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What is the timeframe of the Yerkes–Dodson law?
What is the timeframe of the Yerkes–Dodson law?
The Yerkes–Dodson law is defined this way (Wikipedia):

The Yerkes–Dodson law is an empirical relationship between pressure and performance, originally developed by psychologists Robert M. Yerkes and John Dillingham Dodson in 1908.1 The law dictates that performance increases with physiological or mental arousal, but only up to a point. When levels of arousal become too high, performance decreases.

I am not sure what is the timeframe for this experienced stress. Is it true for a stress which lasts several (dozens) of minutes, or several days?


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At what rate and to what extent do metabolic waste products from neurons diffuse throughout the brain?
At what rate and to what extent do metabolic waste products from neurons diffuse throughout the brain?
Do the metabolic waste products remain local to the neurons being used, or do those waste products diffuse throughout the brain?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Understanding lack of compassion exhibited by Iranian experts in catastrophic situations
In recent catastrophic situations, there have been reports of Iranian experts displaying a lack of compassion towards ordinary people affected by these events. This raises questions about the underlying psychological factors contributing to this behavior, particularly in the context of the influence of Islamofascism.
I came across a post titled "The Role of Experts Outside of the Country in Influencing the Situation Inside the Country" (link: post link) that explores the complexities and importance of external experts in shaping policies and decision-making processes.
I am interested in understanding the lack of compassion exhibited by Iranian experts in catastrophic situations, considering the influence of Islamofascism, and would like to know if there are any psychological theories or research that can shed light on this phenomenon.
Additionally, I am curious about effective ways to utilize the internet to document and address these actions.
By asking this question, I hope to engage with the Psychology & Neuroscience community to gather diverse perspectives, scholarly resources, and practical insights that can contribute to a better understanding of the lack of compassion exhibited by Iranian experts in catastrophic situations, considering the influence of Islamofascism.
Please provide any relevant context or background information that can help the community provide more informed and insightful answers.
(Note: This question was generated by ChatGPT. ChatGPT website)

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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narcissism and cognition
Is there a tight coupling between narcissism and certain forms of cognitive impairment? Does this vary by vulnerable vs. grandiose narcissism ?
People I've known formally diagnosed with a cluster B personality disorder frequently have trouble with abstract problem solving. They aren't unintelligent, some even have PhDs, but they have anomalously poor performance in high school math on up. The more abstract the problem the worse their performance.
This has me wondering if part of the empathy problem associated with narcissism has less to do with not caring about others than a fundamental failure to understand them in a complex way.


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automated co-registration of PET CT
Hi all:) I've acquired Whole body PET CT data from form which I would like to generate brain co-registered PET and CT nifti files - has anyone implemented something similar? I have experience with fMRI preprocessing - could SPM do the trick?
Thanks!


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Is there research on how easy patients feel it is to get access to psychiatric medications they want in various countries?
Regarding availability, satisfaction with diagnosis/ability to receive desired prescription by doctor’s permission, and especially how restrictions in the medical system can lead to long wait times prior to getting access to a medication - comparing that across various countries, and identifying factors at play in those results.


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Why do we explore?
I'm keep trying to list some of strong motivations to explain our "inner curiosity". But, the subject and this question are very broad, therefore I will give you some context.

So, why do we explore? The first class of answers, in my point of view, lies on our physiological necessities.  Our bodies need energy (food...) in order to keep functioning, therefore all the expanse of humankind does have at least a reason: a search for more energy. Hence, our curiosity trais could have a strong genesis in thise matter. Also, if we can "store energy" for a later usage, therefore, in some sense we are optimizing our life; for instance, if we store food, we won't need to stress our bodies to go out and hunt a predator for its meat. In this latter scenario, we will always exaust the resources of the site, then we will need to "explore other lands" sooner or later. Now, up to this stage, humans are social beings, and from our history it is clear that we developed a sense of community. We create all sorts of social structures: tribes, countries, families, etc...
Well, this social structure paradigm, in principle introduces a well optmized life, since we are together and therefore we can overcome many obstacles in order to survive. Still, many of us keep going out to explore, without any sort of clear physiological necessity

The other class of answers, maybe could lie on the evolution of the human as a social being. Together we are stronger, and we can hunt and store energy with efficiency. The sense of community seems to matter deeply in our pysche as well. In this regard I would like to ask:

The fear of being "alone" can be a motivation, as stronger as 1., to explaing our sense of curiosity and "need" for exploration? In other words, which biological traits can explain the feeling of "I need to know what is out there"?

(Please, try to abstract the usage of the words "hunt" and "food")


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Study about confirmation bias (facial disfigurement and job interviews)
In a youtube video (see here), Konstantin Kisin talks about a study in which subjects were given fake scars to study how this affects outcomes of job interviews. The participants did not know that the fake scars were removed shortly before the interview ("we just need to brush up the makeup of the scar quickly"). The scars therefore could not have affected the interview directly, but many participants reported they were treated unfairly because of their scars, which points to confirmation bias. Can anyone point me to that study?


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Why do people see movement where none exists?
We all know that motion pictures, TV programs and videos aren't necessarily moving and they are different of how we see motion in real life that are just a series of still images in rapid succession on a flat surface, live-action movies are photography and has the same settings as photography like aperture, shutter speed and ISO, has the same functions as photography like motion blur, depth of field and lens flares and also has the same rules as photography, Why do people see ''movement'' in movies, TV broadcasts and videos where none exists?

Similar to: Does perception have a "frame rate"? and What causes the spokes of a Wagon Wheel to "move"(rotate) in the opposite direction of the Wagon Wheel itself?


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Non-salience memories?
It is said that memories that are significant are remembered much more clearly due to salience. Yet, let us imagine a man named Fred. Fred does not have hyperthymesia as he forgets things like everyone else; yet he also has a large amount of non-salient memories. Nitty gritty things like the dialogue someone said in a specific interaction. What is wrong with Fred’s brain? Why does he have so many non-salient memories but not a perfect memory?


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Are BDSM sexual practices correlated with or related to social-dominance orientation?
When I think about BDSM sexual practices and sexual sadism disorder, I tend to think that it sounds like something that some people with a social dominance orientation would be interested in. This Wiki page on a subtype of BDSM sexual practice called master/slave reminds me of how feudal lords owned slaves and serfs.
I feel that the economic relationship between a slave and a slave owner looks psychologically similar to the master/slave role play. And I also think that what's referred to as the sexual sadism disorder is an exaggerated version of the regular BDSM sexual desire.
Are there any scientific studies that tested the correlational relationship between BDSM sexual practices and the sexual sadism disorder with the social dominance orientation trait? Does having the SDO trait increase your chances of seeking out BDSM sexual practices or being diagnosed with a sexual sadism disorder?


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What is the study examining biological sex differences in determination where babies pulled on a string to generate a response?
I'm looking for the study that describes this experiment. I saw it demonstrated in a documentary, but I can't remember the name of it.
In the experiment, biological males and females were put in a seat facing a screen with a string attached to their arm, and when they pulled the string, the picture changed. The researchers then stopped the picture from changing when the string was pulled to observe behaviour differences between the two groups.


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Why does handedness suggest that the brain is asymmetrical?
From The Human Mind, by Paul Bloom:

If you just look at a brain - if you remove it from somebody's head and put it on the table - it looks symmetrical. But it isn't. The asymmetry of the brain is manifested in handedness. Some people are right-handed, and others are left-handed, and since motor control comes from the brain, this suggests that the brain itself is asymmetrical. It has a right side and a left side, and they are not identical.

(In this case, I am taking him to mean functionally asymmetrical.)
Of course I'm not disputing that the brain is indeed asymmetrical, but I'm struggling to understand how he draws this conclusion based on the flow of logic above. i.e.
1.) Almost all people have a preferential side for motor control.
2.) Motor control comes from the brain.
3.) Ergo, the brain itself is likely asymmetrical.
How do we get from 1. & 2. to 3.? Playing the devil's advocate here: could a response to the above not be that left handed people have a more active right hemisphere (with respect to motor control), but that the hemispheres are functionally identical? This is obviously an incorrect conclusion, but could it be shown to be incorrect only using the arguments outlined above?

If they were identical, why would there be a preferred hand? Where would the preference come from, physically?


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Commonality of Personality disorders
Why is NPD are OCPD,BPD classfied as personality disorder? Especially for the last one.

Please don't duplicate questions - edit the original instead.  It is definitely an improvement, but this question still needs some work before it can be reopened, as it still contains multiple questions, unsourced claims, and unclear details.


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Phases of Brain Development and Gender Identity
What stages of brain development are represented by sexual differentiation and linked to prenatal development of gender identity?

Welcome. Is this a homework question? In any case, we like questions to be focused and a great way of doing that is by adding your research efforts so far.


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Austism and Over Stimulation
Are there precise terms for sensory overstimulation regarding Autism?
I'd never thought I had a problem with overstimulation, but I've read many people with Autism don't if they can reasonably ignore the stimulation around them. They don't have a problem until they need to sort the information towards a useful purpose, then things can go awry.
For example, an interviewee in Nerenberg's The Neurodivergent Mind says she actually enjoys the random sights and sounds at a busy grocery store if she's just walking around killing time. If she has to look for an item in an unfamiliar area and the store is empty and crowded, she's fine. If she actually has to focus on where she is, navigate to the unfamiliar area, search for the item in question then the sensory environment becomes too much. That's exactly my experience.
I was wondering if there's research on merely being in an overstimulating environment vs. having to use information within that environment and a useful way to sort out one from the other in research.


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Patterns of screen scrolling and tapping and instantaneous mood
I was wondering whether any surveys have been conducted to see if people click more often on things (at a given timing), in Google Discover, and similar, news, apps, when they're depressed.
Another situation could be not clicking on something in Quora or in a similar social app, because of avoidance. This could also have a specific scrolling pattern.
Another, type, of slow slowly accelerating scrolling, and then tapping (screens do not yet have the capability to detect a difference between a depressed tap with a nail, and a positive tap with the index finger, including, an analysis of the pressure, from, such, ... but a capability may be embedded in phones in the future).
So, I was wondering, what research has been done in this area (including research aimed at detecting, escaping, from these patterns).
Thanks.


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Are there better tools for EEG data visualization than MNE-python?
I've started learning about EEG data analysis (as a data scientist working with python and R on a daily basis) and came across MNE package. I know that it has some tools for visualizing EEG data and I am curious if there are any better (i.e. for example faster or more visually pleasing) libraries that could be used instead. I have python based datashader library on my "try it" list as it is designed to be good at visualizing big datasets faster than for example matplotlib and also looks better.


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literature review research transgender youth of color
I'm currently working on a review of the literature. I'm looking for research on how community support can help trans youth of color. For instance, there is research that suggests that trans youth of color are more protected from social strains than white trans youth.
Is there more research on how forms of community support helps trans youth of color? Such as trans youth of color from more collectivist oriented cultures.


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Relationship schemata caused in childhood - better term for this, and can they be grouped?
I listen to a podcast (by Stefanie Stahl, in German), where a psychologist tries to explain the problems adult guests describe to her. She often finds reasons for their problems in the guests childhood, in how their caretakers treated them. For example, someone who always had to fight to be loved (who only felt conditionally loved), might then later on look for partners who also only conditionally accept them. And as soon as a relationship is stable, they might not find their partner interesting any more.
Basically, the idea is that during childhood you learn how relationships work, and later gravitate to what feels familiar (but might be unhealthy).
I am wondering:
a) Does this have a basis in a specific psychological theory? I'm aware of
the Strange Situation test and the attachment styles, but the
examples in the podcast seem more specific, not just "doesn't attach", "attaches", "clingy", but affecting what one tends to attach to (supposedly).
b) Is there a name for relationship problem schemata that are
'caused' by what one experienced in childhood?
c) In case there is a basis for this at all: Is there a grouping for those schemata (the different ways in which ones relationship style can be broken because of childhood experiences)? A type of overview?
I hope I'm making sense in what I'm describing.


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Are autism and schizophrenia more severe in Sub-Saharan populations?
Some time ago, I read a Spanish news article discussing the creation of Neanderthal proto-brains using CRISPR. I have translated the relevant part:

Interestingly, some characteristics of Neanderthal brains resemble those of humans with autism, according to Muotri. 'I don’t want families to think that I am comparing autistic children with Neanderthals, but it is an important observation,' the researcher said. 'In modern humans, these kinds of changes are linked to defects in brain development necessary for socialization. If we believe that this is one of our advantages over Neanderthals, it's something significant.'

Source: genotipia.com
I told myself: wait, all Neanderthal were autistic? Maybe autism was inherited from Neanderthal? But soon I searched if autism is present in Sub-Saharan people with no Neanderthal or Denisovian DNA and of course autism is also a Sapiens issue.
Recently I returned to focus my attention on the topic and I started to read a bit more. I read another statement in a different Spanish news source:

Autism and schizophrenia are uniquely human characteristics.

Source: lavozdegalicia.es
I'm not sure if 'humans' in this context includes other species or refers only to Homo Sapiens. However, what seems clear is that these disorders originate with human emotions and are not present in animals, unless for induced autism in rats using Sodium Valproate I believe.
Regarding Theory of Mind, I read in this paper both spectrums are associated with low ToM. And I have read genes related to autism and schizophrenia are from the same family. The DSM-V indicates they are both spectrums, but neurologically they could represent a single entity.
I have also read that Neanderthal genes reduced the affinity for schizophrenia in Sapiens:

The study also reveals the discovery of a Neanderthal allele of a gene called ADMTSL3 that reduces the risk of schizophrenia, but influences height. "Our results show that the causal mutation was inherited from Neanderthals," states McCoy.

Source: agenciasinc.es.
So, my theory to be refuted is that, when these genes mixed with Sapiens, they might have produced two outcomes:

More functional autism and Asperger in autistic Sapiens.
Less severe and/or less frequent schizophrenia in Sapiens.

If correct, this could be associated with the fact that 200,000 years of Neanderthal existence might have resulted in more stable genes for processing Neanderthal emotions, genes from which Homo Sapiens potentially benefited.
My theory would imply:

Autism in Sub-Saharan people is more severe.
Schizophrenia in Sub-Saharan people is more frequent and severe.

Has there been any study about this using PANSS, PAUSS or other index that could potentially refute my theory?
*Original english speach corrected using GPT-4, an OpenAI product.

I found a study that matches with this: First, in four independent case-control datasets totaling 9362 individuals, individuals with schizophrenia had less Neanderthal-derived genetic variation than controls (p=0.044). Second, in 49 unmedicated inpatients with schizophrenia, having more Neanderthal admixture predicted less severe positive symptoms (p=0.046)

This is not a paper but also matches for less Asperger in Sub-Saharan populations: Among children of women who were born in sub-Saharan Africa only 1 case of Asperger's was recorded, but the risk for the more classical form of autism (the more well-known form that is associated with lower intelligence) was found to be relatively high with 11 cases found. Among Europeans, in contrary, Asperger's and autism were much more evenly spread.


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What is the highest SAT score on record for someone with moderate intellectual disability?
What is the highest SAT score on record for someone with moderate intellectual disability?

The SAT standard deviation is 217 points, which means that most people
scored within 217 points of the mean score

Has anyone with moderate ID ever scored 1600 or near to that?

This is not information that is generally disclosed during testing. It is difficult to determine such a thing without proper testing. Research would mean either finding a pool of participants who met some defined standard of an “intellectual disability” and administering the test, or locating the results of tests taken by people vetted as such. I do not know how you would go about determining that, however.
I realize this doesn’t answer the question but I hope it helps understand why it has not been answered.

Worth noting: the SAT correlates highly with IQ tests which are the determiner of intellectual ability. The question is asking the equivalent of "What's the highest IQ score a person with a low IQ score has gotten?". Or more properly, what the correlation is between IQ score and SAT, I can't find a quantifiable measure (excepting an old army IQ test at 0.82
to 0.86), just the statement that it's "high".

I feel your interpretation is an oversimplification but if that is the intended meaning perhaps the wording should more clearly reflect that it is supposed to be that general.

It's a simplification, perhaps I overdid it. SATs aren't that familiar to me being in the UK, but what little I gleaned from a search is in my comment.  I'm not sure they're intended to be an IQ test per se, but the relationship is intimate apparently. As with everything, diligence in studying makes a big difference no doubt plus other factors.

The distinction to me I suppose is how generally to interpret “mental disability.”
An SAT is mainly for college entry and taken during high school. It is notoriously biased but also something that can be prepped for. Theoretically one could have a learning disability and do well on the test.
However, my point was just that we would generally not know their IQ for comparison to consider how high a low IQ person scored.


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Need help understanding the early visual system towards a scale invariant representation
My research team is looking at understanding how the brain makes a scale and rotation invariant representation of objects.
We are composed of computer scientists and are a little ignorant on modern neuroscience.
Currently, we understand that the retina samples in a log-polar fashion.
This log polar sampling on its own is scale and rotation invariant, up to a horizontal or vertical shift in the log-polar representation/plot.
However, we are working on modelling what happens to the visual input signal past the retinal-thalamic connection.
To our understanding, as the visual signal reaches V1, and goes through V2 and V4, there is repeated log-polar sub-sampling occurring.
We have been developing some visualization program to model what we know of how the system works.
So for example, we are able to generate a log-polar frame of given dimensions and parameters, (much like what is done in this paper: https://link.springer.com/article/10.1007/s12559-016-9430-8) and then sampling with on or off center receptive fields to represent the retinal layer.
After sampling from an input image, we generate a 'compressed cartesian' representation of the image, where we remove spatial information mimicking how we think the signal would be passed and compressed through the optic nerve and enacting cortical magnification.
Then we'd repeat this multiple times in a sensory processing hierarchy, with different log-polar parameters, representing the different layers of the visual system.
In the interest of time, I have below a crude sample of an input checkerboard pattern. I can update with a better image in some time, but the first layer represents the retina, the second V1, and so on (the chosen parameters are not bio-fidelic, we'd be reducing in image dimensions on a good run of the program). The first column represents the signal that the layer is receiving (the blue indicates the visual field), the second is the compressed cartesian representation after sampling, and the third column is the log polar representation.

So, is this really a good way to model how it works?
Further, we've noticed that repeated log-polar sampling causes cortical magnification that distorts in a manner kind of like a lens. We were wondering if anyone has viewed the propagation of visual signals with an optic lens analogy before.
Any pointers to references would be greatly appreciated.


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Why is Autistic Spectrum Disorder compatible with the Schizophrenia Spectrum in the DSM-V?
I am curious why DSM-V says autism spectrum disorder and schizophrenia spectrum disorder are compatible. I am geologist, and all that topic about autism smells to me like a biologic cold adaptation with a sligthy different origin than schizophrenia.
Just I am asking, as I should be missing something, but:

In this paper it is said autists have low CB1 receptors density.
In this other paper it is said schizophrenics have high CB1
receptors density.

Why the compatibility then? CB1 receptors are not quantum particles.

We do not understand what causes either autism (ASD) or schizophrenia in the brain. There are some theories and ideas, but nothing conclusive and certainly nothing as simple as a single receptor. There may be gene variants that are associated with ASD or schizophrenia, or findings in histology or neuroimaging that correlate with ASD or schizophrenia.

In the first paper that you link, about CB1 receptor density in autism, one of the citations, reference 21, is this one:

Purcell, A. E., Jeon, O. H., Zimmerman, A. W., Blue, M. E., & Pevsner, J. (2001). Postmortem brain abnormalities of the glutamate neurotransmitter system in autism. Neurology, 57(9), 1618-1628.

This paper includes two different genome-wide studies, each with very few individuals. For the CB1 receptor specifically, one of the studies showed more CB1 and the other showed less. It isn't clear to me why the authors have taken this to mean "CB1 is low in ASD"; the evidence they provide for this is extremely weak and perhaps non-existent, at least based on the given reference. You absolutely should not take this to mean "low CB1 causes autism" or that everyone with ASD has less CB1 than everyone without ASD.

In the second paper, about schizophrenia, there are several statements that suggest higher CB1 receptor density in various brain regions, but also examples of failures to find any differences. Again, it seems there is some evidence for this but it is weak and not necessarily causal. They also mention caveats in interpreting these data:

Assuredly, there are many confounding factors influencing the results of post-mortem studies, such as antipsychotic treatment, cannabis smoking and the heterogeneity of biochemical techniques.

Let's look into one of these papers results, Wong, D. F., Kuwabara, H., Horti, A. G., Raymont, V., Brasic, J., Guevara, M., ... & Cascella, N. (2010). Quantification of cerebral cannabinoid receptors subtype 1 (CB1) in healthy subjects and schizophrenia by the novel PET radioligand [11C] OMAR. Neuroimage, 52(4), 1505-1513.. Here is a figure from that paper (figure 5):

In this figure, there are 4 panels each corresponding to a different brain region. The y-axis is a measure of CB1 density (after some processing); the x-axis is age. The black symbols, solid lines, and dashed lines represent non-schizophrenic participants, the average linear relationship with age, and confidence intervals around that relationship, respectively. You could roughly consider any points between the dashed lines as "similar to normal for a given age". Notice where the red points are, indicating schizophrenia: for most brain regions and most participants, there is no real way to distinguish them from "normal" using this measure. There might be an overall group difference between schizophrenia and controls, but this is mostly due to a couple of outliers. Many of the schizophrenia participants have lower CB1 than the average non-schizophrenia patient: all the red points below the black lines. In this particular paper, they compared 19 brain regions and only found a significant difference (p<0.05) in one of them, the Pons, which did not appear to be a place they expected to find a difference ahead of time. It does not appear the authors corrected for multiple comparisons. You would expect to find a significant result p<0.05 purely by chance in one out of 20 comparisons - that's what the 0.05 threshold means, that 5% of the time an effect that large occurs if you assume there is no actual difference; it's unlikely this result would survive correction so it should not be considered significant. They need a much larger sample to assess if there is any real difference.
That doesn't mean that there isn't some real group difference here when considering the other studies as well, but a difference between groups is not the same as saying that every individual in each group follows the same pattern, and like for ASD the evidence for a link here seems very very weak.

In summary, the relationship between CB1 density and ASD or schizophrenia is quite weak and does not support a causal link between that receptor either condition. From the available data, it seems that most people with either ASD or schizophrenia do not have CB1 receptor densities that distinguish from the overall population distribution.

Hello Bryan. At the hospitallization I earned rep with the psychiatrists and some of them are going to read this and my theory of autism, my phd subjet in a couple of years, tomorrow. As I told you in the chatroom, not convinced. Some of the schizophrenics with not high CB1 could be delusional patients and the autist of that ancient post mortem study schizophrenics. Rats with induced autism with valproate show low CB1 in recent papers. Recent papers sugest also delusional disorder has mild negative symptomatology

@Universal_learner I'm happy to review other specific papers about this; the evidence presented in the ones you mentioned in the original post is all I've evaluated. That evidence is very weak. It may still be of interest to study, but I wouldn't base conclusions on such weak evidence.

alterations of CB1 receptors might contribute to deficits in social reward processing associated with ASD. Consistent with this, reduced CB1 receptor expression was found in postmortem brains of individuals with autism


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Is it possible to read faster by converting text into shorthand form or symbolic or logoraphic notation?
People often use speed-writing and stenography to write or type faster, and more words written in a logographic language such as Chinese or Japanese can fit into a standard tweet on Twitter than in a language with a regular alphabet that has no logograms or lexigraphs.
Would it be possible to read a book faster by converting it into a shorthand version of one's native language? If subvocalization creates an upper limit on reading speed, then wouldn't reading a shorthand version of a language reduce both the total amount of text to read and the amount of time spent subvocalizing each word in the text?


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How common in general population sexual arousal towards children?
What percentage of the general population have attraction to children (not teens) ?
Not how much are child molesters but how many feel attraction.
I will appreciate if you can give research in your comment.
Mode

Related: At what age are women perceived to be most attractive?


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How related are the notions of TV and Social Networks "addictions" to lack of physical social interactions?
QUESTION
What are (if any) the scientific bases to claim that the people from the western civilization who complained about fictions (e.g. movies, tv series, etc.) and social networks (e.g. Facebook, Instagram, TikTok, etc.) "addictions" are actually lacking "real" (i.e. physical) social interactions in their life, and are resorting to the simulated social interactions to fill voids in their life and, in turn, fail to take efforts to fill them with real social interactions, rendering them dependent to such simulations?
BACKGROUND

There are various references to the concept of "social media addiction":

There are some literary examples (e.g. Flaubert's depiction of "Madame Bovary") describing people lacking in such personal relations in their life as "escaping" by reading stories full of personal relations.
The main character of Cory Doctorow's latest novel "The Lost Cause" has a self-conscious routine before checking social media on his phone to (tentatively) avoid getting addicted to it.
Popular health websites title present discussions of "Social Media Addiction", defined informally as "losing several minutes (or even hours) at a time after using social media", describing the dopamine effect of social media on the human brain.

There are some references to addiction behaviors (not just to social media) being related to a lack of social connection:

Johann Hari (a criticized journalist) claimed in his TED talk that "the opposite of addiction is not sobriety, it’s connection", describing an experiment comparing the potential for addiction between rats in a boring environment  and rats in a life enriched environment.
Robert Weiss (a Doctor) stated in "Psychology Today" that "many 21st Century addiction specialists have espoused for years (the concept) that addiction is not about the pleasurable effects of substances, it’s about the user’s inability to connect in healthy ways with other human beings. In other words, addiction is not a substance disorder, it’s a social disorder."
Researchers described (in 2020)  how the recovery from cocaine addiction of rats was greatly improved through environmental enrichment.

So, I am a bit confounded between any addiction being related to social isolation, or addiction to social media being related to it, or no relation between the three phenomenon.

This seems very broad.


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Can a blind-from-birth individual experience vision or visual imagery during a Near-Death Experience (NDE)?
I recently watched a testimony in which a blind-from-birth individual described two NDEs they had had in which they supposedly were able to see with 20/20 vision (inside the NDEs). The person explained that normally they only have dreams in terms of sounds, smells, touch, taste, but never with visual imagery, which made the experience of sight during the NDEs quite shocking to them. Is this something that has ever been medically documented, and if so, does it have an explanation?
UPDATE:
A video with an interview is available here. Title: Vicki Noratuk Blind Person NDE
I also found a journal article referencing this case. Title: Near-Death and Out-of-Body Experiences in the Blind: A Study of Apparent Eyeless Vision, Kenneth Ring, Ph.D. Sharon Cooper, M.A. University of Connecticut. Journal of Near-Death Studies, 16(2) Winter 1997. 1997 Human Sciences Press, Inc.
In the article, the authors put forward Eyeless Vision and Transcendental Awareness as a possible explanation for these sorts of cases, but I don't know if this hypothesis has any merits from a scientific standpoint.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

I gather from the chat comments that this question is really about the scientific credibility of reports of visual experiences in the congenitally blind during NDEs. I cannot find any such reports in the scientific literature.
The Ring & Cooper (1997) study (re-reported in Ring & Cooper, 1999; Ring, 2001) is the only apparent exception. Other reviewers (eg, Long, 2014; Ilic et al, 2023; Beauregard, Trent, & Schwartz, 2018) seem to concur that this is indeed the only such study published. Thus, the question really comes down to the credibility of this single study.
For critical reviews of the study, see for example Irwin (2000), Fox (2003), and Augustine (2007). I'll also outline some of my own reasoning on this:

I would generally not make any strong conclusions based on a single unreplicated study. Multiple studies, a literature review, or a meta-analysis would be better.
This study is effectively self-published (the lead author Kenneth Ring was the chief editor of the journal it was published in). I would prefer an independent scientific journal.
The study was small for the conclusion in question (only 14 congenitally blind participants). It's therefore unlikely to have had sufficient power for firm conclusions.
The study quality was poor. It involved unstructured (read: easily biased) retrospective (read: unreliable memory) interviews (read: qualitative instead of quantitative) of carefully selected participants, with no hypotheses or controls, and using exploratory analyses.
All that said, the authors don't actually conclude that congenitally blind NDEs involve visual experiences anyway!

As summarized by French (2005):

Initial readings of such accounts often give the impression that the
experience involves seeing events and surroundings in the same way
that sighted people do, but closer reflection upon these cases
suggests otherwise. As Ring (2001, p. 69) writes,

As this kind of testimony builds, it seems more and more difficult to
claim that the blind simply see what they report. Rather, it is
beginning to appear it is more a matter of their knowing, through a
still poorly understood mode of generalized awareness, based on a
variety of sensory impressions, especially tactile ones, what is
happening around them.

Ring argues that casual readers may often gain the impression that
such NDEs in the blind involved literally seeing events and
surroundings but that this impression is based upon having to describe
these experiences, no matter how they were originally coded, in
linguistic form. Our language is based largely upon the experiences of
the sighted and is therefore a ‘‘language of vision’’.

I personally find it incredulous that during their very first visual experience, congenitally blind people would be able to identify objects and persons with the same expertise as sighted people, and the authors seem to agree.
There is one more nail in the coffin of this study worth mentioning just for completion. Pseudoscience is subject matter that appears on the surface to be science, but actually fails to qualify as science. This paper contains several red flags for pseudoscience:

The study was funded by the Institute of Noetic Sciences, an organization focused on pseudoscience topics.
The lead author Kenneth Ring's career is largely focused on pseudoscience.
Wikipedia generally characterizes such NDE studies as pseudoscience.
The paper itself discusses pseudoscience topics and references other pseudoscientific sources.


text:
Calculating Intra-Assay Coefficient of Variance
I am using cortisol data for my master's thesis and I need to report inter-assay and intra-assay coefficient of variance [CV]. In my study, we collected vials of saliva at 5 different time points. The lab that assayed our samples gave us intra-assay CVs for the 5 vials. How do I calculate the overall intra-assay coefficient of variance? Do I calculate an average of all 5 CVs for each participant, then average down the column to get one overall CV%? OR, do I average down the column for each CV, and report the 5 different CVs?


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Where to find reports of A/B testing about ways to alter beliefs about scientific facts?
QUESTION
Where can I find examples of protocols and results of A/B tests of techniques to alter one subject's belief about scientific topics (aka Educating them)?
BACKGROUND
A Theoretical Computer Scientist for the last 20 years, I recently started to work on automatizing psychological processes and experiments (with both humans and other animals than humans), and showing how this can lead to the expected quantitative improvements (the usual outcome of automatizing things) but also qualitative ones (automatizing processes can decrease the quality of the process output, but in some cases it results in neat qualitative improvements).
After some success automatizing some experiments with other animals than humans, I am working on proving the point above through some experiments with humans, and in particular I am thinking about designing some (automatized) A/B tests to compare (automatized) interventions to alter a subject's conviction about some scientific facts (and properties) related to fossil fuel production peaks, greenhouse gazes, population overshoot.
As I did not find such studies in the existing scientific literature about such topics in journals with themes related to climate change (e.g. Nature Climate Change), I assume that there is none in the existing scientific literature about changing people's belief, but I am a bit at a loss as to which journals to consult, and could anyway benefit from reviewing previous work about (not so automatized) interventions to change some subject's beliefs.


text:
To what degree are discussions and concepts within philosophy of mind relevant in the field of neuroscience?

Philosophy of mind is a branch of philosophy that deals with the nature of the mind and its relation to the body and the external world.
The mind–body problem is a paradigmatic issue in philosophy of mind, although a number of other issues are addressed, such as the hard problem of consciousness and the nature of particular mental states. Aspects of the mind that are studied include mental events, mental functions, mental properties, consciousness and its neural correlates, the ontology of the mind, the nature of cognition and of thought, and the relationship of the mind to the body.
(source: Philosophy of mind | Wikipedia)

Relevant topics discussed in philosophy of mind include:

Mind-body problem
Mind–body dualism
Qualia
Hard problem of consciousness
Type physicalism
Anomalous monism
Psychophysical harmony
etc.

Does the field of neuroscience acknowledge any of these and related discussions in philosophy of mind as legitimate issues and topics of inquiry? For instance, does neuroscience recognize the hard problem of consciousness as a genuine issue?
Additionally, does the field of neuroscience adopt any philosophical assumptions? For example, is reductive materialism assumed a priori to be the case in neuroscience research?

Philosophy of mind and neuroscience are both very broad fields, and their overlap is extensive. This overlap can to a degree be characterized as "neurophilosophy":

... the interdisciplinary study of neuroscience and philosophy that
explores the relevance of neuroscientific studies to the arguments
traditionally categorized as philosophy of mind.

I think a great example of such interdisciplinary study is the neuroscience of free will:

... a part of neurophilosophy ... the analysis of how findings from
[neuroscience] studies may impact the free will debate.

Beginning in the 1980s with the well-known Benjamin Libet experiments, neuroscience has had much to say about free will. The hard problem of consciousness is a more complicated example:

It has been accepted by some ... cognitive neuroscientists such as
Francisco Varela, Giulio Tononi, and Christof Koch. On the other hand,
its existence is denied by other ... cognitive neuroscientists such as
Stanislas Dehaene, Bernard Baars, Anil Seth, and Antonio Damasio.

The typical neuroscience approach to the hard problem has been through neural correlates of consciousness (NCC):

A science of consciousness must explain the exact relationship between
subjective mental states and brain states, the nature of the
relationship between the conscious mind and the electro-chemical
interactions in the body (mind–body problem). Progress in
neuropsychology and neurophilosophy has come from focusing on the body
rather than the mind.

Both neuroscientists who accept and deny the hard problem see NCC as a way forward, and this has been a very active area of research. Note that there are other scientific approaches to the hard problem outside of neuroscience, such as in AI.
Since there isn't agreement about the hard problem amongst neuroscientists, I think it's fair to say that neuroscience does not assume materialism (certainly not the reductive or "type" kind). More generally, there are several competing claims regarding what assumptions (if any) underlie scientific research, such as naturalism, causal closure, coherentism, or even none at all. The matter is not settled.


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Can schizoaffective disorder be present with no negative symptomatology
In addition to delusions and hallucinations, schizoaffective disorder involves mood alterations.
Is the presence of negative symptomatology necessary for diagnosing schizoaffective disorder, or is mood alteration sufficient if delusions are present?

I'm afraid something got lost in translation here. What do you mean by: "Can X course with Y ..."? I can't make sense of this sentence/question.

According to the DSM-5, negative symptoms is not a diagnostic requisite for schizoaffective disorder. Negative symptomology is included as a specifier only if the patient presents with these symptoms.
Further, it is important to note that delusions and mood alterations are not the only diagnostic criteria for this disorder. Patients must meet Criterion A for Schizophrenia that occurs concurrently with a major mood episode (must include depressive and may or may not include manic); and at least 2 weeks of delusions or hallucinations without the presence of a mood episode. Also, symptomatic etiology must not be the result of a substance-induced disorder.
Regarding specifiers, clients may present with either Biopolar or depressive type, and may include catatonia. Negative symptoms are remarked in the "Severity specifier" section if present and its severity is rated on a scale of 0 - 4.


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Understanding as a mental simulation of reality
This is a follow up to an earlier question. It appears that there is very little research of this phenomenon, our capacity to piece together and visualize a mental simulation of things we are trying to understand. This higher-level capacity stems from our basic ability create mental imagery, visual imagery in particular -- and there is plenty of research of that basic ability. However, creating the actual simulation also involves other mental skills, skills like:

The ability to connect the dots, to assemble, like a puzzle, larger models from smaller parts.
The ability to run this simulation by visualising how the smaller models interact and work together as parts of a virtual machine (of a virtual reality).

These additional skills allows us to create, in our minds, an interactive simulation of the world (rather than visualise static images), and use that simulation to achieve insights into how the reality operates under the hood,1 and to predict real-life outcomes.
This capacity would explain the success of Carl Rogers' person-centered approach (a person have to piece together their own understanding by themselves, no one can do it for them). It also explains Lev Vygotsky's zone of proximal development -- a person can only add the pieces of the puzzle, so to speak, that are adjacent to the already completed parts.
Given the above, I wonder why there is so little research into this capacity? Is it because it is difficult to master and, therefore, quite rare?2 Or because those of us who did master this skill lack the necessary introspection?
After all, only if we ourselves are conscious of this experience -- of how we understand things -- we would discover better ways of helping others, especially the children, to discover the same ability in them.
UPDATE: Even though this model of understanding cannot be confirmed by direct observations, it can still make testable predictions.3 For example, we can start encouraging students to visualize, in their minds, the problems they are being asked solve, as well as the material they are trying to understand -- and then see if that improves their academic performance.
1 For example, the discovery of the universal gravity by Isaac Newton.
2 Which would explain why the capacity to understand varies widely -- in classrooms, etc.
3 One can even argue that a theory can only be useful if it is testable -- if it can point out the actions that would lead to favorable outcomes. However, even this was not always the case. For example, the heliocentric cosmology didn't immediately lead to any testable predictions. However, it was an important piece of the puzzle and, as such, instrumental in discovery of the Newton's laws of motions as well as the universal gravity. Ironically, it took a whole century after Newton's discovery to observe and measure the gravitational force directly (and only in 19th century we discovered a way to confirm the Earth rotation -- by that time even Catholic church accepted it as a fact). None of this might be relevant to psychology per se, but it is important to know when we try to understand what science is about.

Observation is quite limited as a tool in science compared to experimentation. The phenomenon you're describing are not very accessible experimentally, so there are limits on what can be studied. There is a lot of study "around the edges", though, I mean basically the entire field of cognitive neuroscience would be just one of those edges. You also have people approaching it from more of a philosophical view, people trying to come bottom-up with mathematical formulations, but ultimately many of the hypotheses made can only be tested very indirectly.

I think in general it's a mistake to think that something we're "conscious of" gives us all that much insight into how it actually works; if you sit in a chair you probably think you're more or less sitting still but you're actually rotating quite rapidly around a massive object that is hurtling through space at unimaginable speeds in another reasonable reference frame.

@BryanKrause -- I wholeheartedly agree, this theory can only be tested indirectly (and  that's why I mentioned some of the indirect evidence). Even so, there might be a way to test it -- for example, by finding new methods to encourage and develop this capacity in children and to see if this would improve their academic performance.

There is also a lot of research into education at all ages with various motivating models, ranging from the practical to the theoretical; you'd have to first figure out what the new method is that would be motivated by whatever you're proposing and how that's different from what has already been tried whatever the motivation. Similarly in medicine, comprehensive models have not been that successful in leading to actual treatments; usually we work the opposite direction, we have something that we know works and spend our time trying to figure out why.