text:
Talk:Neurofeedback

Removed paragraph about endorphins
I removed a paragraph that tried to make the case that although there is no known scientific explanation for the perceived effectiveness of neurofeedback therapies, no one understood how endorphins worked at one time either. Off topic and illogical. Highnumber (talk) 00:04, 20 November 2010 (UTC)
 * I must Correct my self I undid your change under the misrepresentation that you had added the section not removed it.Donhoraldo (talk) 07:49, 23 November 2010 (UTC)

Removed section "Evidence based"
The section was reporting on one meta analysis of only 15 studies, all but 2 with a N less than 100. All with tiny effects. A third of the studies, including one studies composing nearly half of the patients of the entire meta analysis uncontrolled, that's 718 out of a N of 1194 with no controls on a completely subjective test. All we can say from this is the analysis is completely worthless and thus the section talking about the meta analysis is completely worthless.Donhoraldo (talk) 19:47, 1 November 2010 (UTC)

Does neurofeedback have to be EEG?
The article defines neurofeedback as: "Neurofeedback is a type of biofeedback that uses electroencephalography to provide a signal that can be used by a person to receive feedback about brain activity." Though, similar things can be done using fNIR and other methods, and a quick google search shows that the term seems to be used here as well. Øln (talk) 17:30, 15 January 2011 (UTC)

Questionable quality and neutrality
I added Advert and verification tags to this article (with IP address, sorry). I came to this article to study the efficacy of the method (questioned here: http://www.quackwatch.org/01QuackeryRelatedTopics/mentserv.html). I'm not an expert in EEG-biofeedback as such, but am familiar with usage of EEG and other physiological signals in psychological research. My understanding is that neurofeedback methods are not a very central component in mainstream psychology or therapy, but this doesn't of course in any way mean they don't work. However, given this background I was surprised that the efficacy isn't discussed much here. Also I find the structure a bit odd and the article stresses too much some in my opinion quite trivial aspects such as over detailed sections about certification and "Neurofeedback in practice". Also many of the references are to specialized biofeedback journals and a bit questionable websites with vested interests. --Jampekka (talk) 22:27, 7 October 2011 (UTC)
 * This article illustrates one of Wikipedia's greatest weaknesses: articles about fringe topics that not many editors are interested in are easily dominated by enthusiasts, who make it more trouble to clean them up than it is worth.  This article really ought to be trimmed of a lot of unsupportable statements.  And you should certainly not use it to study the efficacy of the method -- more accurately you shouldn't believe anything it says. Looie496 (talk) 23:58, 7 October 2011 (UTC)
 * I indeed ran into the same problem over at Great Pacific Garbage Patch. But its good for me to see it here too, makes me more aware of the problem. I also second the skepticism for overly enthusiastic claims. Jacealcard (talk) 21:34, 13 December 2011 (UTC)
 * I've killed the "sites of interest" and "research and development" parts of the external links section. WP:NOT a link farm. I also cleared a the crap and dead links from the only remaining section. Link farms are usually another sign of the type of problems you describe; nobody is paying attention, so the article acquires more and more links over time --GraemeL (talk) 21:50, 13 December 2011 (UTC)
 * Very good! I'll try to help out if trouble arises. Looie496 (talk) 23:37, 13 December 2011 (UTC)

Quality
Well this article needs to be improved a bit, sadly I'm more or less out of time for this. Here are a few points why, in my humble opinion, this is necessary:

1. The article is mainly about EEG-Neurofeedback, which is fine with me as fMRI-NFB is relatively new and it is really hard to find someone with this technology. However, we should clearly distinguish between EEG-NFB and fMRI-NFB which is not always the case in this article. A few examples
 * In the beginning NFB should not be called EEG-Biofeedback (even it is done in some parts of the article), simply because this is not 100% correct, because of fMRI-Neurofeedback. We should write that there are 2 types of NFB, one is called fMRI-NFB (experimental status and not commonly available) and the other EEG-NFB or EEG-BFB (which is “commonly” available and not so experimental anymore).
 * If this article would clearly distinguish between EEG-NFB and fMRI-NFB then there would be no sentence like “Sensors are placed on the scalp to measure activity, with measurements displayed using video displays or sound.” because this is not the case for fMRI-NFB. Just read a bit in the fMRI article and you know why. I would write something like “In EEG-NFB sensors are placed on the scalp to measure (brainwave) activity, with measurements displayed using video displays or sound.”. I personally believe that there should be a short section about fMRI-NFB ( pro (“deeper” in the brain) and cons(expensive and not for everyone) of the technology (measures something different than EEG-NFB) vs EEG(“inexpensive”, but only the brainwaves on the “surface”))and then we should write that for the rest of the article we are always talking about EEG-NFB or we always have to write EEG-NFB. That would make it easier for everyone to understand.

2. We should only use EEG-Biofeedback in the beginning of the article an then EEG-NFB for clarity (and because the article is called Neurofeedback...)

3. “Definition” should not include something like the effectiveness of the therapy, rather what it is or not, what types there are and their differences and how it works. Maybe that's already to much...

4. The same for the “Training process”, it should not include something about the effectiveness...

5. We should split the history section from the application section! I would suggest a list with the efficacy level or different sections with the research or both.

6. Maybe we should have a brainwave section (alpha, beta, theta SMR and so on) Thats it for now. Best Regards --Cyrus Grisham (talk) 09:28, 14 January 2012 (UTC)
 * A brainwave section seems unnecessary; this is covered at EEG. — Preceding unsigned comment added by 121.98.57.188 (talk) 13:17, 27 August 2012 (UTC)
 * A brainwave section seems unnecessary; this is covered at EEG. — Preceding unsigned comment added by 121.98.57.188 (talk) 13:17, 27 August 2012 (UTC)

In the ADHD section the last sentences: "Further research on the benefits of neurofeedback for ADHD is warranted given this history of mixed results. Future research on   this treatment needs to employ appropriate sham neurofeedback or other attention-placebo control groups, double-blinded procedures    and measures of ADHD collected both in school and at home to better evaluate the efficacy of this treatment for ADHD." Either needs a reference, should be removed as OR, or perhaps a new section can be added to the article describing current research topics in Neurofeedback science and application. — Preceding unsigned comment added by 68.166.58.11 (talk) 20:49, 25 July 2013 (UTC)

Wow, this page is terrible
This page is full of psuedoscientific mush. Why have so many "citation needed" tags been tolerated? If you don't believe me about the questionable nature of it, just google neurofeedback quackery. Here's good summary by a neurologist: http://theness.com/neurologicablog/index.php/neurofeedback-and-the-need-for-science-based-medicine/

A lot of the "sources" on the page are from advocacy groups like Association for Applied Psychophysiology and Biofeedback, which should not be considered unbiased.

Sterling.M.Archer (talk) 05:33, 19 November 2012 (UTC)

 * If you would like to do some cleanup on the article, I'll back you up if you run into difficulties. Looie496 (talk) 16:08, 20 November 2012 (UTC)
 * Thanks, I've already started. I've removed many of the undocumented claims and added the beginning of a criticism section with proper documentation. Sterling.M.Archer (talk) 17:59, 20 November 2012 (UTC)
 * Hi I'm not up on EEG, but there are medical devices with 510K clearances from the FDA that are in use. I was wondering if more discussion on the the instruments would be helpful. I have attached one clearance for your review. Let me know what you think. Definitely an interesting topic.Thisandthem (talk) 14:30, 4 December 2012 (UTC)
 * Isn't the document just regarding a product's safety? Sterling.M.Archer (talk) 21:34, 4 December 2012 (UTC)
 * No, it is a clearance from the FDA which gives approval for use as a safe Medical Device.Thisandthem (talk) 13:21, 8 December 2012 (UTC)
 * That's what I mean. The document states that the device is safe, but it has no content regarding efficacy (unless I missed something). Sterling.M.Archer (talk) 20:35, 20 December 2012 (UTC)
 * No, it is a clearance from the FDA which gives approval for use as a safe Medical Device.Thisandthem (talk) 13:21, 8 December 2012 (UTC)
 * That's what I mean. The document states that the device is safe, but it has no content regarding efficacy (unless I missed something). Sterling.M.Archer (talk) 20:35, 20 December 2012 (UTC)
 * That's what I mean. The document states that the device is safe, but it has no content regarding efficacy (unless I missed something). Sterling.M.Archer (talk) 20:35, 20 December 2012 (UTC)
 * That's what I mean. The document states that the device is safe, but it has no content regarding efficacy (unless I missed something). Sterling.M.Archer (talk) 20:35, 20 December 2012 (UTC)

Needs more recent information
"COMMENT: The last reference above is from 2000. Biofeedback technology has changed significantly, and the quality of research has improved relative to the 1990s timeframe. The title of the peer-reviewed [?] journal and sponsoring organization offers no re-assurance in terms of bias." This comment was made by editor 71.105.89.231 in the criticism section. (And it's me who moved this comment to the talk page.  Lova Falk     talk   08:57, 12 January 2013 (UTC))
 * Hi 71.105.89.231! You seem to be quite knowledgeable about this subject, so please, be bold and add or rewrite this section, using reliable sources. With friendly regards,  Lova Falk     talk   09:00, 12 January 2013 (UTC)
 * Hi Lova - thanks for the encouragement. My background is mathematics/engineering, although psychology and neurophysiology are areas of great interest to me.  I'm investigating the possibility of getting training in neurofeedback and/or biofeedback so I can work with my wife, a psychiatrist, in her practice.  I like the quality of comments among the contributors to this page and appreciate the light/humble tone you provide given the tentative and tenuous nature of knowledge - especially involving the brain/mind.  I'll contribute when/if possible.  Best regards, Jeff Daniels [jsd1415 >at< hotmail.com] 71.105.89.231 (talk) 21:23, 13 February 2013 (UTC)
 * Thank you Jeff, I'm looking forward to your edits! Have you considered [|creating an account]? With friendly regards,  Lova Falk     talk   09:22, 14 February 2013 (UTC)

Moved APA "Reference"
Moved text:

Where to start... First of all, the PDF from the AAP references "biofeedback", not "neurofeedback". They are related, but not the same. Secondly, this is basically a quick reference chart for pediatricians on potential therapy. It does not in any way discuss scientific literature or studies. There's a good chance that if the AAP put this out, they have some other documentation on their website, but this is not really evidence. Sterling.M.Archer (talk) 20:00, 27 January 2013 (UTC)

To summarize, the statement "these criticisms... are now moot" isn't even remotely born out by the reference. Sterling.M.Archer (talk) 20:02, 27 January 2013 (UTC)
 * Had those who removed this section bothered to check, the APA referenced DOES INCLUDE neurofeedback. This can be verified by contacting PracticeWise that compiles the Evidence-based practices list for the APA. — Preceding unsigned comment added by 68.4.194.86 (talk) 23:50, 1 February 2013 (UTC)
 * I'm looking at the PDF from the reference right now . It's only one page, so there's not much to read. I've also searched for "neuro" to make sure I'm not missing anything. Can you point out where in the document neurofeedback is referenced? I can't find a single thing. Sterling.M.Archer (talk) 00:40, 2 February 2013 (UTC)
 * I have a list, from PracticeWise, the agency that creates the list for the APP. They gave some very specific and recent examples of the studies that were used. I will post those later. In addition, you can contact PracticeWise and they will confirm those references. FYI, these references include:
 * Beauregard, M., & Levesque, J. (2006). Functional magnetic resonance imaging investigation of the effects of neurofeedback training on neural bases of selective attention and response inhibition in children with attention-deficit/hyperactivity disorder. Applied Psychology and Biofeedback, 31, 3-20.
 * Gevensleben, H., Holl, B., Albrecht, B., Vogel, C., Schlamp, D., et al. (2009). Is neurofeedback an efficacious treatment for ADHD?: A randomized controlled clinical trial. Journal of Child Psychology and Psychiatry, 50, 780-789.
 * Levesque, J., Beauregard, M., & Mensour, B. (2006). Effect of neurofeedback training on the neural substrates of selective attention in children with attention deficit/hyperactivity disorder: A functional magnetic resonance imaging study. Neuroscience Letters, 394, 216-221.
 * In addition, the criticisms most certainly are moot - one is merely a poorly written article found on the Internet and the other only provides a link to an abstract. The actual literature review is not available online. — Preceding unsigned comment added by 68.4.194.86 (talk) 01:38, 2 February 2013 (UTC)
 * Beauregard, M., & Levesque, J. (2006). Functional magnetic resonance imaging investigation of the effects of neurofeedback training on neural bases of selective attention and response inhibition in children with attention-deficit/hyperactivity disorder. Applied Psychology and Biofeedback, 31, 3-20.
 * Gevensleben, H., Holl, B., Albrecht, B., Vogel, C., Schlamp, D., et al. (2009). Is neurofeedback an efficacious treatment for ADHD?: A randomized controlled clinical trial. Journal of Child Psychology and Psychiatry, 50, 780-789.
 * Levesque, J., Beauregard, M., & Mensour, B. (2006). Effect of neurofeedback training on the neural substrates of selective attention in children with attention deficit/hyperactivity disorder: A functional magnetic resonance imaging study. Neuroscience Letters, 394, 216-221.
 * In addition, the criticisms most certainly are moot - one is merely a poorly written article found on the Internet and the other only provides a link to an abstract. The actual literature review is not available online. — Preceding unsigned comment added by 68.4.194.86 (talk) 01:38, 2 February 2013 (UTC)
 * Levesque, J., Beauregard, M., & Mensour, B. (2006). Effect of neurofeedback training on the neural substrates of selective attention in children with attention deficit/hyperactivity disorder: A functional magnetic resonance imaging study. Neuroscience Letters, 394, 216-221.
 * In addition, the criticisms most certainly are moot - one is merely a poorly written article found on the Internet and the other only provides a link to an abstract. The actual literature review is not available online. — Preceding unsigned comment added by 68.4.194.86 (talk) 01:38, 2 February 2013 (UTC)
 * In addition, the criticisms most certainly are moot - one is merely a poorly written article found on the Internet and the other only provides a link to an abstract. The actual literature review is not available online. — Preceding unsigned comment added by 68.4.194.86 (talk) 01:38, 2 February 2013 (UTC)

Criticism Section
The criticism section is not for debate. It is for citing examples of experts in related fields criticizing Neurofeedback. Items supporting Neurofeedback should be placed elsewhere in the article unless they are specific rebuttals to criticism. For example, if Dr. Smith wrote an article saying that Neurofeedback was bunk, and Dr. Jones wrote an article saying that Dr. Smith was wrong because of x, y, and z, then both would belong in the criticism section. Simply putting in a reference that you (as an editor) feel proves that some criticism is wrong is inappropriate. — Preceding unsigned comment added by Sterling.M.Archer (talk • contribs) 07:21, 5 March 2013 (UTC)
 * It is now apparent that you are injecting your personal bias by removing valid responses to the fallacious criticisms of neurofeedback. First, you cherry-picked the elevation of neurofeedback to the "Level 1: Best Practices" as an evidenced-based psycho-social intervention because you failed to find out what they based their decision on, and now you promote two very dated pseudo-scientific web site claims about neurofeedback, written by some of the same authors while ignoring the extant (and genuine) scientific literature on the topic. Just because you have a personal bias against neurofeedback and promote your biases via questionable sources does not give you the right to remove evidence that shows those sources are clearly incorrect. — Preceding unsigned comment added by 68.4.194.86 (talk) 01:48, 6 April 2013 (UTC)
 * He is not, he is following Wikipedia Guidelines. One of the 5 Pillars of Wikipedia is the NPOV, you know what is not neutral? The Truth. This Article lacks a Criticism Section and it is not to us to evaluate the logical soundness of the criticism, but for it to be properly referenced so the reader can decide. PuercoPop (talk) 16:41, 9 October 2013 (UTC)
 * He is not, he is following Wikipedia Guidelines. One of the 5 Pillars of Wikipedia is the NPOV, you know what is not neutral? The Truth. This Article lacks a Criticism Section and it is not to us to evaluate the logical soundness of the criticism, but for it to be properly referenced so the reader can decide. PuercoPop (talk) 16:41, 9 October 2013 (UTC)

New section
As a part of a university course dedicated to expanding Wikipedia articles related to psychology, I've added a section discussing the possible applications of neurofeedback in areas outside of medicine such as in sports and the performing arts. Any feedback would be much appreciated as I'm still relatively new to editing Wikipedia articles.StudentPSYche (talk) 15:45, 5 June 2013 (UTC)
 * I'm personally dubious about those applications, but your contribution is very well written -- far better than most student contributions that I've seen. The only thing that needs fixing is the handling of repeated refs.  When you reuse a citation, you don't have to enter all the information again.  Instead, the first time you use it, give it a "name", such as  .  Then the next time you want to cite the same source, you can just use  and nothing more (notice the / after the name; this indicates that the contents of the reference are specified somewhere else).  I could fix this for you but it's a better learning experience if you do it yourself.  Regards, Looie496 (talk) 16:50, 5 June 2013 (UTC)
 * Thanks for your feedback! I've changed the format of the reused citations as you suggested. I appreciate the tip as I'm sure it will come in handy in the future. As to the validity of the claims, there really isn't a whole lot of research yet on non-medical applications of neurofeedback outside of sports. However, the literature I reviewed in regards to applications in sports seemed more robust and fairly promising. Of course, this is still a topic that needs to be studied at greater length, however, I thought it was worth mentioning if only to highlight the fact that the applications of neurofeedback need not be solely restricted to medical purposes.StudentPSYche (talk) 04:31, 12 June 2013 (UTC)

Neurofeedback in practice
I move here a the section on how a session goes: it is completely unreferenced, quite "how to" manual, and also probably site specific and not generalizable. Not really encyclopedic. I move it here in case it serves to somebody to improve it and re-insert it (provided he finds suitable refs. --Garrondo (talk) 20:46, 27 June 2013 (UTC)

Text moved
A common professional neurofeedback therapy session today goes as follows:

 * 1) In an intake of about 90 minutes the patient will get a questionnaire and a first EEG reading. The questionnaire specifies the complaints and also helps to indicate if the referral to a specialist might be called for. In some cases but not all a full EEG will be recorded.
 * 2) If a full EEG is called for, the EEG recording is typically done on 19 - 21 sites on the scalp. It results in a brainmap ("quantitative EEG"). This is a series of maps (for each frequency one) where for each measured spot the average level of activity is shown. The brainmap is compared to a database to determine spots of over- and under activity compared to the average people of the patient's age and sex. There are several commercial providers of such databases.
 * 3) The actual session itself involves placing sensors on the head. The feedback may involve, for example, a simple light or tone or game that will move and play when certain brain activity is detected by the system. For other brain activity the rewarding tone, or light or game is taken away.
 * 4) A typical course of sessions takes 20 to 40 visits. At the beginning of each session the patient reports the course of his complaints and also mentions other mental effects. On the basis of this report the therapy may be adjusted. In some cases a patient is allowed to take a feedback machine home and have most - but not all - sessions there.

Recent Research
It seems to me that there is little on this page about the more recent research being done with neurofeedback. Also, why no mention of the trials the military is doing with soldiers with PTSD? — Preceding unsigned comment added by 24.21.86.101 (talk) 18:39, 27 March 2014 (UTC)

Please, what is this definition?
I don't understand how this sentence is placed in definition:

"Some feel that the most accurate form of neurofeedback is the one guided by qEEG,   that is usually used in clinical settings. But this approach, although being helpful,    is being seen by many as more using a linear science that is not in tune with modern,    non-linear physics."

Also: quotes? I'm pretty sure some scientific research groups don't spend too much thoughts on NFB, because they prefer other methods. Nonetheless their opinion shouldn't be placed within a definition. — Preceding unsigned comment added by 85.178.247.92 (talk) 21:45, 25 June 2014 (UTC)

Additional source: Lofthouse et al.

—Sangdeboeuf (talk) 23:26, 18 April 2017 (UTC)

In my humble opinion, this page warrants a complete rewrite
I'll keep this short because it's currently 3:00 am, but this page has several major issues, so many that it may be better to rewrite the whole thing from scratch.

- Other than in the history section, it fails to differentiate between the efficacy of different neurofeedback protocols. This would be like a page about pharmocology failing to differentiate between different classes of drugs. To say that either neurofeedback "works" or "doesn't work" would be analogous to saying that drugs, as a whole, either "work" or "don't work".

- It seems to cherry-pick its sources in certain places.

- Other than in the history section, it fails to differentiate between the different stages of the development of neurofeedback. Any study that was done in a previous developmental stage should be either removed or shown that the same protocols are still being used today.

- There is a comical discrepancy between the medium size section entirely about the efficacy of neurofeedback for ADHD and the small sliver of text that to paraphrase, says "oh, and by the way, here's a generic list of stuff that psychiatrists try to fix."

- The article seems to be slightly biased in a few subtle ways, like an opinionated "non-believer" of neurofeedback swept through the article and gave his/her two cents via adding sources, taking away parts, etc.

- The page gives no information into the mechanistic ways that it works, i.e. bipolar montage, frequency pulling, amplitude manipulation, infra-low frequencies, operant conditioning or the lack there-of, etc.

I am not an expert, but I know enough about the field to pick out these major flaws. I will help in rewriting it, but in my opinion it needs to be done by an expert in the field who is

(a): familiar with the current empirical literature on the subject (b): has an eclectic knowledge of the many different protocols (c): is unbiased and can potentially write a section about the criticism of neurofeedback

EDIT: the validity of sources also seems to be controversial since a good chunk of the research is coming from either the developers themselves or from various non-academic associations that have ties with people who are invested in the field. I would personally question whether this bias is enough to invalidate their research on the basis that it is not enough bias to influence the results of the study. It is also possible to question the validity of the "non-biased" sources because they are either too old, too sweeping, or that they may have flaws inherent to not having the expertise of someone active in the field. — Preceding unsigned comment added by 2601:282:8200:5A9E:70D3:7BCF:1CDD:99D3 (talk) 08:31, 20 May 2017 (UTC)

Biofeedback via collective conscience
Biofeedback techniques that have proven effective on the individual can be easily quantified while proof of alterations to the collective cerebral functionality may not be so readily available. Mikrochik (talk) 14:22, 17 June 2019 (UTC)

Plagiarism
So I found obvious plagiarism in the very first paragraph of this entry: the two sentences prior to the first footnote are lifted directly from the abstract to the cited article. Clearly this article was not written by experts and should be taken down. Any article dealing with a therapy or other medical intervention should be thoroughly vetted by experts--otherwise it's dangerous.

Future of article
I've tried to clean up the article the best I could the last few weeks: Improving citations, adding more accurate criticism, and reformatting. However, I mostly expanded existing sections. This article is missing three key areas which would greatly improve the scope:

1 - A discussion of the mechanisms of neurofeedback. There is scientific consensus as to how it is meant to operate, just not to the degree it is successful in all cases. Neuroplasticity could also be joined with this section.

2 - A section dedicated to procedure as well as an overview of the different protocol types and their use.

3 - An adverse effects section. Although neurofeedback is regarded as safe - headaches, triggering of seizure or migraine, or other effects from use of ISF deserve recognition.

See: Article on TMS for a better written example of another modern noninvasive brain procedure

Article overhaul of 2022-12-15
Long story short: I overhauled most of the article. I figured it's easiest to just rip the bandaid off and get it over with. Bullet points of the change follow. If you have any notes or issues the changes, you can leave them here for discussion. Apologies for keeping this short, but I'm utterly exhausted after having done this.

Changes: diff: https://en.wikipedia.org/w/index.php?diff=1127567323&oldid=1125547701&title=Neurofeedback&diffmode=visual
 * Replaced overly positive claims with statements more closely reflecting the content of their citations
 * Toned done statements about the effectiveness of treatment, and noted their caveats
 * Removed first hand sources notice, as many citations are second hand sources
 * Limited Applications section to non-medical applications only and absorbed medical applications into Criticisms section
 * Purged Further reading of anything that seemed overtly sketchy
 * Added notice about notability to Certification section. I'm not opposed to having it in the article, but I'm not convinced its particularly needed.
 * minor reordering
 * minor spelling

SkSlick (talk) 13:02, 15 December 2022 (UTC)

 * This was less of an "overhaul" and more of a decimation with some poorly researched citations sprinkled throughout. While the original article was perhaps overly positive, it appears any statement alongside neurofeedback's utility has now been met with notes from you refuting any possible efficacy. The exact extent of beneficial clinical use of neurofeedback is still finding its place in psychiatry and psychotherapy, but idea that it has no understood benefit in any case is simply not an accurate reflection of the most recent state of the literature. The changes made paint neurofeedback in as much an erroneously negative light as the original article was erroneously positive. I've added an original research disclaimer at the top to reflect your changes.
 * Frankly, it looks like the article should be completely re-written as the current state paints the technology as akin to homeopathy. I'll try and fix up the article and restore it to a neutral reflection of the SOTA if I get some time in the next few weeks. For any further changes to the article, I would recommend a thorough reading of the specific use cases of the technology. These should be enumerated clearly in a clinical usage section with the criticism section fleshed out and arguments presented clearly. In addition, a section on the neurofeedback mechanism and common protocols should be added. The summary also now needs to be cleaned up and expanded with bias removed. 2601:14D:8500:6BF0:E1A9:21EE:C1E6:3B0B (talk) 05:10, 6 January 2023 (UTC)
 * Thank you, I couldn't agree more. I started making up my thoughts on re-writing (and thus restructuring) the article as well. I think a new article will be able to reflect the current state of Neurofeedback in a much more neutral way. NF-LF (talk) 15:48, 26 January 2023 (UTC)

Complete Reset - 2023-04-28
I wrote a complete new article. The topic now focuses on Neurofeedback and also distinguishes in an organized manner the different types of neurofeedback.

Before, the article was telling more about organizations and certifications than neurofeedback itself. These might be interesting topics, but do not intrinsically have to do with neurofeedback but rather with the economics and private interests of associations.

A discussion and critique section is relevant as there are many open and even unaddressed questions and challenges in the field. NF-LF (talk) 12:06, 28 April 2023 (UTC)

Abject lack of references
As other editors have pointed out before, this article is of low quality. I'm especially concerned about the egregious lack of references. Not only is this not a science-based treatment, so we are essentially talking about a quack therapy, but there aren't even enough references to support all the various claims made about it on this page. For that reason, I'd like to go ahead and start pruning a lot of the unreferenced content. If you have references that you would like to add, please do so, otherwise, any unreferenced content is fair game for removal, IMO. Revirvlkodlaku (talk) 03:41, 30 May 2023 (UTC)

 * Yeah, the article used to be moderately well referenced, but the rewrite of 2023-04-28 got rid of basically all of it. The article used to be a lot more critical of its efficacy as well (from revision 2022-12-15 'till revision 2023-04-28).
 * Full disclosure: I authored the revision of 2022-12-15, so it's possible my opinion on the revision of 2023-04-28 may not be the most impartial.
 * There was some input (Talk:Neurofeedback) on the revision of 2022-12-15 that regarded it as hyper-critical and found it unwarranted how it attributed most or all effects of the treatment to placebo effect. In my opinion it would have been warranted to fully revert the revision of 2023-04-28 based on its lack of references and criticality, but I never planned on maintaining this article and now it's rather late to have that discussion. I'm gonna hold off on reverting or reviving content, as I don't want this to devolve in an edit war, but if somebody else thinks doing so would be better, be my guest. SkSlick (talk) 18:29, 2 July 2023 (UTC)
 * Neurofeedback is certainly not quackery. It is best should considered an emerging and still-developing treatment option. It has a specific use case, but being dismissive is not helpful. See here for a recent article (2021) which discusses the behavioral and neurological effects of the treatment as well as the limitations. To quote from the authors: "Overall, there is thus ample reproducible evidence that neurofeedback can trigger behavioural and cortical plasticity changes that result in improved cognitive functions in both impaired and healthy participants (non-exhaustive summary in Table 1). However, it would be misleading to think that the benefit of neurofeedback protocols has reached consensus. Several limits of this type of protocols deserve attention and experimental consideration. Most of these issues are not specific to neurofeedback, but are relevant to all cognitive training approaches."
 * This page should be edited and expanded, with healthy scientific disclaimers throughout, but under no circumstances reverted to the changes made on 2022-12-15. That version was a truly abysmal summarization of the literature. The current version is sparse and perhaps not the academic quality which would make for a good article, but it is a much better start than what we've seen previously. 2600:4040:2A8A:AA00:B87B:B178:392B:9CB2 (talk) 02:33, 15 August 2023 (UTC)

title: Talk:Neurofeedback


text:
Copper(I) oxide

Copper(I) oxide or cuprous oxide is the inorganic compound with the formula Cu2O. It is one of the principal oxides of copper, the other being copper(II) oxide or cupric oxide (CuO). Cuprous oxide is a red-coloured solid and is a component of some antifouling paints. The compound can appear either yellow or red, depending on the size of the particles. Copper(I) oxide is found as the reddish mineral cuprite.

Preparation
Copper(I) oxide may be produced by several methods. Most straightforwardly, it arises via the oxidation of copper metal:
 * 4 Cu + O2 →  2 Cu2O

Additives such as water and acids affect the rate as well as the further oxidation to copper(II) oxides. It is also produced commercially by reduction of copper(II) solutions with sulfur dioxide.

Alternatively, it may be prepared via the reduction of Copper (II) Hydroxide with hydrogen peroxide:

 * 2 Cu(OH)2 + H2O2 →  Cu2O  +  3 H2O +  O2

Aqueous cuprous chloride solutions react with base to give the same material. In all cases, the color is highly sensitive to the procedural details. Cu2O degrades to copper(II) oxide in moist air.

Formation of copper(I) oxide is the basis of the Fehling's test and Benedict's test for reducing sugars. These sugars reduce an alkaline solution of a copper(II) salt, giving a bright red precipitate of Cu2O.

It forms on silver-plated copper parts exposed to moisture when the silver layer is porous or damaged. This kind of corrosion is known as red plague.

Properties
Little evidence exists for copper(I) hydroxide CuOH, which is expected to rapidly undergo dehydration. A similar situation applies to the hydroxides of gold(I) and silver(I).

Like all copper(I) compounds, cuprous oxide is diamagnetic.

Copper(I) oxide dissolves in concentrated ammonia solution to form the colourless complex [Cu(NH3)2]+, which is easily oxidized in air to the blue [Cu(NH3)4(H2O)2]2+.

Cuprous oxide is attacked by acids. Hydrochloric acid gives the chloride complex. Sulfuric acid and nitric acid produce copper(II) sulfate and copper(II) nitrate, respectively.

Structure
In terms of their coordination spheres, copper centres are 2-coordinated and the oxides are tetrahedral. The structure thus resembles in some sense the main polymorphs of SiO2, but cuprous oxide's lattices interpenetrate. Cu2O crystallizes in a cubic structure with a lattice constant al = 4.2696 Å. The copper atoms arrange in a fcc sublattice, the oxygen atoms in a bcc sublattice. One sublattice is shifted by a quarter of the body diagonal. The space group is Pn$-0 cm^{3}/mol$m, which includes the point group with full octahedral symmetry.

Semiconducting properties
In the history of semiconductor physics, Cu2O is one of the most studied materials, and many experimental semiconductor applications have been demonstrated first in this material: The lowest excitons in Cu2O are extremely long lived; absorption lineshapes have been demonstrated with neV linewidths, which is the narrowest bulk exciton resonance ever observed. The associated quadrupole polaritons have low group velocity approaching the speed of sound. Thus, light moves almost as slowly as sound in this medium, which results in high polariton densities. Another unusual feature of the ground state excitons is that all primary scattering mechanisms are known quantitatively. Cu2O was the first substance where an entirely parameter-free model of absorption linewidth broadening by temperature could be established, allowing the corresponding absorption coefficient to be deduced. It can be shown using Cu2O that the Kramers–Kronig relations do not apply to polaritons.
 * Semiconductor
 * Semiconductor diodes
 * Phonoritons ("a coherent superposition of exciton, photon, and phonon")

Applications
Cuprous oxide is commonly used as a pigment, a fungicide, and an antifouling agent for marine paints. Rectifier diodes based on this material have been used industrially as early as 1924, long before silicon became the standard. Copper(I) oxide is also responsible for the pink color in a positive Benedict's test.

In December 2021, Toshiba announced the creation of a transparent cuprous oxide (Cu2O) thin-film solar cell. The cell achieved an 8.4% energy conversion efficiency, the highest efficiency ever reported for any cell of this type as of 2021. The cells could be used for high-altitude platform station applications and electric vehicles.

Similar compounds
An example of natural copper(I,II) oxide is the mineral paramelaconite, Cu4O3 or Cu$\overline{3}$Cu$\overline{3}$O3.

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

title: Copper(I) oxide


text:
Tubular Bells 2003

Tubular Bells 2003 is the 22nd studio album by English musician Mike Oldfield, released on 26 May 2003 by Warner Music Spain. It is a digital re-recording of his 1973 album Tubular Bells, released almost 30 years earlier. This is the final album in the Tubular Bells series.

Background
In 2003, the re-recording rights to Oldfield's debut album Tubular Bells returned to him, which brought about the idea to re-record it to commemorate the 30th anniversary of the original. He had always been uncomfortable with the original recording because he had only a few weeks to record it and the technology at the time was unable to cope with all of his requirements. As a result, mistakes could not be fixed and some instruments were out of tune on the 1973 release. Due to contractual reasons no re-recordings were allowed for 25 years after the original release. The release of Tubular Bells 2003 took place in the year when Oldfield celebrated his 50th birthday and the 30th anniversary of the original version.

To remain faithful to the original album, Oldfield obtained a copy of the original 16 track tape, from Richard Barrie of AIR Studios; this multitrack was then recorded into Digidesign Pro Tools. There were a few parts of the multitrack recording missing however; this included parts of the "Finale", "Caveman" and "The Sailors Hornpipe" sections. These original tracks were then moved into Emagic Logic, where Oldfield used MIDI to create a tempo and time signature map; some sections of the original album had not been in time. A guide MIDI keyboard was laid on top, for which Oldfield usually used some Roland Strings. The first instrument to be recorded was the Glockenspiel at the beginning of Part One's "Introduction", and the final part to be recorded was the "Caveman" vocal track.

The album was released in four versions: a CD in Europe, a CD in North America, and a DVD-Audio edition. The copy protection on the CDs caused many complaints about playback difficulties, including claims of damage to CD and DVD players.

Due to the extensive use of digital technology, Tubular Bells 2003 has a more synthesised and brighter sound than the original. Because of the death of Vivian Stanshall, who was the original master of ceremonies on the 1973 release, Oldfield had actor John Cleese introduce the instruments in the "Finale" part.

A CD audio/DVD Video-audio 5.1, was released in Spain and México.

There is a facetious warning inside the cover of CD: "This stereo record can still not be played on old tin boxes no matter what they are fitted with. If you are in possession of such equipment please hand it into the nearest police station". This warning references a similar note, without the word "still", from the original album.

Promo single
A video and Spanish promo single were produced for a remix version of the Tubular Bells "Introduction" theme, entitled "Introduction 2003". Released as a single in Spain on 24 April 2003, it features drums and more synthesized instruments, and a conceptual video was also produced. This video is available on the DVD Audio version of Tubular Bells 2003.

The second publicly released MusicVR game, Maestro, used various extracts from Tubular Bells 2003.

Personnel
Performers
 * Mike Oldfield – acoustic and electric guitars, electric bass, accordion, Steinway grand pianos, Farfisa, Lowrey & Hammond organs, synthesizers, glockenspiel, timpani, cymbals, tambourine, triangle, tubular bells, programming, producer
 * John Cleese – master of ceremonies
 * Sally Oldfield – background vocals

Non-performers
 * Ben Darlow – engineer
 * Steve Bedford – new Tubular Bell image
 * Trevor Key – original Tubular Bell image
 * Andy Earl – inner cover photo
 * e-xentric thinking – design
 * Oldfield Music Overseas Ltd. / EMI Publishing Ltd – publishing

CD
Part one
 * 1) "Introduction" – 5:52
 * 2) "Fast Guitars" – 1:04
 * 3) "Basses" – 0:46
 * 4) "Latin" – 2:18
 * 5) "A Minor Tune" – 1:21
 * 6) "Blues" – 2:40
 * 7) "Thrash" – 0:44
 * 8) "Jazz" – 0:48
 * 9) "Ghost Bells" – 0:30
 * 10) "Russian" – 0:44
 * 11) "Finale" – 8:32 (featuring John Cleese)

Part two
 * 1) "Harmonics" – 5:12
 * 2) "Peace" – 3:30
 * 3) "Bagpipe Guitars" – 3:08
 * 4) "Caveman" – 4:33
 * 5) "Ambient Guitars" – 5:10
 * 6) "The Sailor's Hornpipe" – 1:46 (Traditional arrangement)

Bonus DVD

 * Disc 2 – Total Time 11:22
 * 1) "Introduction" – 5:51
 * 2) "Fast Guitars" – 1:04
 * 3) "Basses" – 0:46
 * 4) "Introduction 2003" 'The video' – 3:41

DVD-Audio bonus material
The DVD-Audio edition includes the demos Oldfield recorded in his flat in 1971 and two excerpts from other Oldfield DVD releases.

1971 Demos
 * 1) "Tubular Bells Long" – 22:57
 * 2) "Caveman Lead-In" – 2:46
 * 3) "Caveman" – 5:05
 * 4) "Peace Demo A" – 7:00
 * 5) "Peace Demo B" – 4:18

Live Excerpts
 * 1) "Sentinel" – from Tubular Bells II – Live at Edinburgh Castle 1992 – 8:06
 * 2) "Far Above the Clouds" – from Tubular Bells III – Live at Horseguards Parade, London 1998 – 4:40

Hardware
Mixing desk Computers Plug-ins Outboard effects Microphones
 * AMS Neve Capricorn (V2.85.003 & V2.91.007)
 * Apple Macintosh computers
 * G4 466Mhz OS9.1, 1Gb Ram – Logic Audio Platinum 4.8.1 and Pro Tools
 * G4 1000Mhz OS9.2 – Logic 5.3.0 and Pro Tools 5.3.1
 * Powerbook 5300
 * Pro Tools Mix Plus card X2
 * 4 Pro Tools 24-bit 888s
 * Motu 828
 * Amp Farm
 * Focusrite EQ and Compression
 * TC Electronic M5000
 * Eventide DSP 4000
 * Lexicon 300
 * Yamaha SPX 1000
 * UREI 1176 & 1178
 * Belcaman C-102
 * 5 NEVE 1073 Mic Amps and EQ
 * Manor Module (Mic Amp, EQ and Compressor from the original Manor console)
 * Brüel & Kjær 4011
 * Brüel & Kjær 4040 (Serial no. 001)
 * AKG C12
 * Shure SM57
 * Neuman U67
 * Neuman M249
 * Beyer Dynamic M160
 * BSS DI Box

Instruments
Electric guitars Acoustic guitars Pianos and organs Keyboards Soft synths Percussion
 * Fender Telecaster 1965
 * Fender Stratocaster 1963 (listed as 1965) (Pink)
 * PRS McCarty Semi-Acoustic
 * PRS Signature (through Roland GP8)
 * PRS Signature (through Roland VG8)
 * Wal bass
 * Fender Twin Reverb Amplifier
 * Mesa Boogie Amplifier
 * Ramirez Class 1A Flamenco 1974
 * Ramirez Class 1A Flamenco 1975
 * Martin Steel String Acoustic
 * Taylor K22 Acoustic Guitar 1985
 * Ovation Adamas
 * MJV Mandolin
 * Steinway 8 ft 1920s, frame rebuilt
 * Steinway 6 ft 1920s Model L
 * Lowery Organ
 * Farfisa Organ
 * Accordion
 * Roland JV880
 * Roland XP50
 * Roland JV2080
 * Roland JD990
 * Nord Lead
 * Korg Trinity
 * Boss Dr. Rhythm
 * Akai S6000
 * Emagic EXS24
 * Emagic ES1
 * Emagic EVP88
 * Native Instruments Pro-52
 * Glockenspiel
 * Tambourine
 * Triangle
 * Cymbals
 * Timpani
 * Tubular bells

title: Tubular Bells 2003


text:
Antithrombin

Antithrombin (AT) is a small glycoprotein that inactivates several enzymes of the coagulation system. It is a 464-amino-acid protein produced by the liver. It contains three disulfide bonds and a total of four possible glycosylation sites. α-Antithrombin is the dominant form of antithrombin found in blood plasma and has an oligosaccharide occupying each of its four glycosylation sites. A single glycosylation site remains consistently un-occupied in the minor form of antithrombin, β-antithrombin. Its activity is increased manyfold by the anticoagulant drug heparin, which enhances the binding of antithrombin to factor IIa (thrombin) and factor Xa.

Structure
Antithrombin is also termed antithrombin III (AT III). The designations antithrombin I through to antithrombin IV originate in early studies carried out in the 1950s by Seegers, Johnson and Fell.

Antithrombin I (AT I) refers to the binding of thrombin to fibrin, after thrombin has activated fibrinogen, at a non-catalytic binding site of thrombin. Antithrombin II (AT II) refers to a cofactor in plasma, which together with heparin interferes with the interaction of thrombin and fibrinogen. Antithrombin III (AT III) refers to a substance in plasma that inactivates thrombin. Antithrombin IV (AT IV) refers to an antithrombin that becomes activated during and shortly after blood coagulation. Only AT III and possibly AT I are medically significant. AT III is generally referred to solely as "antithrombin" and it is antithrombin III that is discussed in this article. Antithrombin has a half-life in blood plasma of around 3 days. The normal antithrombin concentration in human blood plasma is high at approximately 0.12 mg/ml, which is equivalent to a molar concentration of 2.3 μM. Antithrombin has been isolated from the plasma of a large number of species additional to humans. As deduced from protein and cDNA sequencing, cow, sheep, rabbit and mouse antithrombins are all 433 amino acids in length, which is one amino acid longer than human antithrombin. The extra amino acid is thought to occur at amino acid position 6. Cow, sheep, rabbit, mouse, and human antithrombins share between 84 and 89% amino acid sequence identity. Six of the amino acids form three intramolecular disulfide bonds, Cys8-Cys128, Cys21-Cys95, and Cys248-Cys430. They all have four potential N-glycosylation sites. These occur at asparagine (Asn) amino acid numbers 96, 135, 155, and 192 in humans and at similar amino acid numbers in other species. All these sites are occupied by covalently attached oligosaccharide side-chains in the predominant form of human antithrombin, α-antithrombin, resulting in a molecular weight for this form of antithrombin of 58,200. The potential glycosylation site at asparagine 135 is not occupied in a minor form (around 10%) of antithrombin, β-antithrombin (see Figure 1).

Recombinant antithrombins with properties similar to those of normal human antithrombin have been produced using baculovirus-infected insect cells and mammalian cell lines grown in cell culture. These recombinant antithrombins generally have different glycosylation patterns to normal antithrombin and are typically used in antithrombin structural studies. For this reason many of the antithrombin structures stored in the protein data bank and presented in this article show variable glycosylation patterns.

Antithrombin begins in its native state, which has a higher free energy compared to the latent state, which it decays to on average after 3 days. The latent state has the same form as the activated state - that is, when it is inhibiting thrombin. As such it is a classic example of the utility of kinetic vs thermodynamic control of protein folding.

Function
Antithrombin is a serpin (serine protease inhibitor) and is thus similar in structure to most other plasma protease inhibitors, such as alpha 1-antichymotrypsin, alpha 2-antiplasmin and Heparin cofactor II.

The physiological target proteases of antithrombin are those of the contact activation pathway (formerly known as the intrinsic pathway), namely the activated forms of Factor X (Xa), Factor IX (IXa), Factor XI (XIa), Factor XII (XIIa) and, to a greater extent, Factor II (thrombin) (IIa), and also the activated form of Factor VII (VIIa) from the tissue factor pathway (formerly known as the extrinsic pathway). The inhibitor also inactivates kallikrein and plasmin, also involved in blood coagulation. However it inactivates certain other serine proteases that are not involved in coagulation such as trypsin and the C1s subunit of the enzyme C1 involved in the classical complement pathway.

Protease inactivation results as a consequence of trapping the protease in an equimolar complex with antithrombin in which the active site of the protease enzyme is inaccessible to its usual substrate. The formation of an antithrombin-protease complex involves an interaction between the protease and a specific reactive peptide bond within antithrombin. In human antithrombin this bond is between arginine (arg) 393 and serine (ser) 394 (see Figure 2 and Figure 3). It is thought that protease enzymes become trapped in inactive antithrombin-protease complexes as a consequence of their attack on the reactive bond. Although attacking a similar bond within the normal protease substrate results in rapid proteolytic cleavage of the substrate, initiating an attack on the antithrombin reactive bond causes antithrombin to become activated and trap the enzyme at an intermediate stage of the proteolytic process. Given time, thrombin is able to cleave the reactive bond within antithrombin and an inactive antithrombin-thrombin complex will dissociate, however the time it takes for this to occur may be greater than 3 days. However, bonds P3-P4 and P1'-P2' can be rapidly cleaved by neutrophil elastase and the bacterial enzyme thermolysin, respectively, resulting in inactive antithrombins no longer able to inhibit thrombin activity.

The rate of antithrombin's inhibition of protease activity is greatly enhanced by its additional binding to heparin, as is its inactivation by neutrophil elastase.

Antithrombin and heparin
Antithrombin inactivates its physiological target enzymes, Thrombin, Factor Xa and Factor IXa with rate constants of 7–11 x 103, 2.5 x 103 M−1 s−1 and 1 x 10 M−1 s−1 respectively. The rate of antithrombin-thrombin inactivation increases to 1.5 - 4 x 107 M−1 s−1 in the presence of heparin, i.e. the reaction is accelerated 2000-4000 fold. Factor Xa inhibition is accelerated by only 500 to 1000 fold in the presence of heparin and the maximal rate constant is 10 fold lower than that of thrombin inhibition. The rate enhancement of antithrombin-Factor IXa inhibition shows an approximate 1 million fold enhancement in the presence of heparin and physiological levels of calcium.

AT-III binds to a specific pentasaccharide sulfation sequence contained within the heparin polymer

GlcNAc/NS(6S)-GlcA-GlcNS(3S,6S)-IdoA(2S)-GlcNS(6S)

Upon binding to this pentasaccharide sequence, inhibition of protease activity is increased by heparin as a result of two distinct mechanisms. In one mechanism heparin stimulation of Factor IXa and Xa inhibition depends on a conformational change within antithrombin involving the reactive site loop and is thus allosteric. In another mechanism stimulation of thrombin inhibition depends on the formation of a ternary complex between AT-III, thrombin, and heparin.

Allosteric activation
Increased Factor IXa and Xa inhibition requires the minimal heparin pentasaccharide sequence. The conformational changes that occur within antithrombin in response to pentasaccharide binding are well documented.

In the absence of heparin, amino acids P14 and P15 (see Figure 3) from the reactive site loop are embedded within the main body of the protein (specifically the top of beta sheet A). This feature is in common with other serpins such as heparin cofactor II, alpha 1-antichymotrypsin and MENT.

The conformational change most relevant for Factor IXa and Xa inhibition involves the P14 and P15 amino acids within the N-terminal region of the reactive site loop (circled in Figure 4 model B). This region has been termed the hinge region. The conformational change within the hinge region in response to heparin binding results in the expulsion of P14 and P15 from the main body of the protein and it has been shown that by preventing this conformational change, increased Factor IXa and Xa inhibition does not occur. It is thought that the increased flexibility given to the reactive site loop as a result of the hinge region conformational change is a key factor in influencing increased Factor IXa and Xa inhibition. It has been calculated that in the absence of the pentasaccharide only one in every 400 antithrombin molecules (0.25%) is in an active conformation with the P14 and P15 amino acids expelled.

Non-allosteric activation
Increased thrombin inhibition requires the minimal heparin pentasaccharide plus at least an additional 13 monomeric units. This is thought to be due to a requirement that antithrombin and thrombin must bind to the same heparin chain adjacent to each other. This can be seen in the series of models shown in Figure 5.

In the structures shown in Figure 5 the C-terminal portion (P' side) of the reactive site loop is in an extended conformation when compared with other un-activated or heparin activated antithrombin structures. The P' region of antithrombin is unusually long relative to the P' region of other serpins and in un-activated or heparin activated antithrombin structures forms a tightly hydrogen bonded β-turn. P' elongation occurs through the breaking of all hydrogen bonds involved in the β-turn.

The hinge region of antithrombin in the Figure 5 complex could not be modelled due to its conformational flexibility, and amino acids P9-P14 are not seen in this structure. This conformational flexibility indicates an equilibrium may exist within the complex between a P14 P15 reactive site loop inserted antithrombin conformation and a P14 P15 reactive site loop expelled conformation. In support of this, analysis of the positioning of P15 Gly in the Figure 5 complex (labelled in model B) shows it to be inserted into beta sheet A (see model C).

Effect of glycosylation on activity
α-Antithrombin and β-antithrombin differ in their affinity for heparin. The difference in dissociation constant between the two is threefold for the pentasaccharide shown in Figure 3 and greater than tenfold for full length heparin, with β-antithrombin having a higher affinity. The higher affinity of β-antithrombin is thought to be due to the increased rate at which subsequent conformational changes occur within the protein upon initial heparin binding. For α-antithrombin, the additional glycosylation at Asn-135 is not thought to interfere with initial heparin binding, but rather to inhibit any resulting conformational changes.

Even though it is present at only 5–10% the levels of α-antithrombin, due to its increased heparin affinity, it is thought that β-antithrombin is more important than α-antithrombin in controlling thrombogenic events resulting from tissue injury. Indeed, thrombin inhibition after injury to the aorta has been attributed solely to β-antithrombin.

Deficiencies
Evidence for the important role antithrombin plays in regulating normal blood coagulation is demonstrated by the correlation between inherited or acquired antithrombin deficiencies and an increased risk of any affected individual developing thrombotic disease. Antithrombin deficiency generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism.

Acquired antithrombin deficiency
Acquired antithrombin deficiency occurs as a result of three distinctly different mechanisms. The first mechanism is increased excretion which may occur with renal failure associated with proteinuria nephrotic syndrome. The second mechanism results from decreased production as seen in liver failure or cirrhosis or an immature liver secondary to premature birth. The third mechanism results from accelerated consumption which is most pronounced as consequence of severe injury trauma but also may be seen on a lesser scale as a result of interventions such as major surgery or cardiopulmonary bypass.

Inherited antithrombin deficiency
The incidence of inherited antithrombin deficiency has been estimated at between 1:2000 and 1:5000 in the normal population, with the first family suffering from inherited antithrombin deficiency being described in 1965. Subsequently, it was proposed that the classification of inherited antithrombin deficiency be designated as either type I or type II, based upon functional and immunochemical antithrombin analyses. Maintenance of an adequate level of antithrombin activity, which is at least 70% that of a normal functional level, is essential to ensure effective inhibition of blood coagulation proteases. Typically as a result of type I or type II antithrombin deficiency, functional antithrombin levels are reduced to below 50% of normal.

Type I antithrombin deficiency
Type I antithrombin deficiency is characterized by a decrease in both antithrombin activity and antithrombin concentration in the blood of affected individuals. Type I deficiency was originally further divided into two subgroups, Ia and Ib, based upon heparin affinity. The antithrombin of subgroup Ia individuals showed a normal affinity for heparin while the antithrombin of subgroup Ib individuals showed a reduced affinity for heparin. Subsequent functional analysis of a group of 1b cases found them not only to have reduced heparin affinity but multiple or 'pleiotrophic' abnormalities affecting the reactive site, the heparin binding site and antithrombin blood concentration. In a revised system of classification adopted by the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis, type Ib cases are now designated as type II PE, Pleiotrophic effect.

Most cases of type I deficiency are due to point mutations, deletions or minor insertions within the antithrombin gene. These genetic mutations result in type I deficiency through a variety of mechanisms:
 * Mutations may produce unstable antithrombins that either may be not exported into the blood correctly upon completion biosynthesis or exist in the blood for a shortened period of time, e.g., the deletion of 6 base pairs in codons 106–108.
 * Mutations may affect mRNA processing of the antithrombin gene.
 * Minor insertions or deletions may lead to frame shift mutations and premature termination of the antithrombin gene.
 * Point mutations may also result in the premature generation of a termination or stop codon e.g. the mutation of codon 129, CGA→TGA (UGA after transcription), replaces a normal codon for arginine with a termination codon.

Type II antithrombin deficiency
Type II antithrombin deficiency is characterized by normal antithrombin levels but reduced antithrombin activity in the blood of affected individuals. It was originally proposed that type II deficiency be further divided into three subgroups (IIa, IIb, and IIc) depending on which antithrombin functional activity is reduced or retained.

 * Subgroup IIa - Decreased thrombin inactivation, decreased factor Xa inactivation and decreased heparin affinity.
 * Subgroup IIb - Decreased thrombin inactivation and normal heparin affinity.
 * Subgroup IIc - Normal thrombin inactivation, normal factor Xa inactivation and decreased heparin affinity.

In the revised system of classification again adopted by the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis, type II antithrombin deficiency remains subdivided into three subgroups: the already mentioned type II PE, along with type II RS, where mutations effect the reactive site and type II HBS, where mutations effect the antithrombin heparin binding site. For the purposes of an antithrombin mutational database compiled by members of the Plasma Coagulation Inhibitors Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis, type IIa cases are now classified as type II PE, type IIb cases as type II RS and type IIc cases as type II HBS.

Toponyms
Presently it is relatively easy to characterise a specific antithrombin genetic mutation. However prior to the use of modern characterisation techniques investigators named mutations for the town or city where the individual suffering from the deficiency resided i.e. the antithrombin mutation was designated a toponym. Modern mutational characterisation has since shown that many individual antithrombin toponyms are actually the result of the same genetic mutation, for example antithrombin-Toyama, is equivalent to antithrombin-Kumamoto, -Amien, -Tours, -Paris-1, -Paris-2, -Alger, -Padua-2 and -Barcelona.

Medical uses
Antithrombin is used as a protein therapeutic that can be purified from human plasma or produced recombinantly (for example Atryn, which is produced in the milk of genetically modified goats ).

It is approved by the FDA as an anticoagulant for the prevention of clots before, during, or after surgery or birthing in patients with hereditary antithrombin deficiency.

It has been studied in sepsis to reduce diffuse intravascular coagulation and other outcomes. It has not been found to confer any benefit in critically ill people with sepsis.

Cleaved and latent antithrombin
Cleavage at the reactive site results in entrapment of the thrombin protease, with movement of the cleaved reactive site loop together with the bound protease, such that the loop forms an extra sixth strand in the middle of beta sheet A. This movement of the reactive site loop can also be induced without cleavage, with the resulting crystallographic structure being identical to that of the physiologically latent conformation of plasminogen activator inhibitor-1 (PAI-1). For this reason the conformation of antithrombin in which the reactive site loop is incorporated uncleaved into the main body of the protein is referred to as latent antithrombin. In contrast to PAI-1 the transition for antithrombin from a normal or native conformation to a latent conformation is irreversible.

Native antithrombin can be converted to latent antithrombin (L-antithrombin) by heating alone or heating in the presence of citrate. However, without extreme heating and at 37 °C (body temperature) 10% of all antithrombin circulating in the blood is converted to the L-antithrombin over a 24-hour period. The structure of L-antithrombin is shown in Figure 6.

The 3-dimensional structure of native antithrombin was first determined in 1994. Unexpectedly the protein crystallized as a heterodimer composed of one molecule of native antithrombin and one molecule of latent antithrombin. Latent antithrombin on formation immediately links to a molecule of native antithrombin to form the heterodimer, and it is not until the concentration of latent antithrombin exceeds 50% of the total antithrombin that it can be detected analytically. Not only is the latent form of antithrombin inactive against its target coagulation proteases, but its dimerisation with an otherwise active native antithrombin molecule also results in the native molecules inactivation. The physiological impact of the loss of antithrombin activity either through latent antithrombin formation or through subsequent dimer formation is exacerbated by the preference for dimerisation to occur between heparin activated β-antithrombin and latent antithrombin as opposed to α-antithrombin.

A form of antithrombin that is an intermediate in the conversion between native and latent forms of antithrombin has also been isolated and this has been termed prelatent antithrombin.

Antiangiogenic antithrombin
Angiogenesis is a physiological process involving the growth of new blood vessels from pre-existing vessels. Under normal physiological conditions angiogenesis is tightly regulated and is controlled by a balance of angiogenic stimulators and angiogenic inhibitors. Tumor growth is dependent upon angiogenesis and during tumor development a sustained production of angiogenic stimulatory factors is required along with a reduction in the quantity of angiogenic inhibitory factors tumor cells produce. The cleaved and latent form of antithrombin potently inhibit angiogenesis and tumor growth in animal models. The prelatent form of antithrombin has been shown to inhibit angiogenesis in-vitro but to date has not been tested in experimental animal models.

title: Antithrombin


text:
User:Owen&rob

Owen Jones (b. 1984) was born in Sheffield, and now lives in Stockport when he isn't studying for his BA in Modern History at University College, Oxford.

Robert Bassett (b. 1983) is currently reading PPE at University College, Oxford.

They closely collaborate on all the articles they produce or edit.

title: User:Owen&rob


text:
CSH

CSH (or its styling variants Csh or csh) is a three-letter acronym with multiple meanings:

Locations

 * Cecil Sharp House, home of the English Folk Dance and Song Society
 * Chartwell Seniors Housing, a real estate investment trust in Canada
 * Cold Spring Harbor Laboratory, a genetics laboratory in Cold Spring Harbor
 * Cold Spring Harbor, New York, a town on Long Island
 * See also Cold Spring Harbor (disambiguation)

Medicine, science and technology

 * Caesium hydride, a crystalline solid with the molecular formula CsH
 * C-S-H, calcium silicate hydrate, or calcium silicate hydrogel, the main component of hardened cement paste: the glue phase in hardened Portland cement
 * C shell, a Unix shell
 * Combat Support Hospital, a type of military field hospital
 * Context-sensitive help, method of providing online help
 * CSH Protocols, an on-line scientific journal for biologists
 * Photoshop Custom Shape Object, a file format for use with Adobe Systems' Photoshop

Transport

 * Carshalton railway station, London, National Rail station code CSH
 * Cycle Superhighways, a bicycle route scheme in London
 * Shanghai Airlines, ICAO airline designator CSH

Other

 * Asho Chin language (ISO 639-3 code)
 * Canadian Subject Headings is a list of subject headings of Canadian topics
 * Case Study Houses, experiments in American residential architecture from 1945 until 1966
 * Cash America International has the NYSE designator CSH
 * Coalition to Save Harlem
 * Code for Sustainable Homes
 * Convent of the Sacred Heart (disambiguation)
 * Coordination Syndicale Haïtienne (CSH), a Haitian trade union
 * Council for Secular Humanism
 * Sun Hei SC, a football club in Hong Kong
 * Car Seat Headrest, an American band

title: CSH


text:
Site Finder

Site Finder was a wildcard DNS record for all .com and .net unregistered domain names, run by .com and .net top-level domain operator VeriSign between 15 September 2003 and 4 October 2003.

Site Finder
All Internet users who accessed any unregistered domains in the .com and .net domain space were redirected to a VeriSign web portal with information about VeriSign products and links to "partner" sites. This gave VeriSign the advantage of receiving greater revenue from advertising and from users wishing to register these domain names. It had the effect of capturing the web traffic for several million mistyped or experimental web accesses per day, and meant that VeriSign effectively owned all possible .com and .net domains that had not been bought by others, and could use them as an advertising platform.

VeriSign described the change as an attempt to improve the Web browsing experience for the naive user, without mentioning any use of the domain name system other than by browsers. VeriSign's critics saw this claim as disingenuous. The change led to a dramatic increase in the amount of Internet traffic arriving at verisign.com. According to the web traffic measurement company Alexa, in the year prior to the change verisign.com was around the 2,500th most popular website. In the weeks following the change, the site came into the top 20 most popular sites, and reached the top 10 in the aftermath of the change and surrounding controversy.

Issues and controversy
There was a storm of controversy among network operators and competing domain registrars, particularly on the influential NANOG and ICANN mailing lists, some of whom asserted:
 * that the redirection was contrary to the proper operation of the DNS, ICANN policy, and the Internet architecture in general;
 * that VeriSign breached its trust with the Internet community by using technical architecture for marketing purposes;
 * that the redirection broke various RFCs and disrupted existing Internet services, such as email relay and filtering (spam filters were not able to detect the validity of domain names);
 * that the redirection amounted to typosquatting where the unregistered domain being resolved is a spelling mistake for a famous registered domain;
 * that VeriSign abused its technical control over the .com and .net domains by exerting a de facto monopoly control;
 * that VeriSign may have been in breach of its contracts for running the .com and .net domains;
 * that the Site Finder service assumed that all DNS traffic was caused by Web clients, ignoring the fact that DNS is used by other applications such as networked printers, FTP software, and dedicated communications applications. If users of these applications accidentally entered a wrong host name, instead of a meaningful "host not found" error they would get a "request timed out" error, making it look like the server existed but is not responding. No statement by VeriSign in support of Site Finder even acknowledged the existence of DNS traffic not caused by Web clients, although they published implementation details which mentioned this traffic.
 * that Site Finder contained an end-user license agreement which stated that the user accepts the terms by using the service—but since mistyping an address automatically caused the service to be used, users could not refuse to accept the terms.

Others were concerned that the Site Finder service was written entirely in English and therefore was not accessible by non-English speakers.

The Internet Architecture Board composed a document detailing many of the technical arguments against registry-level wildcards; this was used by ICANN as part of its supporting arguments for its action.

Fallout
A number of workarounds were developed to locally disable the effects of Site Finder on a per-network basis. Most notably, the Internet Systems Consortium announced that it had produced a version of the BIND DNS software that could be configured by Internet service providers to filter out wildcard DNS from certain domains; this software was deployed by a number of ISPs.

On October 4, 2003, as a result of a strong letter from ICANN, VeriSign disabled Site Finder. However, VeriSign has made public statements that suggest that they may be considering whether they will change this decision in the future. On February 27, 2004, VeriSign filed a lawsuit against ICANN, claiming that ICANN had overstepped its authority. The claim regarded not only Site Finder, but also VeriSign's much-criticised Wait Listing Service. The claim was dismissed in August 2004; parts of the lawsuit continued, and culminated in a March 1, 2006 settlement between VeriSign and ICANN which included "a new registry agreement relating to the operation of the .COM registry."

On July 9, 2004, the ICANN Security and Stability Advisory Committee (SSAC) handed down its findings after an investigation on Site Finder. It found that the service should not be deployed before ICANN and/or appropriate engineering communities were offered the opportunity to review a proposed implementation, and that domain name registries that provide a service to third parties should phase out wildcard records if they are used.

title: Site Finder


text:
Self-serving bias

A self-serving bias is any cognitive or perceptual process that is distorted by the need to maintain and enhance self-esteem, or the tendency to perceive oneself in an overly favorable manner. It is the belief that individuals tend to ascribe success to their own abilities and efforts, but ascribe failure to external factors. When individuals reject the validity of negative feedback, focus on their strengths and achievements but overlook their faults and failures, or take more credit for their group's work than they give to other members, they are protecting their self-esteem from threat and injury. These cognitive and perceptual tendencies perpetuate illusions and error, but they also serve the self's need for esteem. For example, a student who attributes earning a good grade on an exam to their own intelligence and preparation but attributes earning a poor grade to the teacher's poor teaching ability or unfair test questions might be exhibiting a self-serving bias. Studies have shown that similar attributions are made in various situations, such as the workplace, interpersonal relationships, sports, and consumer decisions.

Both motivational processes (i.e. self-enhancement, self-presentation) and cognitive processes (i.e. locus of control, self-esteem) influence the self-serving bias. There are both cross-cultural (i.e. individualistic and collectivistic culture differences) and special clinical population (i.e. depression) considerations within the bias. Much of the research on the self-serving bias has used participant self-reports of attribution based on experimental manipulation of task outcomes or in naturalistic situations. Some more modern research, however, has shifted focus to physiological manipulations, such as emotional inducement and neural activation, in an attempt to better understand the biological mechanisms that contribute to the self-serving bias.

History
The theory of self-serving biases first came to attention in the late 1960s to early 1970s. As research on this topic grew, some people had concerns about it. In 1971, a fear emerged that the hypothesis would prove to be incorrect, much like the perceptual defense hypothesis by Dixon. However, the theory now holds strong. When this theory was still being developed it was during the research of attribution bias. Fritz Heider found that in ambiguous situations people made attributions based on their own needs, in order to maintain a higher self-esteem and viewpoint. This specific tendency became what we now know as the self-serving bias. Miller and Ross conducted a study in 1975 that was one of the earliest to assess not only self-serving bias but also the attributions for successes and failures within this theory. They argued that the self-serving bias people create is rational and not dependent on one's need for self-esteem. This means that if the outcome of an event is consistent with the person's expectation, then they will attribute dispositional (internal) factors. On the other hand, if the outcome of the event does not match the person's expectations, they will make situational attributions by blaming their surroundings instead of themselves.

Laboratory testing
Investigations of the self-serving bias in the laboratory differ depending on the experimental goals, but have basic fundamental aspects. Participants perform some task, often of intelligence, social sensitivity, teaching ability, or therapy skills. Participants may be asked to work alone, in pairs, or in groups. After task completion, participants are given randomized bogus feedback. Some studies employ emotion-induction mechanisms to investigate moderating effects on the self-serving bias. Finally, participants make attributions for the given outcomes. These attributions are assessed by the researchers to determine implications for the self-serving bias.

Neural experimentation
Some more modern testing employs neural imaging techniques to supplement the fundamental self-serving bias laboratory procedures. Neural correlates of the self-serving bias have been investigated by electroencephalography (EEG), as well as functional magnetic resonance imaging (fMRI). These procedures allow for insight into brain area activity during exhibition of a self-serving bias, as well as a mechanism to differentiate brain activity between healthy and clinical populations.

Naturalistic investigation
Retrospective performance outcomes can be used in investigation of the self-serving bias. An example of this is reported company performance followed up by self-report of outcome attributions. These self-report attributions can then be used to assess how successes and failures are viewed by company employees and executives. This method can be used for numerous outcome variables to determine the presence or absence of the self-serving bias.

Motivation
Two types of motivation affect the self-serving bias: self-enhancement and self-presentation. Self-enhancement aims to uphold self-worth; attributing successes internally and failures externally helps people in their self-enhancement. Self-presentation refers to the drive to convey a desired image to others and make self-serving attributions to manage impressions. For example, they claim personal responsibility for successes but not failures in an attempt to influence how others perceive them. Motivation works in conjunction with cognitive factors to produce personally satisfying and self-preserving attributions for outcomes.

Locus of control
Locus of control is one of the main influences of attribution style. Individuals with an internal locus of control believe that they have personal control over situations and that their actions matter. Those with an external locus of control believe that outside forces, chance, and luck determine situations and that their actions cannot change anything. Individuals with an external locus of control are more likely to exhibit a self-serving bias following failure than those with an internal locus of control. The difference in attribution style between individuals with internal and external loci of control, however, is not as marked in successful outcomes, as individuals with both types attribution style have less need to defend their self-images in success. Airplane pilots with an internal locus of control were likely to exhibit a self-serving bias in regard to their skill and levels of safety.

Gender
Studies have shown a slight discrepancy in males' and females' use of the self-serving bias. In self-report surveys investigating partner interactions of romantic couples, men tended to attribute negative interactions to their partners more than women did. This is evidence that men may exhibit the self-serving bias more than women, although the study did not look at positive interaction attributions.

Age
Older adults have been shown to make more internal causal attributions for negative outcomes. Differential attribution style at different ages indicates that the self-serving bias may be less likely in older adults. These older adults who attributed negative outcomes to more internal factors also rated themselves to be in poorer health, so negative emotional factors may confound the found age effects.

Culture
There is evidence of cross-cultural differences in the tendency to exhibit the self-serving bias, particularly when considering individualistic (Western) versus collectivistic (non-Western) societies. Family and group goals are important in collectivistic cultures. In contrast, the individual goals and identity focused on in individualistic societies increases the need for people within those cultures to guard and boost their personal self-esteem. While differences have been shown, conflicting literature has cited similarity in causal attributions across both individual and collective cultures, specifically between Belgium, West Germany, South Korea, and England. Naturalistic observation and information comparing United States and Japanese companies outcome attributions shows that the meaning and psychological function of internal versus external attributions are similar across cultures but that the difference is in the strategy of attribution. No consensus has been reached on cross-culture influences on the self-serving bias, though some systematic differences do seem to be present, especially between Western and non-Western cultures. For example, a study conducted by Kudo and Numuzaki showed that the participants in the success condition provided more internal attributions than the participants in the failure condition even though past research has constantly shown that Japanese people do not tend to show a self-serving bias. Another study conducted by Hugten and Witteloostuijn displayed the results that student participants between the ages of 13 and 15 who mainly process feedback in a non-native English tend to show more self-serving bias than those who process feedback in their native Dutch language.

Role
Investigations of self-serving bias distinguish between the role of participants as the actor of a task or as the observer of someone else performing a task, relating closely to actor–observer asymmetry. Actors of a task exhibit the self-serving bias in their attributions to their own success or failure feedback, whereas observers do not make the same attributions about another person's task outcome. Observers tend to be more objective in their tendency to ascribe internal or external attributions to other people's outcomes. This may be due to the fact that the self-image of actors is challenged directly and therefore actors feel the need to protect their own self-image, but do not feel the same inclination to do so when the self-image of others is threatened.

Self-esteem and emotion
Emotions can influence feelings of self-esteem, which in turn alters the need to protect one's self-identity. Individuals with higher self-esteem are thought to have more to protect in their self-image, and therefore exhibit the self-serving bias more often than those individuals with lower self-esteem. In a study, participants who were induced to feel the emotions of guilt or revulsion were less likely to make self-serving attributions for success and less likely to make self-protecting attributions for failure. Coleman concluded that the two emotions of guilt and revulsion lead to a drop in self-esteem, and thus a reduction in the use of the self-serving bias.

Self-awareness and probability of improvement
The relationship between individuals' awareness levels and perceived probability of improvement also influences the activation of the self-serving bias. Individuals with high self-awareness attribute failure internally when they perceive a high probability of improvement. However, they will engage in self-serving bias, attributing failure externally when they perceive a low probability of improvement. Individuals low in self-awareness will attribute failure externally regardless of their perceived probability of improvement.

Interpersonal relations
Whether the self-serving bias is exhibited may depend on interpersonal closeness, relationships in a social context. When working in pairs to complete interdependent outcome tasks, relationally close pairs did not show a self-serving bias while relationally distant pairs did. A study on self-serving bias in relational context suggests this is due to the idea that close relationships place limits on an individual's self enhancement tendencies. The individual becomes more modest, when in a close relationship, and is less likely to use that relationship for his or her own benefit. Understanding why partners refrain from the self-serving bias is still in question but can partially be explained by favorable impression those in close relationships have for one another. A similar result was shown when looking at pairs of friends and strangers. Pairs performed an interdependent outcomes creativity test and were then given a bogus pipeline for a success or failure outcome. Strangers exhibited the self-serving bias in responsibility attributions, but friends tended to make joint attributions for both success and failure. Researchers have taken this as evidence for "boundaries on self-enhancement". In another study conducted in 2016, the implicit and explicit evaluation of 108 partners and exes as parents who were either married, separated or divorced was researched to investigate if the self-serving bias influenced them. Using two Implicit Association tests, one measuring Self vs Partner and the other measuring Self vs Ex, results showed that most of the time, men and women consider their exes or partners as less suitable parents which demonstrates the self-serving bias as they "ascribe more easily successes to internal factors" and failures towards their partners. Also, another result demonstrated that "women revealed a higher self-serving bias than men on both implicit and explicit measures, but only toward exes and not toward current partners" because they consider their exes as an out-group and their partners as an in-group.

Workplace
The self-serving bias can be found in several aspects of the workplace. Research shows that the self-serving bias is used to explain employment: being hired for a job is attributed to personal factors, whereas failure to obtain a job is attributed to external factors. Experimental investigation of the explanations for unemployment through asking participants to imagine particular job opportunities and likelihood of getting those jobs, however, did not show such a self-serving bias. Researchers claim that this may be due to the actor-observer role differences in the self-serving bias. Within the workplace, victims of serious occupational accidents tend to attribute their accidents to external factors, whereas their coworkers and management tend to attribute the accidents to the victims' own actions. Interpersonal dynamics of the self-serving bias in the previous section have implications for attributions for outcomes in the workplace. In an investigation of group dynamics, virtual group members had to complete a decision-making task via computer-mediated communication. Results showed that the self-serving bias was present in negative outcomes, and that greater interpersonal distance from group members increased blame for negative outcomes.

Narcissism
Studies revealed that narcissism was related to enhanced self-ratings of leadership, even when controlling for the Big Five traits. Another study showed that narcissism was related to enhanced leadership self-perceptions; indeed, whereas narcissism was significantly positively correlated with self-ratings of leadership, it was significantly negatively related to other ratings of leadership. This study also revealed that narcissism was related to more favorable self-ratings of workplace deviance and contextual performance compared to other (supervisor) ratings. Because narcissism broadly reflects strong self-admiration and behavioral tendencies which may not be viewed positively by others it is possible that narcissism influences self- and other perceptions differently, and insight into this possibility may be important given that differences in perceptions are the foundation for certain types of performance management and development practices.

Classroom
Studies in both lab and field settings have shown both teachers and students hold self-serving biases in regard to outcomes in the classroom. These attributions hold the potential for conflict between teacher and student since neither will take personal responsibility, as the student may blame the teacher while the teacher holds the student accountable. However, both teachers and students also reported being aware of the others' bias, which indicated there may be a feasible conflict resolution mechanism.

Computer technology
Computers have become an integral part of everyday life, and research has shown that individuals may subconsciously treat interactions with computers as they would treat a social situation. This finding combined with what is known about the self-serving bias in interpersonal relations indicates that consumers that use a computer to buy products will take personal credit for successful purchases but blame the computer for negative purchase experiences. It was also found, however, that consumers are more willing to attribute successful purchases to the computer and not ascribe blame to the computer for failed purchases if they have "intimate self-disclosure" with the computer, which Moon describes as revelation of personal information that makes the discloser feel vulnerable. Another reason is that people are so used to bad functionality, counterintuitive features, bugs, and sudden crashes of most contemporary software applications that they tend not to complain about computer problems. Instead, they believe it is their personal responsibility to predict possible issues and to find solutions to computer problems. This unique phenomenon has been recently observed in several human-computer interaction investigations.

Sports
Individuals have been shown to exhibit the self-serving bias in regard to sports outcomes. In one study, collegiate wrestlers at the Division I level made self-reported attributions of the outcomes in their preseason matches. Winners were more likely than losers to attribute the match outcome to internal causes. The researchers note that wrestling is a one-on-one sport and has clearly defined winners. Therefore, other sports of this nature may show similar results, but other team sports or sports with more ambiguous outcomes may not show the same pattern for the self-serving bias. In another study conducted in 1987, the research focused on comparing the self-serving attributions made by individuals who played single sports and those who played in teams. The study gathered 549 statements that were coded for attributional content from lone performers such as tennis and golf players and team performers such as baseball, football or basketball players. The results showed that "lone performers made more self-serving attributions than team performers" because their performance outcomes have a greater effect on their individual esteem unlike for group outcomes where it "must often be distributed among all participants." To expand upon self-serving attributions made by team sports, a study conducted in 1980 coded "newspaper accounts of baseball and football for attributional content." The coding of the newspaper accounts showed that there was a "tendency to make internal attributions for success and external attributions for failure" which supports the self-serving bias as about 75% of the attributions from winning teams were internal while about 55% of attributions from losing teams were internal.

Depression
Clinically depressed patients tend to show less of a self-serving bias than individuals in the general population. In a study exploring the effects of mood on the self-serving bias, the moods of participants were manipulated to be either positive or negative. Negative mood participants were less likely to attribute successful outcomes to the self than positive mood participants, attributing success to external factors. It has been suggested that the negative mood in depressed individuals as well as their self-focused attention explains why clinically depressed populations are less likely to exhibit the self-serving bias than normal populations.

Impacts in negotiation
Self-Serving bias is defined also by Kaplan et al. to individual's preferences, which effects to his/her beliefs in an optimistic way. Kaplan et al. also defines, that SSB should be termed as ‘self-defeating’ phenomenon as it appears for persons, who does not give up. Furthermore, Kaplan et al. state, that specific type of self-serving bias is wishful thinking. This is typically present, when unpleasant surprise pops up in the negotiation, particularly when the opponent has made preparations carefully. Another example is well-known phenomenon from law-court and is commonly used also in law-based TV-series. We can say, that according to Kaplan et al.'s finding, that self-serving bias is playing a major role in negotiation context. There is an emotional effect to the negotiations and there seems to be a reflection between self-serving bias and emotions.

Functional magnetic resonance imaging (fMRI)
The self-serving bias has been investigated by the fMRI method in normal populations. Attributions using the bias show activation in the dorsal striatum, which plays a role in motivated behavior, as well as in the dorsal anterior cingulate. In clinically depressed patients, there appear to be weaker connections between the dorsomedial prefrontal cortex and limbic areas of the brain, so this connection may play a role in self-serving attributions.

Electroencephalography (EEG)
In a study employing the EEG method of examining brain activation, participants were given bogus outcome feedback that indicated either success or failure and told to make attributions. Different from non-self-serving responses, self-serving responses did not show increased dorsomedial frontal cortex activity preceding attribution decisions. Such lack of brain activity implies that self-control, which is controlled by the dorsomedial frontal cortex, is not as prominent in self-serving attributions as non-self-serving ones.

title: Self-serving bias