidden or unseen intentional being. The way from there to gods, deities and religion, these thinkers claim, is very short. See Dennett's BREAKING THE SPELL.


Sexuality is thought to be mostly fixed (and certainly does not respond to active interventions to change it), but sometimes self-descriptions shift. It's unclear to what extent these shifts are changes in sexuality itself versus changes in how people identify. More broadly speaking, people aren't always good at describing their own wants/desires/feelings, and social and cultural factors can have a strong influence. Individuals may have experiences that make them rethink how they see themselves, or they may be more or less comfortable expressing a view that is outside perceived norms at different times.
Savin-Williams et al 2012 studied a group of young adults longitudinally and compared self-reported sexual orientation during two study waves, one when participants were 18-24 and later when they were 24-34.
Out of 5204 men who reported being "100% heterosexual" in the first wave, the vast majority, 5064, said the same in the second wave. 105 said "mostly heterosexual", 11 said "bisexual", 24 said "homosexual". Other categories were somewhat more fluid, as was sexuality among women, and you can see the whole study linked below.

Savin-Williams, R. C., Joyner, K., & Rieger, G. (2012). Prevalence and stability of self-reported sexual orientation identity during young adulthood. Archives of sexual behavior, 41(1), 103-110.


Why is positive semi definiteness a sufficient condition for Lyapunov stability of the Hopfield networks?

The fact that it's a Lyapunov function means that
$$
\frac{dL}{dt} = \frac{\partial L}{\partial x} \cdot \frac{dx}{dt} \leq 0
$$
If $I-W$ is positive semidefinite, $L$ is bounded from below by $-\frac{1}{2} b^T (I-W)^{-1} b $.
This means that the network will end up in a minimum of $L$ and cannot keep moving for ever.


What's the feeling where you feel weird in places where people in movies get stabbed etc

What you are describing seems to be a form of mirror touch synesthesia

  Mirror-touch synesthesia is a condition which causes individuals to experience the same sensation (such as touch) that another person feels. For example, if someone with this condition were to observe someone touching their cheek, they would feel the same sensation on their own cheek. Synesthesia, in general, is described as a condition in which a stimulus causes an individual to experience an additional sensation. Synesthesia is usually a developmental condition, however recent research has shown that mirror touch synesthesia can be acquired after sensory loss following amputation.


How many sparring partners should I choose for the most effective motivation in the gym?

The Ringelmann effect may be useful to you in this question; he found that "the addition of co-workers in a rope-pulling task leads to a linear decrement in the individual group member's average performance."  It has been examined experimentally here, and was found to occur with the addition of second and third group members, but adding members beyond that didn't have a significant effect.  There was a second experiment that tried to control for the possibility of intermember coordination, but it found the same thing.

(Of course, this leaves out entirely the possibility of differing group dynamics across groups of the same size but with different members. It also does not speak to individual differences--that some people may do better with a larger group, or with varied activity partners, while others do better with smaller groups or more consistent activity partners.)

Alan G Ingham, George Levinger, James Graves, Vaughn Peckham
The Ringelmann effect: Studies of group size and group performance
Journal of Experimental Social Psychology, Volume 10, Issue 4, July 1974, Pages 371–384


Can we really motivate ourselves "on-demand"?

There is not much possibility to talk yourself into being motivated. However, personal narratives can help us redirect our motivations or manage them more productively. To take this more abstractly, consider a person who just ate a large meal. If they are not hungry, could they talk themselves into being hungry? (Rarely.) However, if a person is craving a certain type of food, they could notice that and consciously decide to redirect that interest into a different type of food, and then that intention might lead to actual behavior. This could also apply to longer-term goals, such as pursuing more education; but that process is only possible to the extent that other, existing motivations are borrowed to a new target. See https://en.wikipedia.org/wiki/Self-determination_theory for a popular theory of overall social motivations.

Motivation is not just subconscious, to the extent that we can have sensations around desire and goal states, e.g., be aware of urges and drives. All cognition includes subconscious processes: absolutely.

Popular psychology is wildly profitable but often quite unrelated to the latest empirical science. The incentive is to be convincing and be shared, not to be accurate. 'The Secret' is a good example: super popular and entirely inconsistent with physics. Finally, the note "...nobody can claim anything" is a bit vague.


Is Paul's Churchland claim about qualia supported by science?

Read further down to

  The neural basis of qualia

  V.S. Ramachandran and Edward Hubbard of the Center for Brain and Cognition at UCSD argue that Mary might do one of three things upon seeing a red apple for the first time:

  Mary says she sees nothing but gray.
  She has the "Wow!" response from subjectively experiencing the color for the first time.
  She experiences a form of blindsight for color, in which she reports seeing no difference between a red apple and an apple painted gray, but when asked to point to the red apple, she correctly does.

  They explain further: "Which of these three possible outcomes will actually occur? We believe we've learned the answer from a colorblind synesthete subject. Much like the theoretical Mary, our colorblind synesthete volunteer cannot see certain hues, because of deficient color receptors. However, when he looks at numbers, his synesthesia enables him to experience colors in his mind that he has never seen in the real world. He calls these "Martian colors." The fact that color cells (and corresponding colors) can activate in his brain helps us answer the philosophical question: we suggest that the same thing will happen to Mary."[21]

So it is possible to see in your mind colors you've never seen in reality, due to defective receptors. But it's possible that synesthesia in this subject caused some pathways to form that do not exist in someone who never experienced any color even even due to "fake" inputs like synesthesia.

One fairly recent (2012) fMRI study on a late-blind synaesthete found that

  The colour area hOC4v was engaged when the synaesthetic experience included colour. These results confirm the continued recruitment of visual colour cortex in this late-blind synaesthetes.

So it's technologically possible to determine/confirm when color "perception" in the brain is occurring in the blind. All it would take now is a subject for whom the order of events is reversed (born blind, but acquired/induced synesthesia.) The last paper notes however that.

  It is known that differences in the functional
  neuroanatomy of sighted and early-blind subjects reflect predominantly early recruitment of visual cortical areas for
  tactile [...] and auditory stimulation [...], and during
  verbal [...], and memory processing
  [...]. However, in late-blind individuals, visual cortical areas seem to retain some aspects of their
  original specificity. For instance, tactile perception of motion and faces activates visual cortical areas previously involved in
  analysis of equivalent visual stimuli [...]. And in a late blind synaesthete (the subject of the
  present report), both striate and extrastriate visual areas appeared to be engaged in the synaesthetic perception of coloured
  and spatially located concurrents [...].

So it's not a foregone conclusion that the early- or congenitally-blind could still/even experience synaesthetic color.

One 2018 study (Dell'Erba et al.) on the subjective experiences of a congenitally-blind man on psychedelic drugs reported that these include "synesthetic hallucinations", but of the tactile kind, and the complete absence of visual hallucinations, in line with their (previously reported) absence from the congenitally blind in general.

A Harlow-type experiment in monkeys (for the development of color vision in a black-and-white environment) might barely clear ethics boards nowadays. However, monkeys with natural [partial] color blindness can get the "full version" though gene therapy, suggesting that at least the color machinery in the brain, if developed for two colors/sensors, can quickly accommodate three thereafter. This result however (besides the coolness of gene therapy) isn't terribly surprising on a phenomenological level, given the reports of synesthesic "martian colors" in the color blind humans. (More interestingly, giving mice three-colored vision doesn't work as well.)

Much more interesting for our discussion is achromatopsia and its (genetic) treatments:

  Achromatopsia is a rare (1 in 30,000 to 80,000) congenital visual condition characterized by diminished or absent cone photoreceptor function. Patients have severely reduced visual acuity (~20/200), nystagmus and photophobia. Causative autosomal recessive mutations affect genes of the cone phototransduction cascade, CNGA3, CNGB3, GNAT2, PDE6H, PDE6C, [...] or the transcription factor ATF6. A subset of patients have unidentified causative mutations. Patients typically show complete cone function loss, as shown by absent cone-isolating electroretinogram (ERG) recordings. An incomplete phenotype occurs more rarely, but is not clearly correlated to the underlying mutation. Achromatopsia affects all three classes of photoreceptor and hence, by definition, relates to genes that are expressed in all cone subtypes, as listed above. Conversely, blue monochromatism, tritanopia, and red-green color blindness (deuteranopia and protanopia) are caused by mutations in genes specific to certain subtypes of cone photoreceptors; an important difference to achromatopsia. [...]

  A well reported achromatopsia population lived on the South Pacific island of Pingelap. A genetic bottleneck following Typhoon Lengkeki in 1775 created a founder effect and over 10 percent of the island population had complete achromatopsia. The story is notably recorded in The Island of the Colorblind by the neurologist and author, Oliver Sacks. [...]

  phase I clinical trials to treat achromatopsia using an AAV vector to deliver CNGA3 have already started in Germany (NCT02610582), CNGA3 in the USA and Israel (NCT02935517), CNGB3 in the USA (NCT02599922), and CNGB3 in the UK (NCT03001310) [...]

These are in the wake of partially successful animal knockout models & treatments thereof.

  Carvalho et al. (2011) explored the therapeutic age window for gene therapy in achromatopsia. A mouse model caused by a premature stop codon was rescued with human CNGB3 transgene packaged in an AAV8 capsid. The use of a cone arrestin promoter fragment resulted in universal expression in all cone subpopulations, an alternative solution to the use of the ubiquitous CBA promoter. The subretinal vector rescued retinal function, as tested by ERG, at a range of ages, but again there were poor visual responses in mice treated at later ages. This confirmed that there is an optimal therapeutic window at a younger age. The limited benefit at later ages may be a result of slow retinal degeneration in this model or amblyopia. Cone outer segment abnormalities have also been noted in achromatopsia animal models and it has been shown that regenerating the outer segments with intravitreal ciliary neurotrophic factor just before achromatopsia gene therapy may improve the responses significantly in older Cngb3 deficient mice.

The treatments were also successful for serendipitous "models" found in some sheep (age of the animals is not discussed in this latter context, alas):

  Two serendipitous discoveries of day blindness in unrelated Awassi sheep flocks in Israel yielded two new large-animal models of Cnga3 achromatopsia. Both models—a premature stop codon and a missense mutation—were rescued using the same human PR2.1-CNGA3 vector described by Komaromy et al. (2010). As expected, photopic ERG was restored. Treated animals were also able to use the restored cone function to navigate a maze in photopic conditions. A mouse Cnga3 transgene also provided a similar rescue effect.

The authors of this review generally conclude/speculate that

  The implications for human achromatopsia gene therapy are that the treatment will most likely need to be applied in early childhood to be maximally effective. [...]

  The [four human] trials are designed to initially test the safety profile in adult patients, but three of the trials plan to include patients as young as 6 years in later groups. By comparing older and younger patients, the trials will examine differences in integrated functional cone rescue between age groups. If the pattern observed in the animal trials holds true, there may be a difference in benefit due to patient age at time of treatment. Such a difference may arise from reorganization of cortical pathways or foveal hypoplasia.

  In the one other therapeutic trial registered for achromatopsia (ClinicalTrials.gov number, NCT01648452), six CNGB3 achromatopsia patients received intraocular implants that released Ciliary Neurotrophic Factor (CNTF). CNTF provides neuroprotection to rod and cone photoreceptors in degenerative retinal disease. Concurrent treatment with intravitreal CNTF in a canine model of CNGB3 achromatopsia potentiated gene therapy rescue. CNTF improved ERG rescue in older animals, overcoming a notable inability of gene therapy alone to benefit most dogs over 1 year of age. Limited evidence suggested that CNTF pre-treatment de-differentiated the cone photoreceptors by elongating the outer segments to facilitate CNGA3/B3 tetrameric protein assembly. As mentioned above, in the CNTF only trial, no functional improvement in cone function occurred. There are no current plans to include CNTF pre-treatment in any of the registered human gene therapy trials. This discussion may be reignited if the early trials show difficulty in rescuing cone function in older patients.

So the aforementioned (ongoing as of mid-2017) human trials should have interesting things to say about human color vision development in the absence of all three color "sensors"...


Do antipsychotics have a delayed onset of action similar to (monoamine) antidepressants?

There seem to be multiple studies generally pointing to a delay of clinical antipsychotic action of these drugs, typically between a week and two weeks (e.g.., Zedkova et al (2011) and Mousavi et al. (2013)). However, there is evidence that antipsychotics may start working after a day, or even within a few hours after starting the meds. See for an interesting review Agid et al. (2006).

From reading these papers my understanding is that a lot of it depends on where the researcher puts the threshold of clinical effectiveness and which outcome measure is used to define that effectiveness.

References
- Agid et al., J Psychiatry Neurosci (2006); 31(2): 93–100
- Mousavi et al., J Res Pharm Pract (2013); 2(4): 138–44
- Zedkova et al., Neuro Endocrinol Lett (2011); 32(5): 667-70


Do gating mechanisms in the neocortex have individual degrees for all gated connections?

A paper just came out last week in Neuron demonstrating dendrite-specific gating:
http://www.cell.com/neuron/fulltext/S0896-6273(16)00054-4?elsca1=etoc&elsca2=email&elsca3=0896-6273_20160302_89_5_&elsca4=Cell%20Press
Structured Dendritic Inhibition Supports Branch-Selective Integration in CA1 Pyramidal Cells
Erik B. Bloss, Mark S. Cembrowski, Bill Karsh, Jennifer Colonell, Richard D. Fetter, Nelson Spruston
DOI: http://dx.doi.org/10.1016/j.neuron.2016.01.029


What are the IQ correlations between relatives?

Recent studies on this topic deal with more detailed questions, that are analysed using structural equation models (Deary et al., 2006). A main goal has been the identification of specific genes. No single genes have been found until today and Sternberg (2012) also points out that the concept of heritability itself is indirect and maybe inappropriate if measured as ratio of genetic variation, because of neglection of cultural factors.

But yes, there has been a meta-analysis since Bouchard and McGue: Daniels et al. (1997) argue for maternal womb effects, that explain "20% of covariance between twins and 5% between siblings". E. g. the IQ correlation for monozygotic twins being raised together is reported as r=.85. Correlations for dizygotic twins raised together are reported as from r=.46 to .60, siblings IQ values correlate from .44 to .46, depending on the statistical model used. In regard to correlations, the findings seem very comparable to Bouchard and McGue's.

And of course, occasionally there have been studies on this fundamental topic, e.g Van Leeuwen (2008), Pujol et al. (2007).

Literature

Daniels, M., Devlin, B., & Roeder, K. (1997). The heritability of IQ. In Nature (Bd. 388, S. 468–471). LONDON: MACMILLAN MAGAZINES LTD. doi:10.1038/41319
Nichols, R. C. (1965). The national merit twin study. Methods and goals in human behavior genetic, 231-244.
Van Leeuwen, M., van den Berg, S. M., & Boomsma, D. I. (2008). A twin-family study of general IQ. In Learning and Individual Differences (Bd. 18, S. 76–88). AMSTERDAM: Elsevier Inc. doi:10.1016/j.lindif.2007.04.006
David Gallardo Pujol, Uwe Kramp, Carlos García-Forero, Albert Maydeu-Olivares, und Antonio Andrés-Pueyo. (2007). IQ heritability estimation: Analyzing genetically-informative datawith structural equation models. In Psicothema. Universidad de Oviedo.
Wahlsten, D. (1994). The intelligence of heritability. Canadian Psychology/Psychologie canadienne, 35(3), 244.
Sternberg, R. J. (2012). Intelligence. Wiley Interdisciplinary Reviews: Cognitive Science, 3(5), 501-511.


Why does injury cause brief unconsciousness?

Loss of consciousness is usually caused by a lack of oxygen to the brain - in the case of injury it could be directly cause by the injury or it may be because they are shocked or scared - this is called vasovagal syncope. Basically, severe emotional stress leads to a burst of activity in particular nerves that lead to reduced heart rate and dilation of vessels throughout the body, reducing blood pressure suddenly. The effect is temporarily reduced blood flow to the brain, which causes temporary loss of consciousness.

Wiki


Is there a field of research based around music and emotion in the brain?

Well it depends what you mean by "field of study", but yes there is significant Cognitive Science research on Music and emotional arousal and/or brain activity. In particular Cognitive Neuroscience is most relevant to actually mapping brain activations involved with various forms of music appreciation and creation.

A good study specifically on music and emotion is Investigating Emotion With Music:
An fMRI Study by Stefan Koelsch et all. They investigate listening to music and have nice heatmaps of brain activity during listening. There's many other papers exploring the activity pattern when listening or creating music, but the conclusion of this article sums up some of the major areas:

  In the present study, activations during the perception of
  unpleasant music were observed within an extensive neuronal network of limbic and paralimbic structures comprising the amygdala, hippocampus, parahippocampal gyrus,
  and temporal poles. Although clear increases of BOLD signals were observed in those structures in response to unpleasant music, strong signal decreases were also measured
  in response to pleasant music. This indicates that these
  structures respond to both pleasant and unpleasant auditory
  information with emotional valence, and that listening to
  music has the capacity to up- as well as down-regulate
  neuronal activity in these structures.

  ...

  During the presentation of the pleasant music, activations
  were observed in the ventral striatum, the anterior superior
  insula, and in the Rolandic operculum.

So interestingly, music with different emotional context results in different patterns and locations of brain activation. The full article has more specific information, and you can feel free to ask about more specific patterns of activation in regards to more specific stimuli.


Prozac (the generic drug fluoxetine) is a selective serotonin reuptake inhibitor (SSRI) and is primarily prescribed as an antidepressant, but also as an anxiolytic.

The side effects of fluoxetine indeed include anxiety, but this is a rare phenomenon (source: Drugs.com). The more common complaints are restlessness and skin rash. In fact, Mayo Clinic doesn't even list anxiety as a general side effect of SSRIs.


What is the difference between attractor and recurrent network?

Many recurrent networks have attractors. For example, the BAM (bidirectional associative network) is a recurrent network: one input is presented and the network cycles until no more changes are seen in the connection weights. The BAM can be understood as developing attractor states: Seen in n-dimensions (in which n is the number of units in the model), the state can be seen as a position. Whenever the same stimuli is presented, the state of the network will stabilize to the same position.

One reference is Chartier S, Boukadoum M. (2006) A bidirectional heteroassociative memory for binary and grey-level patterns. IEEE Transactions on Neural Networks, 17(2):385-96.


Does a split brain affect the inner voice?

Short answer: Probably not.
Let's first keep in mind that very few split-brain patients have ever been studied.  Add to this that inner speech is not a well studied area in general.  As the resulting Venn diagram suggests, there is next to nothing known about inner speech in split-brain patients.
Second, remember that one of the key reasons why inner speech is problematic to investigate is because up until recently, our main data source has been self-reports, considered notoriously unreliable as a methodology.  This is especially exacerbated in patients with awareness deficiencies such as split-brain.
Having said that...
Split-brain patients in general report no significant post-operative changes in their cognitive function, sense of self, or conscious experience.  Internal monologue remains intact, and appears to function as normal.  However testing under lab conditions demonstrates that subjects do in fact experience significant changes in awareness - effectively neglecting half of their perceptual experience.
If self-reports of awareness are so significantly inaccurate, then what are we to make of split-brain patients' self-evaluation of conscious experience and other cognitive functions?  The truth is, we just don't know.
Relatively recently, new techniques for studying inner speech have been developed, such as fMRI imaging of subjects instructed to or prevented from engaging in self-reflection and internal monologue.  Such studies suggest that inner speech is primarily localized to Broca's area (LIFG, on the left side of the brain), just as is outer speech (McGuire, 1996; Morin & Hamper, 2012; Wikipedia).  These findings are consistent with other evidence that inner speech is a form of silent (simulated) outer speech, and thus uses the same physical mechanism.
In the split-brain paradigm experiments, subjects are able to articulate stimuli presented to their right field of view (left hemisphere, where Broca's area is), but unable to do so for stimuli presented to their left side (right hemisphere, where language is lacking).  To communicate with the right hemisphere, researchers have subjects use their left hand to gesture responses in some way.
These experiments were instrumental in localizing language function in the brain, and they demonstrated that language capabilities are largely lateralized in the left hemisphere.  However, the right hemisphere has sufficient language understanding capabilities to gesture meaningful responses without the left hemisphere's awareness.
So although it's tempting to suggest that inner speech, localized in Broca's area on the left side of the brain, should be unaffected by corpus callosotomy, as reported by split-brain patients, the language capabilities of the right hemisphere leave open the possibility that a separate experience may exist there, potentially implying some reduction in function of (outer and inner) speech in the left side.
And indeed, while language function is highly lateralized in 90% of right-handed people, function is more evenly distributed amongst the hemispheres in other cases.  By some stroke of luck, this was the case in a particularly interesting split-brain patient by the name of Paul S.
Remarkably, in the experiments conducted with Paul, he was able to use his left hand to spell out single word answers using Scrabble pieces to express what his right hemisphere was thinking (LeDoux et al, 1977).  As with other split-brain subjects, his right hemisphere had a quite different experience from his left, but unlike other patients, Paul was able to demonstrate a slightly different personality residing in his right brain, with different opinions, preferences, and decisions.
Could this mean that Paul S. had a second, independent internal monologue in his right hemisphere that the left hemisphere was unaware of?  The dual-consciousness interpretation of this case study has been the subject of much debate, but most scholars suspect that this is unlikely: Language function is simply too rudimentary in the right hemisphere, even in this remarkable case, to plausibly support this hypothesis.


What is the psychology behind male pornographic actors having larger than average penises?

Besides the simple mechanics of it being easier to position actors and film the details of intercourse there is probably a supernormal stimulus effect. The term, coined by Tinbergen (1948) when he observed birds laying artificial eggs of ridiculous size, is used to describe the effect of a stimulus which elicits a response more strongly than the stimulus for which it evolved. Very large breasts, buttocks, penises, tall heights, etc. are not necessarily particularly useful but because we evolved to prefer larger values of these for fitness reasons we suffer from a supernormal stimulus effect when they are exaggerated. Imagine the rarity of such things for millenia of our evolution during which food and leisure time were relatively scarce. There was little reason to evolve a preference against extreme proportions.


What cognitive properties change as the income vary?

Sociology is the study of how we organize ourselves into groups. Common areas of specification in sociology are social stratification, social class, social mobility, religion, secularization, law, and deviance.

Your question specifically is about social mobility which is the movement of peoples between lower, middle and upper classes. It is commonly thought that education allows from vertical social mobility though an achieved status but that isn't accurate. A more advanced educational system than what is currently employed by the university system is necessary to advance socially.

Now about the specific cognitive difference:

   In school, learning tends to be separate from relationships. In the situated learning of poverty,
  learning occurs in the context of relationships.
  In school, learning is abstract (represented on paper or computer), verbal (words are relied
  upon almost exclusively), and proactive (students must plan). In the situated learning
  environment of poverty, learning is based on sensory data, it relies on nonverbal data as much
  as verbal, and it is reactive. The two worlds are diametrically opposed.
  In poverty, survival is a crucial skill. In formalized schooling, achievement is the crucial
  attribute. Survival means the ability to live in the “tyranny of the moment.” It also means one
  doesn’t develop a future story.
  School success is highly dependent on a student having an external support system. Often we
  find that students from poverty are the support system for the family and have very little
  support for themselves.
  The intergenerational transfer of knowledge is a huge factor in school success. In a study in
  Australia that followed more than 8,500 children for 14 years, researchers found they could
  predict with reasonable accuracy the verbal reasoning scores of 14‐year‐olds based on the
  maternal grandfather’s occupation (Najman et al., 2004). In other words, the greater the
  language with young children, the greater their potential (see also No. 7 below).
  The development of the pre‐frontal cortex, which is the executive function of the brain
  (impulse control, working memory, planning), generally is not developed by the environment
  of generational poverty. In a study released in 2008 using EEG (electroencephalogram) scans
  with poor and middle‐class children, researchers found that the prefrontal cortex of the brain in
  poor children was undeveloped and resembled the brains of adults who have had strokes
  (Kishiyama, Boyce, Jimenez, Perry, & Knight, in press). The researchers went on to say that the
  prefrontal cortex can be developed through intervention.
  Poverty tends to be heavily dependent upon casual register, whereas school is heavily
  dependent upon formal register. Hart and Risley (1995) found in their research that the average
  4‐year‐old in a professional household has heard 45 million words, while a 4‐year‐old in a
  welfare household has heard 13 million words. In fact, they found that a 4‐year‐old in a
  professional household has more vocabulary than an adult in a welfare household (Hart &
  Risley).
  In any situated learning environment, there is a set of “hidden rules” that individuals tend to
  follow. Those “hidden rules” are usually not articulated, but they are equated with intelligence.Poverty has a differentset of “hidden rules” frommiddle class and a differentsetfromwealth.
  One set is not better than another; the sets of hidden rules are simply different and help you
  survive in a given environment.

-How the Environment of Poverty (Having Fewer Resources) Impacts Cognition and Learning

Stress is thought to be the mechanism by which the brain of poor children is degraded.

  A massive literature documents the inverse association between poverty or low socioeconomic status and health, but little is known about the mechanisms underlying this robust relation. We examined longitudinal relations between duration of poverty exposure since birth, cumulative risk exposure, and physiological stress in two hundred seven 13-year-olds. Chronic stress was assessed by basal blood pressure and overnight cortisol levels; stress regulation was assessed by cardiovascular reactivity to a standard acute stressor and recovery after exposure to this stressor. Cumulative risk exposure was measured by multiple physical (e.g., substandard housing) and social (e.g., family turmoil) risk factors. The greater the number of years spent living in poverty, the more elevated was overnight cortisol and the more dysregulated was the cardiovascular response (i.e., muted reactivity). Cardiovascular recovery was not affected by duration of poverty exposure. Unlike the duration of poverty exposure, concurrent poverty (i.e., during adolescence) did not affect these physiological stress outcomes. The effects of childhood poverty on stress dysregulation are largely explained by cumulative risk exposure accompanying childhood poverty.

-Childhood poverty and health: cumulative risk exposure and stress dysregulation.


Can meditation be associated to lucid dream?

Stumbrys, Erlacher, & Malinowski (2015) found a positive correlation between mindfulness during wakeful states and lucid dreaming during sleep. However, there is no explanation about how the actual processes of meditation and lucid dreaming are related.

Stumbrys, T., Erlacher, D., & Malinowski, P. (2015). Meta-Awareness During Day and Night: The Relationship Between Mindfulness and Lucid Dreaming. Imagination, Cognition and Personality, 34(4), 415–433. https://doi.org/10.1177/0276236615572594


What electrical stimuli do brain implants use?

Short answer
The track record of cortical visual prosthetics is limited. However, a lot more is known on auditory prostheses (mainly cochlear implants) and retinal prostheses. In these implants, biphasic, charge balanced pulse trains are generally applied, mainly for safety reasons and to reduce current spread through the neural tissue. Sine waves have been tested in cochlear implants, but have long since been abandoned as useful stimulus. Color perception in visual cortical prosthetics is uncovered ground so far, but in retinal implants some limited data is available that color perception can be manipulated by altering the shape and frequency of the electrical pulse trains.

Background
First off, neural prosthetics (including auditory and visual prosthetics, as well as pace makers) in general operate through biphasic pulses instead of sine waves.

Biphasic pulses have the advantage that they can be very short (in the order of tens of microseconds in the case of cochlear implants, and hundreds of microseconds in retinal implants). This is advantageous, because the typical biphasic pulse has two identical phases but of opposite polarity. This means that the injected current is quickly neutralized within microseconds. Note that direct current is damaging to the delicate neural tissues. That's why charge-balanced pulses are used in modern cochlear implants to avoid direct current (DC) stimulation that may damage neural tissues (Bahmer & Baumann, 2013).

Sine waves have been used in cochlear implants (Clark, 2006), as most of the acoustic speech information is conveyed in frequencies between 500 and 400 Hz. Indeed, the auditory nerve does show phase locking when the electrical (or acoustic) stimulus is about 100 Hz or lower. However, biphasic pulse train are the norm nowadays, because it is safer, more power efficient and more effective, as pulses on adjacent electrodes can be alternated to prevent electrical current to summate on closely spaced electrodes. This is called interleaving and has been used widely since the 1990's as it came known as the continuous-interleaved sampling (CIS) strategy (Wilson et al., 1993). A CIS-like strategy has been adopted in retinal implants too, for example the Argus II prosthesis.

Visual prosthetics in general deliver visual perceptions on a gray scale. Cortical prosthetics have not been investigated much. However, retinal implants are currently commercially available from at least two companies. In retinal implants, phosphenes appear mostly as white spots of light, but yellow has been reported too (Stronks & Dagnelie, 2014b) as well as red to orange phosphenes (Humayun et al., 2003). Interestingly, in retinal prostheses it has indeed been shown that by carefully adjusting the pulse rate and pulse shape some crude form of color perception could be induced (Stronks & Dagnelie, 2014a). However, the only consistent result seem to have been that high-pulse rates resulted in blue phosphenes when the stimulation was stopped (OFF response) (Humayun et al., 2003). The thought is that different stimulus characteristics stimulate a different set of fibers in the retina but this is very preliminary at this stage. In cortical implants research has not even touched upon color sensations as yet, as far as I am aware.

References
- Bahmer & Baumann, Hear Res, 306: 123-30
- Clark, Philos Trans R Soc Lond B Biol Sci (2006); 361(1469): 791–810
- Humayun et al., Vis Res (2003); 43(24): 2573-81
- Stronks & Dagnelie, Exp Rev Med Dev (2014a); 11(1): 23-30
- Stronks & Dagnelie, Encyclopedia of Computational Neuroscience (2014b):
1-4
- Wilson et al., J Rehabil Res Dev (1993); 30(1): 110-6


How can I create a set of comparable symbols of different shapes?

Presumably to have symbols with the same area but different shapes, you could do a little geometry to work out relevant angles and sides. Then in any reasonable drawing package you could draw the shapes and check that they have appropriate angles. Programming drawing packages might also make life easier, but I don't have much experience with these (e.g., tikZ).

You raise an interesting question of what represents equivalence of size. Area of the shape could be a way of making size equivalent, but alternatively you could see two shapes as being visually of a similar size if they could be contained within an equivalent sized square.

One general strategy for designing the stimuli is to consider what dimensions might contaminate pairwise judgements of preferred shape: e.g., colour, size, features of the shape (e.g., angles on a triangle, the depth of cut-ins on star like shapes, etc.).
Once you've defined those features, either hold them constant or vary them in a consistent way. So you can either set up a factorial set of stimuli or randomise over features hold a feature constant. If you set up a factorial design (e.g., 3 levels of size, 2 colours, 5 shapes). You could examine how preferences vary across the confounding dimension and see whether inferences on the dimension of interest (i.e., shape) hold up levels of the confounding dimension.


The Truth Effect:

  Repetition makes statements easier to process relative to new,
  unrepeated, statements, leading people to believe that the repeated
  conclusion is more truthful. ... The illusory truth effect plays a
  significant role in such fields as election campaigns, advertising,
  news media, and political propaganda.

A seminal experiment is Begg et al (1992), in which subjects were presented with statements that they were told were false, but later rated them as truer than statements they were not previously exposed to.  Merely being exposed to statements makes them more familiar, and hence judged more true, and even being told that they are false does not counteract this effect of familiarity.

More recent studies have replicated these results with fake news stories.  For example, Polage (2012):

  ... repeating false claims will not only increase their believability
  but may also result in source monitoring errors.

And Pennycook et al (2017):

  ... even a single exposure increases subsequent perceptions of
  accuracy ... Moreover, this “illusory truth effect” for fake news
  headlines occurs despite a low level of overall believability, and
  even when the stories are labeled as contested by fact-checkers or are
  inconsistent with the reader’s political ideology. These results
  suggest ... that tagging such stories as disputed is not an effective
  solution to this problem.

This is consistent with belief perseverance.  The broader familiarity effect that causes illusion of truth is called processing fluency or cognitive ease.


Do female victims of rape have an increased risk of becoming a sex offender?

Our social constructs play a big role in influencing how we respond. As with most common cognitive mechanisms - confluence of environmental triggers meet a biological predisposition.

Regarding belief systems: in many traditions, femininity is guarded due to its relationship to motherhood. Women are thought not to be sexual. Masculinity is sexualized in a different manner, which perpetuates violence against women as well as the association of masculinity to aggression. Women who have been abused may not become aggressors- but instead are re-victimized. The idea that they will protect a perpetrator like a boyfriend or husband is a coping mechanism of sorts. On a cognitive level it is a fear-based response.The response is different for men and women due to evolutionary traits as well as learned behavior.

Many people experience sexual trauma and are not warped or broken or damaged, in part because their learned behavior is based on a positive role model who has taught proper coping mechanisms which increase protective factors.

I do believe, as a survivor of sexual violence myself, that there is a tendency to want to re-appropriate one's own sexuality and also to engage in a process of externalization through sexual experience and behavior in a way that might be labeled as deviant by others. Sometimes people respond by presenting as less feminine or less masculine as a way to distance oneself from the sexualization of their gender in order to feel safe. Sometimes people may respond by presenting self as hyper-sexual as a way to re-appropriate their own body. Of course - it's contextual. What one person chooses to present at one point and time can easily change as a reflection of the social construct.

Here is an interesting article examining the question of gender and sexual trauma.
Turchik, Hebenstreit, & Judson (2015)

You might need an academic login

This one focuses on the differences between the two genders: Cashmore & Shackel (2014)


Why does the summer holiday go so quickly?

Please check the answer to this question, Why do some days feel fast and others feel slow?, think that is the answer you are looking for.


Is there a central collection of information about the often called right brain phenomena?

The chapter on Hemispheric Specialization from Cognitive Neuroscience (Gazzaniga) is a good place to start, and I am reviewing some of it here:

In general, right side / left side  thinking has been abandoned for a systems view of cognition where both sides contribute to a given task but maintain certain specializations due to how the brain interacts with the environment as it develops, ( we still don't have all the facts though).

For instance, 96% of humans have a left-hemisphere specialization for language and speech ( processing spoken input into words and linking to meaning), yet the right hemisphere is linked to prosody as well and both report to frontal areas (where  higher associational meaning and/or task specific operations are performed so here again it could be left or right), so when hearing a conversation you are most likely using both an projecting to one or both sides of other parts of the brain depending on context,task, motivation etc, and shifting operations dynamically.

The inverse can also happen, the right hemisphere is traditionally attached to artistic thinking, yet this claim falls flat on it's face when you consider visual processing is equally divided in between hemispheres at it's early stages, the confusion stems from higher visual processing, where some visuospatial processes end up in the right side (location), but still some other processes like visual discrimination end up on the left side.

The problem with making a map of left and right areas of specialization, is that due to plasticity and the unique upbringing of each person,plus perhaps genetic variations, these areas don't overlap from person to person, so a capabilities map of general areas makes more sense for now.


Cognitive (neuro)science and related mailing lists

The Visionlist is indeed extremely helpful. It's not quite the same, but I found the mailing lists of the Organization for Human Brain Mapping (OHBM) and of the Cognitive Neuroscience Society (CNS) quite useful.


Is there a correlation between facial features and personality?

Inheritability of facial features

Let's start with the origin of specific facial features. Below is a table which shows averaged heritabilities for a range of facial quantitative traits from a large number of studies, from the review by Kohn (1991):

where $h^2$ is the narrow-sense heritability. You can clearly see that heritability in the majority of the features is well above 0.5, in fact the overall mean from all the features is 0.72 (with standard deviation 0.18). To put it in the context, this review shows that facial features are typically more heritable than behavioural traits (usually less then 0.50), but less heritable than the height (0.8-0.9). At this point we can conclude that a substantial part of the variability in facial features can be explained by the inheritance (i.e. genetic factors).

Cognitive aspects of physiognomy

As @Xurtio pointed out, physiognomy gained and lost popularity several times in history. In general, modern science is sceptical towards the traditional approach to physiognomy (i.e. specific facial features correlate with objective personality traits). However, there is a strong interest in attribution of personality traits to specific facial features. Hassin and Trope (2000) conducted a number of experiments examining the cognitive aspects of physiognomy. In examining "reading from faces" authors demonstrated that physiognomic information changes the interpretation of verbal information. The more ambiguous this information is, the more perceivers use the face. Furthermore, even when asked to, participants were unable to ignore people's faces while simulating decisions regarding personnel selection, although they are quite sure that they are able to do so (Hassin and Trope, 2000). Finally, physiognomic information makes us highly overconfident about our judgments - our confidence in physiognomy-based judgments far exceeds the actual accuracy of these judgments.

We all know that face is powerful information channel that is used to communicate a broad spectrum of emotions, more or less universally across cultures (Ekman et al., 1971). We also have dedicated brain areas specialised in decoding facial information, for example Face Fusiform Area (FFA) that contributes to facial recognition (Sergent et al., 1992). It is therefore not surprising that we all attribute so much to the specific facial features. And that we are biased in making personality judgements based on facial features, as showed by Hassin and Trope (2000).

Regarding the direct correlation between facial features and objective personality traits, there are no systematic empirical studies that support such links (as for September 2015).

References

Kohn, L. A. P. (1991) The Role of Genetics in Craniofacial Morphology and Growth.
Annual Review of Anthropology 20, 261-278.

Hassin, R., Trope, Y. (2000) Facing faces: Studies on the cognitive aspects of physiognomy. Journal of Personality and Social Psychology, 78, 5, 837-852.

Ekman, P., & Friesen, W. V. (1971). Constants across cultures in the face and emotion. Journal of Personality and Social Psychology, 17(2), 124–129.

Sergent, J., Ohta, S., MacDonald, B. (1992) Functional neuroanatomy of face and object processing. A positron emission tomography study. Brain 115, 1, 15–36.


Would a teacher benefit from reading psychology journals?

If you don't have a decent amount of education in psychology already, I wouldn't recommend diving straight into journals...but I wouldn't recommend you don't either. If you want to check them out, I'd say the only harm is the cost and the chance of getting discouraged, so first of all, I'd recommend this: don't get discouraged! You're on the right track. The best teachers are those who still spend plenty of time learning (if only to keep up with their fields), IMO. Educational psychology ("ed psych") is a deep subject—as deep or deeper than many, if not most. In my limited experience as a higher ed educator, I'd say I've learned more about teaching through experience than through what meager training I've been offered, and colleagues of mine who have sought more training haven't had good things to say about their programs...so I'd say you're not necessarily missing much for lack of training, relative to most of us, if you've got a good head on your shoulders, good communication skills, a professional attitude, plenty of respect and tolerance for the circumstances and shortcomings of others, and have paid attention to the teaching styles you admire in your own time as a student. To some extent, training programs mostly teach the basics of these qualities, and can't teach much more. However, I also have a colleague in an ed psych program, and judging from what I've heard from her (I admit I don't have any other real exposure to ed psych on which to base my opinion), I think we've all got plenty more to learn that they won't teach you in the average teacher training program anyway. Therefore I applaud your ambition for self-education, and certainly don't want to steer you away from going straight to the source. I hope I've already disillusioned you somewhat regarding the training you're lacking; it's important for maintaining minimal standards, but in my experience, it hasn't offered much guidance for growth beyond that. If you don't have any particular shortcomings that need ironing out—if you're already a halfway decent teacher—you're probably better off skipping the watered-down, "common-sense" sort of educational psychology you'd get from people who specialize in other things, and who are only teaching how to teach because it's a job they could get.

I would, however, recommend testing the waters of those journals you're thinking of diving into before shelling out the subscription fees. Some journals can be quite dense and advanced reading without a proper introduction (especially cognitive psychology articles, in my experience). This isn't to say you can't hack it, but you may find a lot of articles referring to concepts that are introduced in other articles (or worse, books!) that you can't access for free except through your university, which might also require inter-library loaning (you might not be able to do that without being enrolled, but you should at least be able to get access to some journals by visiting an on-campus library). This becomes quite a lot of legwork, so don't dive in unless you're ready to swim the equivalent of the English Channel. Try looking for free articles from these journals you're interested in (e.g., the links on the right that you can access through a Google Scholar search for "Journal of Applied Psychology"), see how comfortable you are with reading them, and see how far you can follow the reference lists whenever you come across an interesting idea that you'd like to know more about. If you can make a go of it and be happy with what you get out of it, if you're not happy with what you can already access for free by means like Google Scholar or your university, and if you're willing to pay the price of subscription, I don't see any further reason to dissuade you!

Regardless (or especially if these journals don't work out for you), I'd also recommend checking out more introductory literature on ed psych. The thing about journal articles (in case you don't already know this; forgive me if I'm getting pedantic) is that their authors often write to a fairly advanced research audience, so it's not exactly like learning to swim in the shallow end, where most inexperienced students would probably be better off starting. Some books are like this too of course, but it seems to me that most books in psychology are less afraid to belabor their points and more keen on appealing to a more general audience. Especially when setting the average book aside and looking directly to introductory books and textbooks, you can expect to find the process of learning the foundational theories of most domains a lot easier, and probably more efficient; again, I haven't tried doing this with ed psych texts myself, but I'd assume the same is true of this domain as it is of others. In general, the advantage of intro text/books is not just that they're directed at more general audiences; they'll also usually take a much broader overview of the field as a whole. You might have to do a LOT more reading to get the same breadth out of journal articles as you could out of an intro text/book.  You'd probably get a much deeper exposure through journals, but if your time is short enough as is, you're probably more concerned with covering all the fundamentals than with sharpening your knowledge on any specific subject, let alone all of them, by yourself!

If you're sold on the idea of checking out intro text/books, you don't actually have to buy anything necessarily. For instance, check out this list of free e-books on ed psych that I just found. To make sure I wasn't tossing you a red herring, I went ahead and downloaded Seifert and Sutton's (2009) Educational Psychology for myself, for free; it looks fairly solid to me at first glance. In any case, it's not your only free option on this list alone, and with a little extra effort or a trip to the library, I'm sure you could find plenty more options for free. If that won't cut it, or if you see recommendations for a particular text/book, consider ordering it used. You ought to be able to get plenty of them for much less than the price of a subscription to the journals you mentioned, which look like they'd run you $\$455$ apiece. I'm a fan of Half.com for used book buying myself. I see some options here for less than $40!

Good luck; I hope you learn a lot of good stuff, and come back to share some of your insights with us here! We could all stand to know more about these topics...Except maybe those who really know these topics, whom I hope will give you some answers of their own too!


How to denoise and get rid of 1/f trend of a PSD in an EEG synchronization experiment

Apparently the paper you mention is simply evaluating the median in the EEG spetrum. Say that for all your channels you get a 3D matrix PSD, with dimension 1 the number of channel, dimension 2 the time windows, and dimension 3 the frequencies. In pseudocode the article computes M = median(median(PSD,2),1), then removes the trend with CorrectedPSD = PSD - M. Which is actually fairly simple.


Episodic-memory amnesia preserving fear conditioning

As a sort of partial answer, but since it's too much to add to the question itself... a more encompassing question would be whether fear conditioning can occur without awareness of the conditioning event happening at all. I suppose an affirmative answer to the latter implies the answer is also "yes" to my question because forgetting the association event doesn't seem any more restrictive than not learning (into episodic memory) about it in the first place.

However, the jury seems to still be out on whether unaware conditioning can happen in humans. Some initial (and highly cited) studies answered the question affirmatively, but later studies cast doubt on the results because the level of awareness for the stimuli used seem to vary with the individual. (In other words, there was heterogeneity in awereness in the original studies; for a completely different reason, I've looked into what happens in such a case and asked what the phenomenon is called on cross-validated, but with not very satisfying answers insofar) From a 2005 review by Pessoa, which summarized the research up to then:

  Does the processing of emotional stimuli depend upon awareness?
  Two influential neuroimaging papers, both of which
  appeared in 1998, reported that responses in the human
  amygdala occur in the absence of visual awareness.
  Awareness was manipulated by employing backward
  masking, as introduced by Esteves and Ohman in
  a behavioural paradigm. In one study, fearful faces were
  shown for 33 ms and were immediately replaced by a
  neutral ‘mask’ face that was presented for 167 ms.
  Subjects were naive as to the stimulus conditions, which
  included masked fearful and masked happy faces. Stronger
  responses were observed in response to fearful rather
  than happy faces (both masked by neutral faces), even
  though, upon subsequent debriefing, subjects did not
  report seeing any emotional faces. In another study,
  Morris et al. combined backward masking with classical
  conditioning to investigate responses to perceived
  and non-perceived angry faces. Although the participants
  did not report seeing the masked angry stimuli (angry
  faces were shown for 30 ms and followed by a neutral
  mask that was shown for 45 ms), the contrast of conditioned
  and non-conditioned masked angry faces activated
  the right amygdala. Recent studies have also gathered
  evidence for unaware processing by the amygdala For instance, Glascher and
  Adolphs showed that in normal controls, but not in
  patients with amygdala lesions, arousal ratings correlated
  with skin conductance responses for both subliminal
  (unaware) and supraliminal (aware) conditions (see Glossary).
  Together with the important earlier work by
  Ohman and colleagues, these results have strengthened
  the view that emotional processing occurs independently
  of conscious awareness. In general, a
  stimulus that is shown for about 30 ms before masking
  is considered to be at the ‘threshold’ for awareness.

  However, a recent study by Phillips et al. did not
  observe any response in the amygdala during unaware
  conditions. The authors compared aware conditions, in
  which target faces (fearful or disgusted) were shown for
  170 ms and followed by a mask that was shown for 100 ms,
  with unaware conditions, in which target faces were
  shown for 30 ms and, again, followed by a mask that
  was shown for 100 ms. Unlike prior studies, however,
  no differential responses were observed in the amygdala
  in association with fearful faces in the unaware condition
  (or in the anterior insula for unaware disgusted faces).

  A crucial issue in the assessment of awareness is the
  criteria used to determine whether a participant is aware
  or unaware of a stimulus. According to ‘objective’
  criteria, unaware perception occurs when a subject’s
  performance in a ‘forced-choice’ task is at chance. Under
  such conditions, behavioral effects of unaware stimuli
  (e.g. faster reaction time to undetected fearful faces),
  as well as the associated fMRI signals, constitute correlates
  of unaware perception. According to ‘subjective’
  criteria, unaware perception occurs when subjects report
  that they are unable to perform the task better than by
  chance (independent of their actual objective performance).
  Although some of the previous studies used
  forced-choice objective methods, they did not assess
  performance in a manner that is independent of response
  bias on an individual-by-individual basis [...]. This is important because in the face of weak, noisy signals, subjects might indicate that they do not detect
  target stimuli and thus appear to be unable to detect them
  reliably. A recent behavioral study by Pessoa et al.
  addressed these issues by analyzing performance by way
  of signal detection methods. The authors varied the
  duration (17, 33 and 83 ms) of which a target face (fearful,
  happy or neutral) was shown before being immediately
  replaced by a neutral-face mask (which was shown for
  116, 100, and 50 ms, respectively, such that the target plus
  mask lasted 133 ms in each case). The subject’s task was
  to report explicitly whether or not a fearful face was
  presented in each trial, and also to rate their confidence
  in this decision. Although some subjects only reliably
  detected the fearful targets that were shown for 83 ms,
  36% of the participants were able to detect both the 33 ms
  and 83 ms targets. Remarkably, some subjects could even
  detect fearful faces that were shown for 17 ms before
  masking. These results demonstrated that participants
  differ widely in their sensitivity to fearful faces (Figure 1).
  Moreover, the results revealed that even very brief
  (17 ms) stimuli can be incompletely masked, consistent
  with another recent study [Maxwell and Davidson]. The findings by Pessoa
  et al. also raise the possibility that the discrepancy
  between the results of Phillips et al. nd those of
  prior studies might be caused, at least in part, by variability
  in sensitivity among individuals, which may be
  related to anxiety levels.

I'm not sure if there's a more recent review than this perhaps with different conclusions following newer experiments. The fact that the review was written by someone who also contributed primary research in the "cast doubt" direction casts a little doubt (in my mind) on its objectivity... But the above surely illustrates the difficulty in conducting studies related to awareness.


Why do many parents prevent children from being exposed to anything sex-related?

If I were to guess, the reason is probably something to the effect of: because children would not understand since they lack the same (or same level of) sexual urges that adults have. Another thought that comes to mind is maybe parents are afraid (or even ashamed) of their children seeing them (the parents) acting essentially like non-human animals. Sexual intercourse activities are usually very animalistic compared to most of the things we do in everyday life of modern society. For a similar reason, many parents probably would not want their kids seeing the parents drunk or otherwise acting uncivilised. In a way, it is like the parents are trying to hide from the kids the fact that adults are in many ways just big babies who are good at hiding it. The idea that humans are supposed to be civilised and clean is somewhat unnatural, yet common culture seems to view this idea as highly important.

On the topic of war and violence, my guess as to why these are often considered okay for children to see is because awareness of danger and the threat of violence are necessary even for a child, while knowledge of sex and sexuality really is not that essential at a young age.


What is the term for doing things or behaviors that contrast to what you really feel?

Is there a term for that?

The closest term I can think of relevant to psychology is the Freudian concept of reaction formation the classic example being the gay homophobe


Looking for a name of a theory or reason behind a seeming cognitive mistake or error

I think what you describe is a capture error.

  Capture errors refer to frequently performed tasks that take over the
  correct intended action. Wickens & Hollands clearly define capture
  errors as resulting from two primary reasons: (1) the intended action
  and the resulted action share somewhat characteristics that are
  closely related: and (2) the action sequence is resulted from
  automated behaviour and therefore, not closely monitored by attention.
  The example stated earlier about pouring orange juice instead of milk
  is a capture error by itself.

You had the intention to close the sink, but instead you closed the light. Both actions share the characteristic of closing, closing the light is the most frequent.


Have there been any mechanisms proposed for normalization in probabilistic population codes?

It depends what you mean by a biological mechanism. If you mean that there should be a protein cascade that implements normalization, that doesn't seem plausible, in my opinion. Normalization in probabilistic population codes is just one of many computations that can be performed in a neural system.

If you're okay with the notion that there's nothing biologically unique about normalization, then Normalization for probabilistic inference with neurons (a paper written by my supervisor, Chris Eliasmith) proposes a spiking neural network performs normalization on probability density functions.


Why might mindfulness and meditation lead to anger and anxiety?

I have found several studies which support the general consensus that mediation helps to ease anxiety.

Bahrke, M. S., & Morgan, W. P. (1978). Anxiety reduction following exercise and meditation. Cognitive therapy and research, 2(4), 323-333.
Krisanaprakornkit, T., Sriraj, W., Piyavhatkul, N., & Laopaiboon, M. (2006). Meditation therapy for anxiety disorders. The Cochrane Library.
Tacón, A. M., McComb, J., Caldera, Y., & Randolph, P. (2003). Mindfulness meditation, anxiety reduction, and heart disease: a pilot study. Family & community health, 26(1), 25-33.
Lee, S. H., Ahn, S. C., Lee, Y. J., Choi, T. K., Yook, K. H., & Suh, S. Y. (2007). Effectiveness of a meditation-based stress management program as an adjunct to pharmacotherapy in patients with anxiety disorder. Journal of Psychosomatic Research, 62(2), 189-195.

However, one study by Heide and Borkovec describes the phenomena of relaxation induced anxiety (RIA):

  While procedures such as progressive relaxation, biofeedback and meditation can often be effective in reducing subjective anxiety and physiological hyperactivity, recent evidence indicates that these same procedures apparently
  can initiate or exacerbate anxiety in certain individuals (Heide and Borkovec, 1983).

They suggest that this may be because

  Somatic, affective and cognitive states arising during relaxation are perceived as threatening, perhaps due to the loss of control which they represent. Loss of control, in turn is avoided as either a perceived threat to coping and survival or perhaps more commonly as a threat to social acceptance (e.g. the fear of emerging inner conflicts and emotions, and the expression of which may be linked to anticipated social rejection). To guard against such loss of control, individuals may adopt strategies to cope with the
  environment and control anxiety; such strategies frequently maintain tension and may be antithetical to relaxation.

Based on this study, one would assume the effect of meditation is based on the individuals response to it, rather than the efficacy of the meditation techniques

Reference:
Heide, F. J., & Borkovec, T. D. (1984). Relaxation-induced anxiety: Mechanisms and theoretical implications. Behaviour research and therapy, 22(1), 1-12.


What is the difference between facets and factors?

Factors and facets

In personality trait research, traits are often conceptualised hierarchically. There is also a broad consensus that a small number of broad traits (typically the Big 5, but others argue for different numbers such as the HEXACO 6) explain personality quite well. The big 5 also goes by the name Five Factor Model. The terminology of "factor" is quite likely linked to the method of factor analysis often used for scale construction in this area.

Several popular personality tests measure traits at two-levels (e.g., NEO-PI-R, HEXACO-PI-R, IPIP, etc.). So for example, the NEO-PI-R is composed of five broad factors, each of which is composed of 6 narrower facets.

So in summary, there is a range of terminology that  have similar meaning:

broad traits, domains, factors
narrow traits, facets

Another common terminology is that of scales and subscales.

On basic level, this is just convenient terminology for describing two levels of a hierarchy of measurement, particularly where the broader level is defined by the lower level.

For further discussion see:

Anglim, J., & Grant, S. L. (2014). Incremental criterion prediction of personality facets over factors: Obtaining unbiased estimates and confidence intervals. Journal of Research in Personality, 53, 148-157. https://osf.io/g8kbj/

Your case of mapping a test onto a theory

In your case, you are mapping eight scales onto a theory that includes eight components. This doesn't have too much to do with the factor-facet distinction.

Perhaps the main issue is whether there is an overall scale (e.g., an overall leadership effectiveness scale, of which there are eight subscales). You could potentially call this the leadership effectiveness factor and call the eight elements "facets". But it might be more common to merely call the eight components "scales" or "subscales".


Here's the only speculation I could find about brain shivers aka brain zaps.

Cortes JA, Radhakrishnan R. A Case of Amelioration of Venlafaxine-Discontinuation “Brain Shivers” With Atomoxetine The Primary Care Companion for CNS Disorders. 2013;15(2):PCC.12l01427. doi:10.4088/PCC.12l01427.

It proposes an explanation related to norepinephrine. Also, it claims that brain shivers or brain zaps are related to Lhermitte's phenomenon. I have mixed feelings about this specific comparison from what I've witnessed.

"These facts point to the possibility that increases in synaptic norepinephrine are due to norepinephrine transporter reversal, akin to dopamine transporter reversal associated with amphetamine. Abrupt withdrawal of venlafaxine would hence result in paradoxical increase in synaptic norepinephrine via efflux through norepinephrine transporter channels, which is normalized by atomoxetine’s norepinephrine transporter blockade."

That would explain brain zaps from stopping tramadol and SNRIs too, by the way: a noradrenergic syndrome.

Anyone has a better or more supported speculation?


Is "not going to doctor because of fear of illness" a psychological disorder?

What you are describing is most likely avoidance, which in itself isn't a disorder.

People are most likely afraid of the illness in itself, and so not going to the doctor means that they don't have to confront the possibility of having that illness. This avoidance is a mechanism that maintains hypochondria or health anxiety (however you wish to call it) by negative reinforcement: 'I don't go to the doctor, I'm not told if I'm sick or not, so I'm less anxious'.

The reduction in fear or anxiety is usually short lived and only makes it worst over time. This coping mechanism is not adaptive, and may aggravate health anxiety, but in itself, is not a disorder.

Sources
- David Veale's website
- Centre for Clinical Interventions
- Psychology Today


What makes a sight or an image mesmerizing and irresistible?

Setting aside the encyclopedic issue of what might make an unspecified stimulus funny, beautiful, or otherwise pleasing for its aesthetics, it's at least evident that you're asking about reinforcing stimuli that provide incentives via emotional reward(s). It's not clear how you expect to rule out conscious interest, but reinforcement learning may not necessitate consideration of conscious control, so I suppose we can disregard the whole issue of consciousness at this level of generality (or ambiguity/vagueness). That is essentially the approach of radical behaviorism, after all.

Aside from the tags and links included so far, there's plenty of science available on psychological reward:

Relevant neural structures include the ventral tegmental area and nucleus accumbens.
Dopamine is probably the most relevant neurotransmitter, but other catecholamines such as adrenalin and norepinephrine may affect impulse regulation and attention.
Relevant personality factors include the behavioral activation system and sensation-seeking. Other factors become more or less relevant depending on the nature of the stimulus, e.g.:

Openness to experience affects aesthetic preferences, especially in art and culture.
Cultural background affects interests, preferences, and incentives through taste acquisition.
Emotional stability and extraversion may affect attitudes toward arousing or social stimuli.
Sexual desire may be relevant, depending on the stimulus and the individual.
Emotional and physiological states affect the strength and relevance of other needs / motives.
Conscientiousness or control affects impulse regulation, which is relevant if urge resistance is.

We have a dedicated question about humor: How does our brain consider something to be funny?


'Describe this object to me' - To work out what type of thought process you have. What is this test called?

The test you seem to be talking about is often referred to by different names, but the name used by The Myers & Briggs Foundation[1] and most of the papers on the subject[2] is MBTI (Myers-Briggs Type Indicator).
PS:

I did my best to identify it according to your description, but leave a comment if I'm wrong.
It is important to add that this test is often regarded as pseudoscience and has several fundamental issues [3]

[1] https://www.myersbriggs.org/my-mbti-personality-type/mbti-basics/
[2] https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=%22Myers-Briggs+Type+INdicator%22&btnG=
[3] https://www.psychologytoday.com/intl/blog/give-and-take/201309/goodbye-mbti-the-fad-won-t-die


What is the most complex artificial neural network created to date?

A (probably incomplete) list of ongoing whole brain simulation projects can be found at http://www.artificialbrains.com/. However, based on the information reported on this site, it is sometimes hard do distinguish what already has been achieved and what is still in the planning stage. Nevertheless it gives a good overview to start with.


How much overlap should I expect between Medline and PsycINFO?

Unfortunately, I'm not sure there's a quick answer to the exact amount of overlap, but you may be able to get an estimate by comparing the list of journals included in Medline (http://www.nlm.nih.gov/archive/20130415/tsd/serials/lji.html.notice.html) to the list of journals covered by PsycINFO (http://www.apa.org/pubs/databases/psycinfo/coverage.aspx). Also, keep in mind that each database has it's own thesaurus and preferred search terms, and the terms you're using might pull up different results in different databases. You may be able to optimize your results by using search terms specific to each database.


How does an understanding of the brain explain why people experience strong emotional responses to major sporting events?

This is only a partial answer (since the question scope is so large) but it is one of my favorite empirical findings.

It turns out that simply watching your favorite team win or lose has physiological impacts. Specifically, if a team you are rooting for wins, your testosterone levels will increase, and they will decrease if your team loses. This was demonstrated by Bernhardt, Dabbs Jr., Fielden, & Lutter (1998). In two experiments, they measured testosterone levels in male sports fans before and after watching their team win or lose. In both experiments, people who were rooting for the winning team showed an increase in testosterone relative to their testosterone level before the match, while people who were rooting for the losing team showed a corresponding decrease in testosterone.

This doesn't explain why we get so invested in sports, but it might help us understand some of the extreme reactions that sports fans have after a particularly exciting match.


Self-study guide for translating a psychological scale

The article by Gudmundsson (2009) looks very useful. It describes an eight step process for translating and adaptive psychological instruments. The article is written clearly with concrete suggestions and references to the broader literature.

  selecting an instrument for translation
  selecting qualified translators
  selecting qualified experts
  Method of translation (e.g., back translation, two independent translations)
  Method of adaptation
  Investigating bias
  pilot studies
  validity studies

In general, psychological scales are copyrighted. That said, many academics would be excited at the prospect of having their scale being translated into another language. Thus, in general, a good approach is to contact the author of the scale to get their consent to you performing the translation.

References

Gudmundsson, E. (2009). Guidelines for translating and adapting psychological instruments. Nordic Psychology, 61(2), 29.


What is the maximum size of content the human eye can focus upon?

The fovea (highest-resolution area of the retina) can only "see" the central two degrees of the visual field; the field of foveal vision is approximately circular, although it varies slightly by individual.  This depends on the distance from the eye or sensor.  This is called "visual angle" or "angular size", and it can be calculated using the formula

where S is the object's linear size and D is the distance between the eye/sensor (sometimes called point O) and the object.

More here: http://en.wikipedia.org/wiki/Visual_angle
Calculator here: http://www.oocities.org/robertellis600/va.html


Is there a circadian component to mood variations in humans?

Overview: It seems like quite a bit of research has been conducted with experience sampling methodologies looking at daily variations in mood and activity. It is an interesting question as to how best tease out the effect on mood of time of day per se and activities associated with time of day on variations. It also seems like there are individual differences in how time of day influences mood. Anyway, here are a few studies I found on the topic:

Csikszentmihalyi and Hunter (2003) performed an experience sampling study of a large sample of U.S. secondary school students. With regards to time of day they found:

  During the weekdays, time is structured by work or school requirements
  according to a circadian pattern. The ﬁrst part of the day, spent at
  work or school, tends to be less happy, except for a peak at
  lunch-time. There is a dip after lunch, followed by higher reports of
  happiness in the afternoon when one is again free (see Figure 2).

However, day of the week was also relevant with the greatest happiness observed on Saturday.

  Clearly, the social structure of time has an impact on happiness: The
  early part of the weekend, with its freedom from work or school, is
  experienced as liberating. The effect is probably greater on adults,
  for whom the working week is presumably even more constraining than it
  is for teenagers.

Rusting and Larsen (1998) measured negative affect in a small sample of undergraduates where three measure were obtained each day, once each in the morning, afternoon, and evening. The mean levels of negative affect seemed to be slightly higher later as the day progressed.

  Table 1 Average Percentage of Negative Affect Peaks at Each Time of Day

               M       SD
Morning      30.46   12.10
Afternoon    33.77   13.45
Evening      35.77   13.10

  Note. Percentages at each time of day were calculated for each subject
  across the 60-day assessment period. These percentages were then
  averaged across all subjects (N = 46).

Stone et al (1996) measured mood and activity using a diary study with measures taken every 15 minutes for one day. They found:

  Diurnal cycles were found for several moods (e.g., happy, tired),
  activities (e.g., discourse, thinking), and locations (e.g., home,
  work). Diurnal cycles in most moods were strongly associated with
  activities and location, yet diurnal cycles of some moods (rushed,
  sad, and tired) were not dependent on these factors.

If you read their article, you'll see various graphs of self-reported emotions throughout the day both controlling and not controlling for type of activity.

References

Csikszentmihalyi, M. & Hunter, J. (2003). Happiness in everyday life: The uses of experience sampling. Journal of Happiness Studies, 4, 185-199. http://www.mendedreality.com/private/docs/CSIKSZENTMIHALYI2003.pdf
Rusting, C.L. & Larsen, R.J. (1998). Diurnal patterns of unpleasant mood: associations with neuroticism, depression, and anxiety. Journal of Personality, 66, 85-103.
Stone, A.A., Smyth, J.M., Pickering, T. & Schwartz, J. (1996). Daily mood variability: Form of diurnal patterns and determinants of diurnal patterns. Journal of Applied Social Psychology, 26, 1286-1305.