text:
Talk:Demystifying Depression

Review Notes

 * Just because wikibooks can be edited by anybody, doesn't mean they are. (The graphs are totally bogus.) by 128.119.165.135
 * That disclaimer was definitely a good one. Although the author warns the reader at some points about following conjecture, it feels like most of this book is conjecture, fuzzy logic, and the result of a nonprofessional. The author scolds professionals, as if those who have made a career out of psychology don't know their subject; yet the author himself seems to have little experience. If he could back up his statements by citing his sources, I would be more impressed. -Monk 05:55, 4 December 2006 (UTC)

This book is not a good source of information
Let me make this clear right now: The majority of this book was written by one person (Name of Feather), a person who is not a professional, has not cited any articles from scientific journals. In fact, his sources are all secondary, and they all suck (Really, they do). There is no indication that this guy has any idea what he's talking about. He talks big, as if he knows the subject. But where's the proof? This entire book is just one rambling speech after another about what he thinks depression is. Where is the proof that any of this bull is true? He speaks about all this brain chemistry mumbo-jumbo, and acts as if it instantly means that all his conclusions are accurate. But he backs up almost NONE of his claims with evidence.

Do not listen to this guy. Listening to this guy would be equivalent to taking medical advice about your broken leg from a Janitor who says he took a biology course in high school. Although Name of Feather may act like he knows the subject, it sure as hell seems he doesn't. If he had any actual professional experience, instead of just deciding that he'd go on the internet and spew whatever he decides is right, he'd have evidence and actual statistics, he'd have objective evidence and not just anecdotes about his own personal version of "the truth" about depression.

If you are depressed, do not make decisions about what to do off of this book. There's no evidence that the author understands the subject any more than you do. The author just *thinks* they understand the subject, but that doesn't mean anything. Go to an actual doctor, an actual professional; or if you're not into quacks, who have spent years studying this stuff, at least don't listen to this nut who thinks he has "all the answers" because he uses fancy words like "serotonin" and "neurogenesis." I don't care if he read a news article or two about it. I don't care if he took some course in psychology ten or twenty years ago. You should listen to actual professionals, or to many different people who have had depression. But don't let some stranger from the internet, who has not shown that his ideas are valid in any way, tell you what to do with your life.--Monk 06:21, 4 December 2006 (UTC)

I agree. I am wondering if large portions of this book need removed until they can be written properly. Lonjers 08:47, 24 January 2007 (UTC)

I agree, and would have said it if nobody else had. But in defence of the author, depression is a very individual thing. I was diagnosed with depression as a child and I am now over 60. It didn't stop me working. My story would be very different. The other day I looked at a book by an English sufferer. His story was very different again, and just as irrelevant to mine. Depression is not capable of precise description like a broken leg or an infection. I have yet to come up with a formal definition of it.

On the subject of rants
Hey Monk, before you "contribute" any further, would you mind counting the number of times that readers are advised to seek professional help if they think they have a depression? I go as far as advising them to seek a competent professional (i.e. a psychiatrist) instead of being treated only by their (cheaper) GPs.

That being said, show the advice herein contained to a modern psychiatrist. They will not disagree with it. --Name of Feather 21:40, 6 December 2006 (UTC)

 * On the subject of proof, by Monk

 * You seem to be very confused as to where the burden of proof lies here. It's not my job to disprove the contents of your book to show that the contents are untrustworthy. It's your job to prove the contents of your book to show that they're trustworthy in the first place. You can't just put any content up here and expect everyone to treat it as authoritative and the truth until they can get an expert to vouch against it. You need to back up your statements with proof. Doing that is your job, not mine. If you cannot provide good proof for your scientific statements, you can not expect others to treat anything you say as scientifically reputable.

 * Secondly, I don't give a damn if you advise readers to see a professional a hundred times, that doesn't make your knowledge any more professional. You are not qualified to "inform" people about the subject to any degree, because as far as I'm concerned, you may know nothing about it. You may just be making this up. You may just be "remembering it" from some casual chat you had with a few psych doctors months ago, but that means essentially nothing as to qualifications. You have shown NO qualifications to educate others on the subject. Normally, qualifications are irrelevant as long as you can back up your claims with objective evidence, but so far you have not actually backed up your claims with anything but a vague hand-motion to a few mainstream-level science magazines, and some other worthless sources.

 * Depression is a sensitive subject. I think I'm justified in warning other people when you go around telling them what to do with their lives without providing any evidence that you know what you're talking about. I don't care if you throw in "Oh, but you should really see a doctor" at the beginning, you're still instructing them on something that you may know nothing about. If you have enough evidence to support the claims you make in this book, that's great, but you have to show that evidence, and it has to be valid evidence. Every claim has to be supported by previously collected data, proof, and scientific papers, rather than be anecdotal.

 * Irrelevant of whether the book is designed to appeal to the masses, the information within is of a sensitive scientific subject, and should be scientifically accurate. Like any scientific piece, although it may be up to others to investigate whether your evidence and data is valid and whether it supports or does not support your conclusion (something I have done, and in this case I have found that it's mostly invalid evidence), it's up to you to prove your arguments in the first place. You have failed to do that. If you can not support your claims about depression, you are not qualified to speak on the subject, and you are not qualified to tell people how to live their lives when under such a mentally precarious condition.

 * I don't need to prove you wrong for your claims to be dubious. If you can not prove that you are correct in the first place, your claims are automatically put into doubt. Until you can back your claims up, and back them up well, this book is an unreliable source of information. - Monk talk 20:15, 17 December 2006 (UTC)

I am male, and in Australia. I have had depression for 45 years, but I still don't take an hour and a half to get up in the morning. I am sure that what Name of Feather has written agrees with his experience, and no doubt, what he has written is what a psychiatrist would say to him. It is good if it gets men to acknowledge that they can be depressed, too. But it is not of general application. On the ordinary Wikipedia, it would be labelled "weasel words" - putting the author's views forward as general knowledge (although I hate the expression itself.) How does he know that a modern psychiatrist would not disagree with his advice? Is he a psychiatrist, or so familiar with psychiatric thought generally? He hasn't quoted the basis of this statement, just as with any of his others. I have already mentioned one area where I would receive different advice.

What worries me is that advice to wrap oneself in cotton wool, as he recommends, is exactly the wrong treatment for depression. It depends on the depth of depression involved, and I was lucky enough to keep working. But so many depressed people are sitting patiently waiting for a cure, and doing nothing with their lives in the meantime. Depression is an interaction of brain chemistry, circumstances and attitude. Change any one, and you change the other two. Although "positive thinking" or "counting our blessings" often achieves nothing against depression, nevertheless attitude is still within our control. Depression practically wipes me out for about 3 days every month, but like a woman with periods that are just as disabling, I don't let it stop me the rest of the time. I try to look on it as a disability, rather than an illness.

I find the term "a depression" strange. I suppose that it is legitimate like "a cancer" or "an AIDS". It must be a local thing. We don't use it here. - Douglaid

Sources suck because....
His sources suck, and here's why -- The author has only supported his statements with the following references: This guy only cites one good source, but his book doesn't even reflect the contents of that source. All the other sources are either secondary or meaningless. Looks like he has no idea what he's talking about.
 * created a few haphazard links to a "science news" website, and a page which reprints a "science news" magazine. Where "science news" refers to a magazine that reformats, rewrites, and rewords science knowledge as to make consumable for easy reading by the public.
 * created a few links to wikipedia articles
 * created a link to a student's assignment at a college (Not an authoritative source in any way!).
 * The only possibly valid reference he uses is This NIMH site, and you would be better off reading that page than this "book".

--Monk 06:36, 4 December 2006 (UTC)

Exercise only for 'mild' depression?
My psychiatrist told me that regular aerobic exercise is as good for moderate depression as an SSRI, according to studies. This book states the proper role of exercise is much more limited, without seeming to back that up with proper research.

207.34.148.245 19:07, 7 December 2006 (UTC)

Todo

 * Change the tone of the book, especially the first person perspective.
 * Agreed.

Retitle?
I think that a title like Introduction to Depression would serve this book better and bring it more inline with the textbook nature of wikibooks. What does everyone else think? Triddle 07:17, 3 Jun 2005 (UTC)
 * Change Title The title Introduction to Depression is less marketing-pitch and honest. One more vote for this, and I'll move the title if nobody else does. -Monk 05:41, 4 December 2006 (UTC)

Retitle plus other suggestions
Concerning the retitle, that is fine by me!

Some other suggestions (for now):

 * I will make proper figures out of the ASCII art. I know how they should look like, so I should do it.
 * Merge parts 1 and 2.

Later on there are other things that could be done:

 * Create a section for each of the available treatments (meds, etc)
 * Add information on the existing antidepressants (though Wikipedia already has quite a lot)

New navigation template
I created a prototype navigation template and put it on the first two pages of this book. Here it is as an example:

What does everyone else think? Triddle 20:22, 5 Jun 2005 (UTC)

Template
Using a template is a good idea, of course.

About the particular format of the template, I would suggest that all links use the same font size. Also, "First Page" should be renamed "Top", as that is the standard nomenclature used by most tools (eg. tex2html).

Name of Feather 10:21, 6 Jun 2005 (UTC)

Communication between editors
I personally find the use of the talk page a very limited form of communication. What about creating a mailing list (a yahoo group or something) for the purpose of synchronising the editing process?

Name of Feather 10:23, 6 Jun 2005 (UTC)

Concerning the title
Well, I am not adamant about it, but perhaps we should leave the title as it is. It has already picked up some "brand recognition"... :-)

Name of Feather 10:44, 6 Jun 2005 (UTC)

Namespace
Looking at the Naming conventions page, we should move all pages back to the original "Demystifying Depression/Section Name". That is the preferred format for new books.

Name of Feather 10:54, 6 Jun 2005 (UTC)

 * After reading the Naming Conventions page and Hierachy_naming_scheme it seems that using : is going to be easier for this project than using /. Why? The | trick will be of great use when creating links to pages inside the book. Quick overview of how links work:

 * Foo - links to Foo
 * Bar links to Foo but displays Bar
 * Foo:Bar links to Foo:Bar
 * Bar links to Foo:Bar but only displays Bar (note trailing |)
 * Foo/Bar links to Foo/Bar
 * Foo/Bar links to Foo/Bar but displays Foo/Bar, can't use trailing /
 * Bar links to Foo/Bar but displays Bar

Now think of the difference between

and

As well as the other benefits listed by Hierachy_naming_scheme. It really seems to me that setting this up in its own namespace is the way to go. Triddle 16:32, 6 Jun 2005 (UTC)

 * I didn't know it was possible to create custom namespaces. In that case, it is definately the way to go!

Name of Feather 08:53, 8 Jun 2005 (UTC)

Announce book
I think it is time to announce the book and add it to the bookshelves, don't you agree?

Name of Feather 11:03, 6 Jun 2005 (UTC)

I do not agree due to the huge amount of unsupported and perhaps false information.Lonjers 09:10, 24 January 2007 (UTC)

Notation fixer
I ran this program on all the articles to update the old style reference notation. I hope someone else can find it useful in the future. Triddle 06:56, 12 Jun 2005 (UTC)

 * 1) !/usr/bin/perl -w

 * 1) This source code is copyright Tyler Riddle ,
 * 2) caries no license requirements, and is made available for any purpose.
 * 3) You may incorporate this into any other project with out regard
 * 4) for licensing issues.

use strict;

my $data = <<EOF; EOF
 * 1) Wikipedia: Dualism (philosophy of mind)
 * 2) Wikipedia: Cirrhosis
 * 3) Taming Stress
 * 4) Wikipedia: Stress (medicine)
 * 5) Wikipedia: Fight-or-flight response
 * 6) Neurogenesis in the Human Brain: Fact or fiction?
 * 7) Stress and the Immune System
 * 8) Sleep Paralysis Page
 * 9) NIMH: Depression
 * 10) Wikipedia: Selective serotonin reuptake inhibitor
 * 11) NIMH: Bipolar Disorder
 * 12) Why? The Neuroscience of Suicide
 * 13) Nietzsche's Toxicology
 * 14) Wikipedia: Clinical depression
 * 15) Wikipedia: Concentration (game)
 * 16) Wikipedia: Functional magnetic resonance imaging
 * 17) Depression and the Birth and Death of Brain Cells
 * 18) Overtraining

my @links = &build_array;

while(<>) { s/(\[(\d+)\])/&handler($1, $2)/ge; print; }

sub handler { my $orig = shift; my $refnum = shift; die "Invalid reference number: $refnum" unless defined $links[$refnum];

my $newlink = '['. $links[$refnum]. ']';

print STDERR "$orig => $newlink\n";

return $newlink; }

sub build_array { my @array;

$array[0] = 'garbage'; #numbering for the articles starts at 1

while($data =~ m/^#\[([^ \]]+)/gm) { my $link = $1;

push(@array, $link); }

return @array; }

Reference Descriptions
This is about the reference links throughout the book. What about adding article/page titles to the tooltips?

I am very impressed with the book. Thanks for a useful and real discussion.

Calvinism
The references to Calvinism probably need better explanation. 220.253.24.254 01:54, 28 December 2005 (UTC)

Before you make changes...
Being a wikibook and all that means that one expects people to make changes/corrections as they see fit. However, if not for anything else at least for the sake of politeness, it would be very much appreciated if radical changes were first proposed in this talk page. (See the history for an example of what I'm referring to).

Thank you,

Name of Feather 18:46, 30 May 2006 (UTC)

Radical changes are however needed to this book please make them.Lonjers 08:44, 24 January 2007 (UTC)

I think some doctor should put some specific counter arguments against some of the specific the book is claiming. I sense that the author of this book deeply believes what he or she wrote, so he or she deserves some scientific arguments. May be those sections that can not be proved or were just made up should be marked as that are controversial. Ervinn 15:24, 24 January 2007 (UTC)

What should be done with this book?
I think that this book needs almost completely rewritten and reorganized as an introduction to depression. Or it needs to be removed from wikibooks. My reason for this is it contains large amounts of unsighted or original research and information based on individual experience. According to the "What Wikibooks is not" section of What is Wikibooks large parts of this book do not qualify for being part of a Wikibook. At the vary least it needs removed from the completed books book shelf. What are other peoples opinions Lonjers 09:15, 24 January 2007 (UTC)

I would not remove this book. The claims it is making could be true, based on 'individual experience'. If scientifically proven that the book claims are incorrect then I would remove it. In the meantime it could be moved to a controversial state. There are some precedence, where 'individual experiences' were strongly rejected and eventually turned out to be true. Ervinn 15:40, 24 January 2007 (UTC)

I'd move to remove...
I read this book with some care. I see very little merit in it and much potential for disseminating misconceptions and unfounded speculation about a very important subject. Does the nature of wiki mean that we have no reponsibility to try to ensure good quality information? Despite the caveats, this book is seriously likely to misinform people including sufferers about a potentially very dangerous illness.

Unfortunately not a 'wikibook'
I personally think that this work has its merits in giving a new public perspective (as far as I am aware) on depression. Upon reading the What is Wikibooks, however, I do not think that it qualifies unless properly cited or founded, as it is certainly not a textbook, rather an interesting essay. Simply put, I do not think that this is the place for the book; but I do think that it should be part of a public reading list somewhere on depression (I assume somewhere on Wiki), if not simply for the debate it causes.

My editing spree
In case any one noticed I went through and just destroyed everything I though was obviously wrong or does not fit the guidelines for what should be on wiki books. I realize this was not the most democratic method but it needed done and I was in the mood. The whole book still need restructured perhaps in the form of three major sections What is Depression, Treatments, Other Issues. It also all needs cited. If disagree with any of my changes feel free to revert. The book is currently a mess with many pages now blank in need of deletion but I could not figure out how to do that so perhaps some one more knowledgeable can help with that. Lonjers 11:44, 12 March 2007 (UTC)
 * I do not agree all the deletions. Deleting something because being in the mood is the definitation of vandalism. I think a warning on the discussion page before deletion is the wiki policy we should follow. Ervinn 16:20, 12 March 2007 (UTC)

I understand revert anything you feel is actually within the guide lines of things that should be on wiki books. Relize however the most of the information I deleted was in direct confrontation with much higher quality article on wikipedia. It just seemed to me that there had been a consensus for a while for deletion but no one had done anything. Lonjers 17:42, 12 March 2007 (UTC)

If this stays it is certainly inappropriately indexed
As a psychiatrist, and a wikipedia member I must say that the inclusion of this book under Health is completely unfair to to people seeking high quality information. It does provide one person's perspective without scientific data or sources, and it may have some value in shedding light on the publics viewpoint. However, this is not a book about Health. At best this should fall under Self-Help or perhaps Editorial. I refrain to get into the argument about whether this should be completely removed or not, but it certainly has no place whatsoever within the category of health. Slippy007 March 30, 2007

VfD
I personally feel that this book had some good information before it was mostly all deleted by Lonjers. However, if the requirements for inclusion here are the same as Wikipedia, than original research is not welcome and thus this book should be outright deleted. I don't know why it hasn't been put up for deletion given the general consensus. However, there is a deletion policy in effect here. As I do not believe it should be deleted I'm not going to put it up myself, but there you have it. Spoom (talk) 18:17, 18 April 2008 (UTC)

I am depressed and THIS IS THE BEST PIECE OF INFORMATION I FOUND
I am depressed for years. Due to traumas and ongoing personal issues... I am educated person and read everything I could find about depresion ... I am went to therapy - 8 different highly qualified medical professionals and 2 MD who gave me meds. Results? -traditional medical community has ABSOLUTELY NOTHING USEFULL for me. I just learn to copy not to recover. So I think they should even post here.

Kim545 (discuss • contribs) 06:20, 17 November 2011 (UTC)

title: Talk:Demystifying Depression


text:
Demystifying Depression/The Controversy about Antidepressants

The Controversy about Antidepressants
This is largely country-dependent: in some countries their use is widespread and generates little discussion; in others, many factors contribute to making them practically taboo words. The country where I live, the Netherlands, tends towards the taboo end of the spectrum. The reason has a lot to do with the prevalent (and backwards if you ask me) Calvinist mentality. I know that in other places, such as most of North America and Southern Europe they are much more readily accepted. Your mileage may vary.

The controversy is typically framed in the following ways: doctors nowadays over-prescribe antidepressants, instead of following the psychotherapy route; antidepressants are just a ploy from the evil pharmaceutical multinationals; our societies are drifting towards a "Brave New World" scenario where drugs are used to keep the populace happy and unable to rebel. Well, my personal opinion is that there is some substance to some of these worries, but they are largely exaggerated and fail to acknowledge one very important fact: antidepressants are very effective in treating clinical depression. This is not a matter of opinion: it has been demonstrated in several double-blind clinical trials.

First, on the issue of over-prescription. I would say that they are both over-prescribed and under-prescribed. The problem is that most doctors do not understand depression well, and will prescribe drugs to people whose brains are healthy, and fail to provide them to people who could actually benefit from them. Take people who are mourning, for example. In most cases, these people do not have a depression. Grief is something perfectly normal, and its onset is all too sudden to cause a depression (remember that a depression typically takes years to develop). Likewise, consider giving antidepressants to very young people: the brain of a child or even a teenager has such a fantastic ability to repair itself that it takes quite a pounding for a depression to develop. In these cases, antidepressants and all their unavoidable side effects are more likely to hurt than to help. On the other hand, there are people who have minor problems with stress and anxiety, or whose blood pressure is above normal for no apparent reason. They are often simply told that they should watch out for salt in their diets, or to take up yoga or meditation. This advice might help, but only to a certain degree. I suspect that a course of an antidepressant would have a stronger and more lasting effect.

Moving on to the subject of side-effects. Modern antidepressants are generally well-tolerated and safe to use. They do have side-effects, which depending on the drug and the person can be significant enough that people discontinue taking the medication. However, this is yet another issue where proper handling by a competent professional will make a huge difference. What one often finds is that people are given the wrong drug for their case. Imagine for example an overweight patient being given an antidepressant which increases appetite, or someone who has a satisfactory sex life and is given a drug which upsets their libido. What is required is matching the profile of the patient with the expected side-effects of the drug. Granted, there is plenty of variation among individuals, but the overall pattern is still strong enough that we can categorically say what will be the most likely side-effects of a given antidepressant. A straightforward discussion with a good professional will go a long way towards finding a drug tuned to your particular case, thus minimising the negative side-effects and decreasing the chances of premature discontinuation.

Finally on to the subject of psychotherapy. As someone who had a depression, I can assure you that there is nothing more patronising and irritating than people who bring up the "psychological help". A depressed person will definitely need professional help, but mostly for a proper explanation of the problem, to learn relaxation techniques, to know how to listen to their bodies, and to be coached in the lifestyle changes required for giving their brains a chance to recover. Once they are recovered, perhaps some therapy might be needed to make sure that whatever behavioural patterns which contributed to the development of the illness will not recur. However, and I cannot stress this enough, therapy is not a substitute for medication, and "psychological help" is a misunderstanding.

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


text:
Wikibooks talk:Collaboration of the Month/June 2005 voting

There is nothing in the voting rules about a tie, yet we have a tie. I say we go with the BotM policy, and select the older book. Reub2000 11:24, 1 Jun 2005 (UTC)

I suggest you choose Puzzles, since the FHSST one has already been elected as BotM It'd look very unprofessional to have the same book listed twice on the homepage in different categories IMO. --Azertus 11:59, 1 Jun 2005 (UTC)


text:
Talk:Using GNOME/Differences KDE

Slicker?

 * "While KDE's interface is normally considered slicker and more polished to that of GNOME possibly due to the underlying Qt toolkit, GTK is a very popular toolkit for Linux and so most apps have better integration with GNOME."

Hmmm... how can we say this in a less-biased way? --Jcarroll 05:18, 19 March 2006 (UTC)

Task Bar

 * "GNOME takes the Mac OS X approach, placing the task bar on top of the screen and a separate bar for currently-open applications (the Task Bar)."

Isn't this is entirely under the control of the user? I'm pretty sure that it is, since I've configured my gnome/ubuntu install to have a single combined windows-style task bar at the bottom of the screen.

title: Talk:Using GNOME/Differences KDE


text:
User:LinasLit~enwikibooks

LinasLit[uanus]

Linas Plankis, filologist, 32 years old, Vilnius.

The page, I'm currently revising here is:
 * Lithuanian language basics

These are pages of my interest in wikipedia
 * Culture of Lithuania
 * Lithuanian mythology
 * Lithuanian language

In wikipedia: w:User:LinasLit

title: User:LinasLit~enwikibooks


text:
User:Sblive~enwikibooks

retired.

n:User:Sblive

pl:User:Sblive

title: User:Sblive~enwikibooks


text:
Blender 3D: Noob to Pro/Looking All Around - Panorama Settings

This Article is Out Of Date
Panoramic features were changed somewhere between 2.37a and 2.42. More information, including how to actually use panorama, can be found in this thread in the forums: http://blenderartists.org/forum/showthread.php?p=797886

Building the Example Scene

Ever wondered how that cool looking 360 degree panoramas that you see on some websites are made? Well, I don't know either, so someone else will have to tell about that. What I found out though is how to make Blender output a 360 degree panoramic image - quite probably this at least is the first step when making something like on those websites.

Now, let's try to progress like in a tutorial, as in the other pages of this Wikibook. So, fire up Blender, and look at the well known initial box scene. Or rather, change it somehow. Assuming you have read the book in order, it shouldn't be hard to get something like in the picture.

I placed the camera and the light both above the origin, deleted the cube, and added 8 cylinders, all around the origin. One way to do this is to place one cylinder, then duplicate and rotate it around the origin. For this to work, set the rotation center to the 3D-cursor (with the Pivot button), and position the 3D cursor at the origin (use SHIFT+S to make the 3D cursor snap to the grid).Place the first cylinder using GKEY and then holding CTRL while moving the mouse. Change to object mode, then use SHIFT+D to duplicate it. Next, press RKEY to rotate it, then hold CTRL while rotating it by 45 degrees. Repeat the same for the remaining cylinders. Use G to move the light. Use NKEY to enter the camera values like shown, so it looks parallel to the ground.

Speaking of ground, lets also add a ground. I added another cylinder, below the other ones, as shown. It's easy to add by switching to front view (NUM1), duplicating a cylinder (SHIFT+DKEY), and then moving it holding CTRL pressed again, so it snaps to the grid. To scale it, use the SKEY, but hit SHIFT+ZKEY to lock the z scaling, and hold CTRL pressed while scaling in x and y direction so you can snap to the exact size you want.

Now, to have a complete scene, we need some colors. I made the ground cylinder green, the 8 example cylinders gray, and also added a noise normal to the ground. This doesn't really matter here though, just needed some example scene for the 360° camera.

Something more interesting is the sky texture, because Blender's sky can be made to seamlessly wrap around with 360 degree. Below is a screenshot of the sky settings I used. To get there, click on the Shading button, then select World.

To change the texture, click the textures button or press F6, then add a new texture with the small button with two arrows, and select the type (e.g. "Marble" or "Clouds") instead of "None" for the texture. Go back to the World pane, and enable the Real and Blend buttons. And don't forget to use nice colors, I used blue and white. Now it looks a bit like white clouds in a blue sky.

[Maybe should add here more details? What is important so you don't get a seam at the 0 - 360 degree point? How do you map pre-made sky textures?]

And we are already done, this is the example scene. All that is left to do is to render it as a panorama.

Panoramic Rendering
Go to the render settings (F10), and click the Pano button. Change the Xparts value to 4. The value in Xparts will tell how many times the camera will 'turn' horizontally when rendering. The Yparts value would do the same vertically. Each part (Xparts or Yparts) will render the size of the whole image you set. To make things easier, make the output image size quadratic and set both X and Y Aspect to 100. E.g. make your image size 600x600, but not 800x600, otherwise the following will not work.

If you want a seamless 360 degree view, it is important to know how many degrees one single image spans. For example, if you know one image is 90 degree, then you can set Xparts to 4, and the result will be a single panoramic picture, and with the right panorama viewer, you can spin around in it endlessly.

But, how do you make a single picture 90 degree? The angle a picture spans is called field of view (FOV). And it is a property of the camera. To change it, select your camera, then click the edit button (or hit F9). Make sure you haven't set your camera to orthographic (the "Ortho" button), since FOV only exists with a normal camera.

You can directly enter the FOV in Blender's camera settings (as of version 2.42) - Toggle the 'D' button on, next to the parameter called Lens. Type in 90 to get a 90 degree FOV. Now hit F12 to render our test image.

If you want, you can also try it out with any other scene. Place the camera somewhere in the middle with a good view all around, set the camera's Lens to 90, and go into the render settings (F10). Set Xparts to 4, enable Pano, and render. You should get an image 4 times as wide as a normal image, and the left and right edges should fit together seamlessly. Also note that Blender doesn't know if it should apply the FOV as horizontal or vertical viewing angle, but we always want it to be the horizontal angle. Therefore just make the single images of the panorama quadratic, as mentioned above - then horizontal and vertical FOV is the same and Blender gets it right.

This is the resulting panoramic image:

Warning: Didn't convert following lens settings to the new possibility with the 'D'-button for passing the FOV value directly. One problem remains, the image will be quite distorted. This is because a FOV of 90 degree is too high. Let's try with 45 degree and 8 XParts instead. As you will have noticed when playing around with the Lens parameter before, setting Lens to 8 instead of 16 will not achieve this, it will make the FOV even bigger. Setting it to 32 looks better, but definitely is not 45 degree. The picture to the right explains how FOV and Lens relate to each other:

The camera is at the bottom, the red angle is our desired FOV, and the length of the green line is what the Lens parameter represents in Blender. Therefore, the formula to calulcate Lens when we know FOV:

 * Lens = 16 / tan(FOV / 2)

For a FOV of 45 degree, we therefore get a Lens of 38.627. Now, write that into the Lens field in the camera settings, and render with 8 XParts. This time it will render an output image which is 8 times as wide as a normal output image, and again it will be a seamless 360 degree all around panorama of your scene. And this time with less distortion. With the above formula, you can now use any number of XParts you want - just divide 360 by the number of parts, and calculate the Lens parameter for the resulting FOV. Note that you also need to take the Aspect settings into account, unless you set it to 100 and create a quadratic output, as we did.

Some Lens settings:

 * 4 parts: 16
 * 8 parts: 38.627
 * 16 parts: 80.437

The output with 8 parts can be seen below.

As always, feel free to modify this page in any way you want or add feedback to the Talk page.


text:
Human Physiology/Blood physiology

Overview of Blood
The primary function of blood is to supply oxygen and nutrients as well as constitutional elements to tissues and to remove waste products. Blood also enables hormones and other substances to be transported between tissues and organs. Problems with blood composition or circulation can lead to downstream tissue malfunction. Blood is also involved in maintaining homeostasis by acting as a medium for transferring heat to the skin and by acting as a buffer system for bodily pH.

The blood is circulated through the lungs and body by the pumping action of the heart. The right ventricle pressurizes the blood to send it through the capillaries of the lungs, while the left ventricle re-pressurizes the blood to send it throughout the body. Pressure is essentially lost in the capillaries, hence gravity and especially the actions of skeletal muscles are needed to return the blood to the heart.

Gaseous Exchange
Oxygen (O2) is the most immediate need of every cell and is carried throughout the body by the blood circulation. Oxygen is used at the cellular level as the final electron acceptor in the electron transport chain (the primary method of generating ATP for cellular reactions). Oxygen is carried in the blood bound to hemoglobin molecules within red blood cells. Hemoglobin binds oxygen when passing through the alveoli of the lungs and releases oxygen in the warmer, more acidic environment of bodily tissues, via simple diffusion.

Carbon dioxide (CO2) is removed from tissues by blood and released into the air via the lungs. Carbon dioxide is produced by cells as they undergo the processes of cellular respiration (particularly the Kreb's Cycle). The molecules are produced from carbons that were originally part of glucose. Most of the carbon dioxide combines with water and is carried in the plasma as bicarbonate ions. An excess of carbon dioxide (through exercise, or from holding ones breath) quickly shifts the blood pH to being more acidic (acidosis). Chemoreceptors in the brain and major blood vessels detect this shift and stimulate the breathing center of the brain (the medulla oblongata). Hence, as CO2 levels build up and the blood becomes more acidic, we involuntarily breathe faster, thus lowering CO2 levels and stabilizing blood pH. In contrast, a person who is hyperventilating (such as during a panic attack) will expire more CO2 than being produced in the body and the blood will become too alkaline (alkalosis).

Blood Composition
Blood is a circulating tissue composed of fluid plasma and cells (red blood cells, white blood cells, platelets). Anatomically, blood is considered a connective tissue, due to its origin in the bones and its function. Blood is the means and transport system of the body used in carrying elements (e.g. nutrition, waste, heat) from one location in the body to another, by way of blood vessels.

Blood is made of two parts:

 * 1) Plasma which makes up 55% of blood volume.
 * 2) Formed cellular elements (red and white blood cells, and platelets) which combine to make the remaining 45% of blood volume.

Plasma makeup
Plasma is made up of 90% water, 7-8% soluble proteins (albumin maintains bloods osmotic integrity, others clot, etc), 1% carbon-dioxide, and 1% elements in transit. One percent of the plasma is salt, which helps with the pH of the blood. The largest group of solutes in plasma contains three important proteins to be discussed. There are: albumins, globulins, and clotting proteins.

Albumins are the most common group of proteins in plasma and consist of nearly two-thirds of them (60-80%). They are produced in the liver. The main function of albumins is to maintain the osmotic balance between the blood and tissue fluids and is called colloid osmotic pressure. In addition, albumins assist in transport of different materials, such as vitamins and certain molecules and drugs (e.g. bilirubin, fatty acids, and penicillin).

Globulins are a diverse group of proteins, designated into three groups: gamma, alpha, and beta. Their main function is to transport various substances in the blood. Gamma globulins assist the body's immune system in defense against infections and illness.

Clotting proteins are mainly produced in the liver as well. There are at least 12 substances, known as "clotting factors" that participate in the clotting process. One important clotting protein that is part of this group is fibrinogen, one of the main components in the formation of blood clots. In response to tissue damage, fibrinogen makes fibrin threads, which serve as adhesive in binding platelets, red blood cells, and other molecules together, to stop the blood flow. (This will be discussed in more detail later on in the chapter.)

Plasma also carries Respiratory gases; CO2 in large amounts(about 97%) and O2 in small amounts(about 3%), various nutrients(glucose, fats), wastes of metabolic exchange(urea, ammonia), hormones, and vitamins.

Overview
Red blood cell (erythrocyte) also known as "RBCs". RBCs are formed in the myeloid tissue or most commonly known as red bone marrow, although when the body is under severe conditions the yellow bone marrow, which is also in the fatty places of the marrow in the body will also make RBCs. The formation of RBCs is called erythropoiesis ( erythro / red; poiesis / formation). Red blood cells lose nuclei upon maturation, and take on a biconcave, dimpled, shape. They are about 7-8 micrometers in diameter. There are about 1000x more red blood cells than white blood cells. RBCs live about 120 days and do not self repair. RBCs contain hemoglobin which transports oxygen from the lungs to the rest of the body, such as to the muscles, where it releases the oxygen load.The hemoglobin gets its red color from their respiratory pigments.

Shape

RBCS have a shape of a disk that appears to be “caved in” or almost flattened in the middle; this is called bi-concave. This bi-concave shape allows the RBC to carry oxygen and pass through even the smallest capillaries in the lungs. This shape also allows RBCs to stack like dinner plates and bend as they flow smoothly through the narrow blood vessels in the body. RBCs lack a nucleus (no DNA) and no organelles, meaning that these cells cannot divide or replicate themselves like the cells in our skin and muscles. RBCs have a short life span of about 120 days, however, as long as our myeloid tissue is working correctly, we will produce about 2-3 million RBCs per second. That is about 200 billion a day! This allows us to have more to replace the ones we lose.

Main Component

The main component of the RBC is hemoglobin protein, of which there are about 250 million per cell. The word hemoglobin comes from "hemo" meaning blood and "globin" meaning protein. Hemoglobin is composed of four protein subunits: polypeptide globin chains that contain anywhere from 141 to 146 amino acids. Hemoglobin is responsible for the cell’s ability to transport oxygen and carbon dioxide. Hemoglobin, iron, and oxygen interact with each other, forming the RBCs' bright red color. You can call this interaction by product oxyhemoglobin. Carbon monoxide binds with hemoglobin faster than oxygen, and stays bound for several hours, making hemoglobin temporarily unavailable for oxygen transport. One red blood cell contains about 200 million hemoglobin molecules. If all this hemoglobin was in the plasma rather than inside the cells, blood would be so "thick" that the heart would have a difficult time pumping it through. The thickness of blood is called viscosity. The greater the viscosity of blood, the more friction there is, and more pressure is needed to force blood through.

Functions
The main function is the transportation of oxygen throughout the body and the ability of the blood to carry out carbon dioxide which is called carbamino – hemoglobin. Maintaining the balance of blood is important. The balance can be measured by the acid and base levels in the blood. This is called pH. Normal pH of blood ranges between 7.35-7.45; this normal blood is called alkaline (less acidic than water). A drop in pH is called acidic. This condition is also called acidosis. A jump in pH higher then 7.45 is called "alkalosis". To maintain the homeostasis (or balance,) the blood has tiny molecules within the RBC that help prevent drops or increases from happening.

Destruction

Red blood cells are broken down and hemoglobin is released. The globin part of the hemoglobin is broken down into amino acid components, which in turn are recycled by the body. The iron is recovered and returned to the bone marrow to be reused. The heme portion of the molecule experiences a chemical change and then gets excreted as bile pigment (bilirubin) by the liver. Heme portion after being broken down contributes to the color of feces and your skin color changing after being bruised.

White Blood Cells
Shape

White blood cells are different from red cells in the fact that they are usually larger in size 10-14 micrometers in diameter. White blood cells do not contain hemoglobin which in turn makes them translucent. Many times in diagrams or pictures white blood cells are represented in a blue color, mainly because blue is the color of the stain used to see the cells. White blood cells also have nuclei, that are some what segmented and are surrounded by electrons inside the membrane.

Functions
White blood cells (leukocytes) are also known as "WBC's". White blood cells are made in the bone marrow but they also divide in the blood and lymphatic systems. They are commonly amoeboid (cells that move or feed by means of temporary projections, called pseudopods, meaning "false feet"), and escape the circulatory system through the capillary beds. The different types of WBC's are Basophils, Eosinophils, Neutrophils, Monocytes, B- and T-cell lymphocytes. Basophils, Eosinophils, and Neutrophils are all granular leukocytes. Lymphocytes and Monocytes are agranular leukocytes. Basophils store and synthesize histamine which is important in allergic reactions. They enter the tissues and become "mast cells" which help blood flow to injured tissues by the release of histamine. Eosinophils are chemotoxic and kill parasites. Neutrophils are the first to act when there is an infection and are also the most abundant white blood cells. Neutrophils fight bacteria and viruses by phagocytosis which mean they engulf pathogens that may cause infection. The life span of a of Neutrophil is only about 12-48 hours. Monocytes are the biggest of the white blood cells and are responsible for rallying the cells to defend the body. Monocytes carry out phagocytosis and are also called macrophages. Lymphocytes help with our immune response. There are two Lymphocytes: the B- and T- cell. B-Lymphocytes produce antibodies that find and mark pathogens for destruction. T-Lymphocytes kill anything that they deem abnormal to the body.

WBCs are classified by phenotype which can be identified by looking at the WBCs under a microscope. The Granular phenotype are able to stain blue. The Agranular phenotype are able to stain red. Neutrophils make up 50-70% of Granular cells Eosinophils make up 2-4%, and Basophils 0-1%. Monocytes make up 2-8% of Agranular cells. B and T Lymphocytes make up 20-30%. As you can see, there is a great deal of differentiation between WBCs. These special cells help our bodies defend themselves against pathogens. Not only do they help our immune system but they remove toxins, wastes, and abnormal or damaged cells. Thus, we can say that WBCs' main function is being Phagocytic which means to engulf or swallow cells.

Platelets
Platelets, also called thrombocytes, are membrane-bound cell fragments. Platelets have no nucleus, they are between one and two  micrometers in diameter, and are about 1/10th to 1/20th as abundant as white blood cells. Less than 1% of whole blood consists of platelets. They result from fragmentation of large cells called Megakaryocytes - which are cells derived from stem cells in the bone marrow. Platelets are produced at a rate of 200 billion per day. Their production is regulated by the hormone called Thrombopoietin. The circulating life of a platelet is 8–10 days. The sticky surface of the platelets allow them to accumulate at the site of broken blood vessels to form a clot. This aids in the process of hemostasis ("blood stopping"). Platelets secrete factors that increase local platelet aggregation (e.g., Thromboxane A), enhance vasoconstriction (e.g., Serotonin), and promote blood coagulation (e.g., Thromboplastin).

Hemostasis (Coagulation or Clotting)
Hemostasis is the natural process of stopping blood flow or loss of blood following an injury. (hemo = blood; stasis = standing). It has three stages: (1) vascular spasm, vasoconstriction, or intense contraction of blood vessels, (2) formation of a platelet plug and (3) blood clotting or coagulation. Once the flow of blood has been stopped, tissue repair can begin.

Vascular spasm or Vasoconsriction: In a normal individual, immediately after a blood vessel has been cut and endothelial cells are damaged, vasoconstriction occurs, thus slowing blood flow to the area. Smooth muscle in the vessel wall goes through spasms or intense contractions that constrict the vessel. If the vessels are small, spasms compress the inner walls together and may be able to stop the bleeding completely. If the vessels are medium to large-sized, the spasms slow down immediate outflow of blood, lessening the damage but still preparing the vessel for the later steps of hemostasis. These vascular spasms usually last for about 30 minutes, long enough for the next two stages of hemostasis to take place.

Formation of a Platelet Plug: Within 20 seconds of an injury, coagulation is initiated. Contrary to popular belief, clotting of a cut on the skin is not initiated by air or drying out, but by platelets adhering to and activated by collagen in the blood vessels endothelium. The activated platelets then release the contents of their granules, which contain a variety of substances that stimulate further platelet activation and enhance the hemostatic process.

When the lining of a blood vessel breaks and endothelial cells are damaged, revealing collagen proteins in the vessel wall, platelets swell, grow spiky extensions, and start clumping together. They start to stick to each other and the walls of the vessel. This continues as more platelets congregate and undergo these same transformations. This process results in a platelet plug that seals the injured area. If the injury is small, a platelet plug may be able to form and close it within several seconds. If the damage is more serious, the next step of blood clotting will take place. Platelets contain secretory granules. When they stick to the proteins in the vessel walls, they degranulate, thus releasing their products, which include ADP (adenosine diphosphate), serotonin, and thromboxane A2.

A Blood Clot Forms: If the platelet plug is not enough to stop the bleeding, the third stage of hemostasis begins: the formation of a blood clot. First, blood changes from a liquid to a gel. At least 12 substances called clotting factors take part in a series of chemical reactions that eventually create a mesh of protein fibers within the blood. Each of the clotting factors has a very specific function. We will discuss just three of the substances here: prothrombin, thrombin, and fibrin. Prothrombin and fibrinogen are proteins that are produced and deposited in the blood by the liver.

 * Prothrombin: When blood vessels are damaged, vessels and nearby platelets are stimulated to release a substance called prothrombin activator, which in turn activates the conversion of prothrombin, a plasma protein, into an enzyme called thrombin. This reaction requires calcium ions.

 * Thrombin: Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long insoluble fibers or threads of the protein fibrin.

 * Fibrin: Fibrinogen is cleaved by thrombin to form its active form, "fibrin." Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot. This net of fibers traps and helps hold platelets, blood cells and other molecules tight to the site of injury, functioning as the initial clot. This temporary fibrin clot can form in less than a minute, and usually does a good job of reducing the blood flow. Next, platelets in the clot begin to shrink, tightening the clot and drawing together the vessel walls. Usually, this whole process of clot formation and tightening takes less than a half hour.

The use of adsorbent chemicals, such as zeolites, and other hemostatic agents, are also being explored for use in sealing severe injuries quickly.

ABO Group System
The ABO blood group is represented by substances on the surface of red blood cells (RBCs). These substances are important because they contain specific sequences of amino acid and carbohydrates which are antigenic. As well as being on the surface of RBCs, some of these antigens are also present on the cells of other tissues. A complete blood type describes the set of 29 substances on the surface of RBCs, and an individual's blood type is one of the many possible combinations of blood group antigens. Usually only the ABO blood group system and the presence or absence of the Rhesus D antigen (also known as the Rhesus factor or RH factor) are determined and used to describe the blood type. Over 400 different blood group antigens have been found, many of these being very rare. If an individual is exposed to a blood group antigen that is not recognized as self, the individual can become sensitized to that antigen; the immune system makes specific antibodies which binds specifically to a particular blood group antigen and an immunological memory against that particular antigen is formed. These antibodies can bind to antigens on the surface of transfused red blood cells (or other tissue cells) often leading to destruction of the cells by recruitment of other components of the immune system. Knowledge of a individual's blood type is important to identify appropriate blood for transfusion or tissue for organ transplantation.

Surface Antigens
Several different RBC surface antigens stemming from one allele (or very closely linked genes) are collectively labeled as a blood group system (or blood group). The two most important blood group systems were discovered during early experiments with blood transfusion, the ABO group in 1901 and the Rhesus group in 1937. These two blood groups are reflected in the common nomenclature A positive, O negative, etc. with letters referring to the ABO group and positive/negative to the presence/absence of the RhD antigen of the Rhesus group. Development of the Coombs test in 1945 and the advent of transfusion medicine led to discovery of more blood groups.

Blood group AB individuals have both A and B antigens on the surface of their RBCs, and their blood serum does not contain any antibodies against either A or B antigen. Therefore, a individual with type AB blood can receive blood from any group (with AB being preferable), but can only donate blood to another group AB individual. AB blood is also known as "universal receiver".

Blood group A individuals have the A antigen on the surface of their RBCs, and blood serum containing IgM antibodies against the B antigen. Therefore, a group A individual can only receive blood from individuals of groups A or O (with A being preferable), and can donate blood to individuals of groups A or AB.

Blood group B individuals have the B antigen on their surface of their RBCs, and blood serum containing IgM antibodies against the A antigen. Therefore, a group B individual can only receive blood from individuals of groups B or O (with B being preferable), and can donate blood to individuals of groups B or AB.

Blood group O individuals do not have either A or B antigens on the surface of their RBCs, but their blood serum contains IgM antibodies against both A and B antigens. Therefore, a group O individual can only receive blood from a group O individual, but they can donate blood to individuals of any ABO blood group (ie A, B, O or AB). O blood is also known as "universal donor".

Inheritance
Blood types are inherited and represent contributions from both parents. The ABO blood type is controlled by a single gene with three alleles: i, IA, and IB. The gene encodes an enzyme that modifies the carbohydrate content of the red blood cell antigens.

IA gives type A, IB gives type B, i give types O

IA and IB are dominant over i, so ii people have type O, IAIA or IAi have A, and IBIB or IBi have type B. IAIB people have both phenotypes because A and B are codominant, which means that type A and B parents can have an AB child. Thus, it is extremely unlikely for a type AB parent to have a type O child (it is not, however, direct proof of illegitimacy): the cis-AB phenotype has a single enzyme that creates both A and B antigens. The resulting red blood cells do not usually express A or B antigen at the same level that would be expected on common group A or B red blood cells, which can help solve the problem of an apparently genetically impossible blood group.

Rh Factor

Many people have the Rh Factor on the red blood cell. Rh carriers do not have the antibodies for the Rh Factor, but can make them if exposed to Rh. Most commonly Rh is seen when anti-Rh antibodies cross from the mothers placenta into the child before birth. The Rh Factor enters the child destroying the child's red blood cells. This is called Hemolytic Disease.

Compatibility in Blood/Plasma Transfusions
Blood transfusions between donor and recipient of incompatible blood types can cause severe acute immunological reactions, hemolysis (RBCT destruction), renal failure, shock, and sometimes death. Antibodies can be highly active and can attack RBCs and bind components of the complement system to cause massive hemolysis of the transfused blood.

A patient should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. If time allows, the risk will further be reduced by cross-matching blood, in addition to blood typing both recipient and donor. Cross-matching involves mixing a sample of the recipient's blood with a sample of the donor's blood and checking to see if the mixture agglutinates, or forms clumps. Blood bank technicians usually check for agglutination with a microscope, and if it occurs, that particular donor's blood cannot be transfused to that particular recipient. Blood transfusion is a potentially risky medical procedure and it is vital that all blood specimens are correctly identified, so in cross-matching labeling is standardized using a barcode system known as ISBT 128.

When considering a plasma transfusion, keep in mind that plasma carries antibodies and no antigens. For example you can't give type O plasma to a type A, B or AB, because a person with type O blood has A and B antibodies and the recipient would have an immune response. On the other hand an AB donor could give plasma to anyone, since they have no antibodies.

The table to the right is for plasma transfusions, and it's just the opposite for RBC transfusions. It doesn't take the Rh factor into effect, though, because most people don't have antibodies for the Rhesus factor (it only happens upon exposure).

Hemolytic Disease of the Newborn
Often a pregnant woman carries a fetus with a different blood type to herself, and sometimes the mother forms antibodies against the red blood cells of the fetus, leading to low fetal blood counts, a condition known as hemolytic disease of the newborn.

Hemolytic disease of the newborn, (also known as HDN) is an alloimmune condition that develops in a fetus when the IgG antibodies produced by the mother and passing through the placenta include ones which attack the red blood cells in the fetal circulation. The red cells are broken down and the fetus can develop reticulocytosis and anemia. The fetal disease ranges from mild to very severe and fetal death from heart failure - hydrops fetalis - can occur. When the disease is moderate or severe many erythroblasts are present in the fetal blood and so these forms of the disease can be called erythroblastosis fetalis.

Before birth, options for treatment include intrauterine transfusion or early induction of labor when pulmonary maturity has been attained, fetal distress is present, or 35 to 37 weeks of gestation have passed. The mother may also undergo plasma exchange to reduce the circulating levels of antibody by as much as 75%.

After birth, treatment depends on the severity of the condition, but could include temperature stabilization and monitoring, phototherapy, transfusion with compatible packed red blood, exchange transfusion with a blood type compatible with both the infant and the mother, sodium bicarbonate for correction of acidosis and/or assisted ventilation.

Rh negative mothers who have had a pregnancy with or are pregnant with a Rh positive infant, are given Rh immune globulin (RhIG) also known as Rhogam, during pregnancy and after delivery to prevent sensitization to the D antigen. It works by binding any fetal red cells with the D antigen before the mother is able to produce an immune response and form anti-D IgG. A drawback to pre-partum administration of RhIG is that it causes a positive antibody screen when the mother is tested which is indistinguishable from immune reasons for antibody production.

Von Willebrand Disease
The most common inherited bleeding disorder, von Willebrand disease affects both men and women equally. Von Willebrand disease is similar to hemophilia in that it involves a deficiency in the ability of blood to clot properly. Those affect by von Willebrand disease will have one or more of the following- low levels of von Willebrand factor (a protein that helps the blood to clot), and/or their von Willebrand factor doesn't work properly. While it is mostly an inherited disease (with factors contributed by both parents), von Willebrand disease may be an acquired syndrome in rare cases.

There are three types of von Willebrand disease: Type 1, which is the mildest and most common form of the disease; Type 2, which has four subtypes (2A, 2B, 2M, and 2N) and ranges from mild to moderate in severity; and finally, Type 3, which is very rare and is the most severe form.

In type 1 von Willebrand disease, there is a low level of von Willebrand factor. The level of factor VIII may also be lower than normal. This is the mildest and most common form of the disease. About 3 out of 4 people diagnosed with von Willebrand disease have type 1.
 * Type 1:

In type 2 von Willebrand disease, a defect in von Willebrand factor causes it to not work properly. Type 2 is divided into 2A, 2B, 2M, and 2N. Each is treated differently, so knowing the exact type is important.
 * Type 2:

People with type 1 and type 2 von Willebrand disease may have the following mild-to-moderate bleeding symptoms: easy bruising, nosebleeds, bleeding from the gums after a dental procedure, heavy menstrual bleeding in women, blood in their stools or urine (from bleeding in the intestines, stomach, kidneys or bladder), excessive bleeding after a cut or other accident or surgery.

People with type 3 von Willebrand disease usually have no von Willebrand factor and very low factor VIII. Type 3 is severe and very rare.
 * Type 3:

Symptoms of type 3 von Willebrand disease might include any of the symptoms of types 1 and 2, and also include severe bleeding episodes for no reason, which can be life-threatening if not treated immediately. Bleeding into soft tissues or joints (hemarthrosis), causing severe pain and swelling, is another symptom.

 * Treatment:

Many people with von Willebrand disease do not require treatment to manage the disease. However, if treatment is necessary, it may include a range of different interventions depending on the severity. These involve medicine to increase the level of von Willebrand factor in the blood (DDAVP), medicine to prevent the breakdown of clots (called antifibrinolytic drugs), medicine to control heavy menstrual bleeding in women (often birth control pills), or injection of clotting factor concentrates (containing von Willebrand factor and factor VIII).

Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC), also called consumptive coagulopathy, is a pathological process in the body where the blood starts to coagulate throughout the whole body. This depletes the body of its platelets and coagulation factors, and there is a paradoxically increased risk of hemorrhage. It occurs in critically ill patients, especially those with Gram-negative sepsis (particularly meningococcal sepsis) and acute promyelocytic leukemia.

Hemophilia
Hemophilia is a disease where there is low or no blood protein, causing an inability to produce blood clots. There are two types of Hemophilia: Type A, which is a deficiency in factor VIII and Type B, (Christmas disease) a deficiency on factor IX. Because people with hemophilia have an impaired ability to make blood clots, even a little cut may take hours or days to fully clot, and a small bump or jar to the body could cause severe bruising that doesn't heal for months. Internal muscle bleeds are the most common symptom though, causing swelling and varying degrees of pain.

Hemophilia is passed down from mothers to their sons. Hemophilia is sometimes known as the "Royal Disease". This is because Queen Victoria, Queen of England (1837-1901), was a carrier of hemophilia. The hemophilia disease was passed down to her son Leopold who ended up dying at age 31. Queen Victoria also had two daughters who were carriers. These daughters passed hemophilia into the Spanish, German, and Russian royal families. One of the most famous stories is that of the Russian royal family. Alexandra, granddaughter to Queen Victoria, married Nicholas (Tsar of Russia in the 1900s). Alexandra was a carrier of the disease and passed the disease to their first son, Tsarevich Alexi, who was heir to the throne of Russia. The family tried to keep their son's secret from the people, but Alexi suffered with serious bruises and extreme pain. The family found help from a monk named Rasputin. He kept their secret and gained a great deal of power over the family, making them think he was their only hope. During this time of great turmoil in Russia, Nicholas and Alexandra spent most of their attentions on their son, and not on the people. It wasn't long before the Bolshevik Revolution of 1917 began.

Factor V Leiden
The opposite of Hemophilia, Factor V Leiden is the name given to a variant of human factor V that causes a hypercoagulability disorder. In this disorder the Leiden variant of factor V, cannot be inactivated by activated protein C. Factor V Leiden is the most common hereditary hypercoagulability disorder amongst Eurasians. It is named after the city Leiden (The Netherlands), where it was first identified in 1994 by Prof R. Bertina et al. Those that have it are at a slightly higher risk of developing blood clots than those without. Those that test positive for factor V should avoid (oral contraceptives, obesity, smoking, and high blood pressure.)

Anemia
Anemia (AmE) or anaemia (BrE), from the Greek (Ἀναιμία) meaning "without blood", refers to a deficiency of red blood cells (RBCs) and/or hemoglobin. This results in a reduced ability of blood to transfer oxygen to the tissues, causing hypoxia. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences. Hemoglobin (the oxygen-carrying protein in the red blood cells) has to be present to ensure adequate oxygenation of all body tissues and organs.

The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). In menstruating women, dietary iron deficiency is a common cause of deficient red blood cell production.

Sickle cell

Sickle-cell disease is a general term for a group of genetic disorders caused by sickle hemoglobin (Hgb S or Hb S). In many forms of the disease, the red blood cells change shape upon deoxygenation because of polymerization of the abnormal sickle hemoglobin. This process damages the red blood cell membrane, and can cause the cells to become stuck in blood vessels. This deprives the downstream tissues of oxygen and causes ischemia and infarction. The disease is chronic and lifelong. Individuals are most often well, but their lives are punctuated by periodic painful attacks. In addition to periodic pain, there may be damage of internal organs, and/or stroke. Lifespan is often shortened with sufferers living to an average of 40 years. It is common in people from parts of the world where malaria is or was common, especially in sub-Saharan Africa or in descendants of those peoples.

Genetics: Sickle-cell disease is inherited in the autosomal recessive pattern, depicted above. The allele responsible for sickle cell anemia is autosomal recessive. A person who receives the defective gene from both father and mother develops the disease; a person who receives one defective and one healthy allele remains healthy, but can pass on the disease and is known as a carrier. If two parents who are carriers have a child, there is a 1-in-4 chance of their child developing the illness and a 1-in-2 chance of their child just being a carrier.

Polycythemia
Polycythemia is a condition in which there is a net increase in the total circulating erythrocyte (red blood cell) mass of the body. There are several types of polycythemia.

In primary polycythemia, there may be 8 to 9 million and occasionally 11 million erythrocytes per cubic millimeter of blood (a normal range for adults is 4-5 million), and the hematocrit may be as high as 70 to 80%. In addition, the total blood volume can increase to as much as twice as normal. The entire vascular system can become markedly engorged with blood, and circulation times for blood throughout the body can increase up to twice the normal value. The increased numbers of erythrocytes can increase of the viscosity of the blood to as much as five times normal. Capillaries can become plugged by the very viscous blood, and the flow of blood through the vessels tends to be extremely sluggish.
 * Primary Polycythemia:

As a consequence of the above, people with untreated Polycythemia are at a risk of various thrombotic events (deep venous thrombosis, pulmonary embolism), heart attack and stroke, and have a substantial risk of Budd-Chiari syndrome (hepatic vein thrombosis). The condition is considered chronic; no cure exists. Symptomatic treatment (see below) can normalize the blood count and most patients can live a normal life for years.

Secondary polycythemia is caused by either appropriate or inappropriate increases in the production of erythropoietin that result in an increased production of erythrocytes. In secondary polycythemia, there may be 6 to 8 million and occasionally 9 million erythrocytes per cubic millimeter of blood. A type of secondary polycythemia in which the production of erythropoietin increases appropriately is called physiologic polycythemia. Physiologic polycythemia occurs in individuals living at high altitudes (4275 to 5200 meters), where oxygen availability is less than at sea level. Many athletes train at higher altitudes to take advantage of this effect — a legal form of blood doping. Actual polychthemia sufferers have been known to use their condition as an athletic advantage for greater stamina.
 * Secondary polycythemia:

Other causes of secondary polycythemia include smoking, renal or liver tumors, or heart or lung diseases that result in hypoxia. Endocrine abnormalities, prominently including pheochromocytoma and adrenal adenoma with Cushing's Syndrome, are also secondary causes. Athletes and bodybuilders who abuse anabolic steroids or erythropoietin may develop secondary polycythemia.

Relative polycythemia is an apparent rise of the erythrocyte level in the blood; however, the underlying cause is reduced blood plasma. Relative polycythemia is often caused by fluid loss i.e. burns, dehydration and stress polycythemia.
 * Relative polycythemia:

Leukemia
Leukemia is a cancer of the blood or bone marrow characterized by an abnormal proliferation of blood cells, usually white blood cells (leukocytes). It is part of the broad group of diseases called hematological neoplasms. Damage to the bone marrow, by way of displacing the normal marrow cells with increasing numbers of malignant cells, results in a lack of blood platelets, which are important in the blood clotting process. This means people with leukemia may become bruised, bleed excessively, or develop pin-prick bleeds (petechiae).

White blood cells, which are involved in fighting pathogens, may be suppressed or dysfunctional, putting the patient at the risk of developing infections. The red blood cell deficiency leads to anaemia, which may cause dyspnea. All symptoms may also be attributable to other diseases; for diagnosis, blood tests and a bone marrow biopsy are required.

Glossary
Albumin: a major blood protein responsible for the maintenance of osmotic (water) pressure in the blood

Anemia: a deficiency of red blood cells or hemoglobin caused by lack of iron, folic acid or vitamin B12 in the diet, or by red blood cell destruction; associated with decreased ability of blood to carry oxygen

B-Cell: cell responsible for the distribution of antibodies

Basophil: this white blood cell enters damaged tissues and releases a histamine and other chemicals that promote inflammation in the body to fight pathogens

Blood: the means and transport system of the body used in carrying elements - nutrition, waste, heat - from one location in the body to another by way of blood vessels

Eosinophil: white blood cell that is involved in the immune response against parasitic worms (such as tapeworms and roundworms). Named because it stains with the red dye "eosin."

Factor V Leiden most common genetic hypercoagulability disorder.

Formed Elements: the red blood cells, white blood cells and platelets found in blood

Hematocrit: measurement of the % of red blood cells found in blood

Hemoglobin (Hb): iron-containing pigment in red blood cells that combines with and transports oxygen

Hemophilia: genetic disorder in which the affected individual may have uncontrollable bleeding; blood does not clot

Hemostasis: the process by which blood flow is stopped; also describes the clotting of blood

Lymphocytes: cells of the Lymphatic system, provide defense against specific pathogen or toxins

Monocytes: The largest white blood cell. Becomes a macrophage when activated. Engulfs pathogens and debris through phagocytosis, also involved in presenting antigens to B and T lymphocytes.

Neutrophils: the most common white blood cell; they are phagocytic and engulf pathogens or debris in the tissues; also release cytotoxic enzymes and chemicals to kill pathogens

NK-Cells: also known as "Natural Killer Cells", these T lymphocytes are responsible for surveillance and detection of abnormal tissue cells; important in preventing cancer

Phagocytosis: process by which amoeboid-like cells engulf and ingest, and thereby destroy, foreign matter or material

T-Cell: cells that mediate by coordinating the immune system and enter the peripheral tissues. They can attack foreign cells directly and control the activities of other lymphocytes ,

Review Questions

 * Answers for these questions can be found here

1. Taking aspirin every day can reduce the risk of heart disease because:
 * A) it is a powerful vasodilator
 * B) it blocks pain receptors in heart tissue
 * C) it stops ventricular fibrillation
 * D) it loosens plaque on arterial walls
 * E) it prevents platelet clumping

2. A hematocrit measures percentage of:
 * A) White blood cells
 * B) Plasma
 * C) Platelets
 * D) Red blood cells

3. Fred's blood type is O- and Ginger's is B+. Fred and Ginger have a son who is AB+. What do you conclude?
 * A) If they have a second child Ginger needs to have RhoGam shot
 * B) There is no risk to a second child, unless it has a negative blood type
 * C) If the child needs a blood transfusion Fred could provide it safely, but not Ginger
 * D) Fred is not the boy’s father

4. Which blood component plays the largest role in maintaining the osmotic pressure of blood?
 * A) albumin
 * B) carbon dioxide
 * C) white blood cells
 * D) fibrinogen
 * E) globulins

5. If you hold your breath for one minute
 * A) The kidneys will increase sodium ion reabsorption
 * B) Hydrogen-ion concentration in the blood will increase
 * C) Your heart rate will greatly slow
 * D) Hemoglobin will bind to oxygen more strongly

6. Most of the carbon dioxide produced by tissues is transported to the lungs as:
 * A) Small gas bubbles in the plasma
 * B) Gas bound to hemoglobin in the red blood cells
 * C) Bicarbonate ions in the plasma
 * D) Gas bound to white blood cells and albumin
 * E) Gas transported through the lymphatic system

7. To prevent blood loss after a tissue injury, blood vessels first
 * A) Form a platelet plug
 * B) Form a clot
 * C) Initiate the coagulation cascade
 * D) Constrict and form barriers

8. You take a blood sample from a male cyclist at the end of a long race. The hematocrit is 60%. The most likely conclusion is:
 * A) This is within normal range for most adult males
 * B) This cyclist is anemic
 * C) This low of a hematocrit could indicate liver damage or leukemia
 * D) The cyclist is dehydrated
 * E) The cyclist has been taking pharmaceutical erythropoietin

9. In a normal blood sample, which of the following cells will be the most abundant?
 * A) Neutrophils
 * B) Basophils
 * C) Eosinophils
 * D) Monocytes
 * E) Lymphocytes

10. A bag of donated blood does not clot because
 * A) There is not enough oxygen
 * B) It cannot dry out
 * C) It is kept refrigerated
 * D) There is no free calcium
 * E) All of the above

11. What is the primary function of bood?
 * A) Supply nutrients to tissues
 * B) Remove waste products
 * C) To keep your body at one consistent temperature
 * D) A and B
 * E) B and C

12. What is the main component of the Red blood cell?
 * A) Albumin
 * B) Globulins
 * C) Hemoglobin
 * D) Nucleus

title: Human Physiology/Blood physiology


text:
Statistics/Curve fitting

Whenever trying to evaluate data that has been collected, often patterns appear, such as a -1 slope when making a scatter plot of $$1/d_i=1/f-1/d_o$$ in ray optics. It may often be the goal to find a mathematical function that "fits" the data. That is to say a function whose values are close to the data values at the corresponding values and independent values. This is often referred to as the "least squares", and the reason for which is explained later.

Sales Example
A store sells whatsits at P=3.49 each and the average number of whatsits sold (the volume) per day is V=100. Therefore the total money received T=P times V=349.00 ..... If the price is reduced then, maybe, more whatsits will be sold, but T may be more or less. Obviously if P=0 then T will also be zero. The following was the result:

P         V           T       2.99        130        388.70 3.29       123        404.67       3.49        100        349.00 Obviously the "best" price is somewhere between 2.99 and 3.49. ..... Curve fitting provides an equation for T versus P for each of the many models that are available for comparison.

Linear model
The linear model is based on the "best" straight line. Using a calculator that can do regression, we find for the above data that the closest line of the graph showing T versus P is
 * T=605.268605263 - 68.9289473684 * P, and the correlation is shown as about 60% for this model.

Let us examine it in more detail: P   Actual T   Calculated T       Difference     Difference2 2.99  388.70  399.17105263159  - 10.4710526316   109.642943214   3.29   404.67  378.49236842106    26.1776315789   685.268395081   3.49   349.00  364.70657894738  - 15.7065789474   246.696622231 Adding the differences, we find that their sum is nearly zero, indicating that it is the "best" linear model. Squaring a negative number always gives a positive number. so that the SUM OF SQUARES will give us an indication of the GOODNESS OF FIT. Here the SUM OF SQUARES is 1041.60796053, and we can compare the different models, selecting finally the model that has the LEAST SQUARES. - If you do NOT have a calculator or a computer that can do regression, then.....

Calculation of the least square line to fit the given points:
LOOKING FOR a and b in the equation of the straight line y=a+b*x:

We have, in the above example: x      x2      y       y2             xy   2.99   8.9401  388.70  151087.69     1162.213 3.29 10.8241  404.67  163757.8089   1331.3643   3.49  12.1801  349.00  121801        1218.01     --- ---  ---   -   9.77  31.9443 1142.37  436646.4989   3711.5873

We have: n = number of points = 3 ax=average of x=9.77/3=3.25 6 ay=average of y=1142.37/3=380.79 x1=sum of x=9.77 x2=sum of x2=31.9443 y1=sum of y=1142.37 y2=sum of y2=436646.4989 s1=sum of xy=3711.5873 z1=s1-(x1*y1/n)=3711.5873-(9.77*1142.37/3)= -8.731 z2=x2-(x12/n)=31.9443-9.772/3=0.12 6  b=z1/z2=-68.9289473682

a=ay-b*ax=380.79-(-68.9289473682)*3.25 6 =605.268605263

Thus we have y=605.268605263-68.92894736828*x as the best line to fit the given points of this example.

Parabolic Model
If we have n points, then a polynomial of (n-1) degree will fit these n points exactly. We are given in this example 3 points, and a polynomial of the 2nd degree (parabola) should give us an exact fit. The calculator provides the equation (-663.1666666653)x2 + 4217.91999999x-6294.10448332, giving us   P    Actual T   Calculated T       Difference 2.99  388.70   388.6999999956      4.4E-9 = zero plus rounding error 3.29  404.67   404.6699999951      4.9E-9 = zero plus rounding error 3.49  349.00   348.999999995       5.0E-8 = zero plus rounding error That is a perfect fit, with the LEAST SQUARES indicating that this model be used.

Other models
Some of the many other models are based on the exponential function, logarithms, and various manipulations of the independent and/or the dependent variable(s). The "best fit" is usually the one that provides the LEAST SQUARES. Also weighting of the data could be used when some points on a graph are more important than others (such as, maybe, end points, for example).
 * Caution: Some calculators may require for Curve fitting consecutive, equally spaced, independent variables. Always compare the original graph with the "fitted" graph.

title: Statistics/Curve fitting


text:
Cookbook:Gravlax

| Seafood

Gravlax is salmon that is cured in salt and sugar. It is a common dish throughout Scandinavia. Gravlax is easy to make and makes a festive dish that is an excellent to serve at parties with many people. The process of curing fish in salt and sugar (grava) is not limited to salmon and works fine with any fatty fish although salmon is definitely the most common choice. Gravlax has been particularly popular and common in the northern regions of Scandinavia whose cold and fresh waters produce salmon of excellent quality. The basic recipe here has been used for generations and has its origins in the northernmost part of Sweden. Gravlax can be used either as a main dish or as an appetizer.

Ingredients

 * 800 g (1.75 lb) fresh salmon filet, approximately 2–5 cm (1–2 inches) thick
 * 30 ml (2 Tbsp) salt
 * 30 ml (2 Tbsp) white granulated sugar
 * 45 ml (3 Tbsp) juniper berries
 * 300 ml (1 ¼ cups) gin (optional)
 * 5 ml (1 tsp) whole or crushed white pepper
 * 20–40 g (0.75–1.5 oz) fresh dill

Procedure

 * 1) Cut the salmon filet into two equally-sized parts (if you are making gravlax for many people it is fine to use two filets instead). Freeze the salmon for at least 4 days at -18°C or colder to kill any parasites.
 * 2) After deep freezing the salmon remove it from the freezer and let it thaw, preferably overnight in the refrigerator. The salmon does not have to be completely thawed for the next steps.
 * 3) Combine the salt and sugar. Place the salmon, skin down, on a table. Rub the salt and sugar mix onto the pieces, then apply the juniper berries and pepper. Finally, cover with dill.
 * 4) Put one salmon piece on top of another, flesh side to flesh side so the skin it outside on both pieces, and place in a plastic bag. Add any leftover ingredients to the bag along with the gin.
 * 5) Seal the bag and place it in the refrigerator. Let the salmon cure in the mixture, turning the bag over once, preferably twice, a day for 4 days.
 * 6) After 4 days, the salmon is ready to serve. If you are not going to eat it immediately (it lasts a couple of days) move it to a fresh plastic bag or jar, removing the salty liquid that has formed in the original bag. If you keep it in the original bag the risk is that it may be too salty once you are about to serve it.
 * 7) Use a sharp knife to slice thin slices from the salmon at an angle. During slicing, also remove any remaining bones. The larger the piece of salmon the larger the angle and the larger surface area for the produced slices. Large slices look better when served.
 * 8) As a main dish, serve with potato stew, boiled potatoes and gravlax sauce, or in a salad. As an appetizer, serve on crispbread or toast. Potato stew with some additional Dijon mustard is excellent addition to gravlax.

Notes, tips, and variations

 * Use the thick part of the salmon filet found towards the head. Don't use the part closest to the tail, since it is not thick enough.
 * The gin can be substituted by lemon or lime juice (like a ceviche).
 * The time can be greatly shortened by slicing the salmon thinly before curing it. It can be ready with as little as 4 hours of curing time.  However, using this method means it should also be eaten sooner.

title: Cookbook:Gravlax


text:
User talk:Sfinx~enwikibooks

Contattatemi sul mio profilo principale

 * 1) Profilo principale []
 * 2) Le mie discussioni []

Talk to me on my main page

 * 1) Main profile page []
 * 2) My talk page []

Your account will be renamed
Hello,

The developer team at Wikimedia is making some changes to how accounts work, as part of our on-going efforts to provide new and better tools for our users like cross-wiki notifications. These changes will mean you have the same account name everywhere. This will let us give you new features that will help you edit and discuss better, and allow more flexible user permissions for tools. One of the side-effects of this is that user accounts will now have to be unique across all 900 Wikimedia wikis. See the announcement for more information.

Unfortunately, your account clashes with another account also called Sfinx. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Sfinx~enwikibooks that only you will have. If you like it, you don't have to do anything. If you do not like it, you can pick out a different name.

Your account will still work as before, and you will be credited for all your edits made so far, but you will have to use the new account name when you log in.

Sorry for the inconvenience.

Yours, Keegan Peterzell Community Liaison, Wikimedia Foundation 23:44, 17 March 2015 (UTC)

Renamed
 This account has been renamed as part of single-user login finalisation. If you own this account you can |log in using your previous username and password for more information. If you do not like this account's new name, you can choose your own using this form after logging in: . -- Keegan (WMF) (talk) 05:28, 19 April 2015 (UTC)

title: User talk:Sfinx~enwikibooks


text:
Wikibooks:Collaboration of the Month/June 2005

The Collaboration of the Month for June is Puzzles.

Puzzles is a Wikibook dedicated to establishing a source of open content logic problems and tricks for the general public. It currently has in excess of fifty entries. All users are asked to help contribute to this project over the course of the month. For resources, visit the information page.

Vote for July - Collaboration of the Month


text:
Wikibooks:Collaboration of the Month/July 2005 voting

Voting Rules
The following are the rules and conditions for voting for the Collaboration of the Month:

 * 1) Only registered users with 20 or more edits to their name may vote.
 * 2) You may vote under as many nominations as you wish, however, you may only vote for each book itself once.
 * 3) Sign your vote with a number sign and four tildes, #~, after the most previous vote under the book's nomination. Unsigned votes will be removed.
 * 4) Any nomination which receives 3 or more votes in one month will automatically be renominated the next month if it is not chosen.
 * 5) If you wish to include a short comment for your vote, then you may do so. Make sure that if you leave such a comment, that you are also voting for that page.
 * 6) Do not post objection votes as these will have no effect on the final tally.
 * 7) Voting will end at 00:00 UTC on the first day of each month. In essence, when a new month begins voting ends. Any votes added after this time will be discarded.
 * 8) The nomination with most votes will be chosen as the Collaboration of the Month. In case of a tie, the older Wikibook will be chosen.

FHSST Physics
Automatically renominated with 3 votes in May
 * 1) Klingoncowboy4 03:14, 26 Jun 2005 (UTC)

COMMENTS... This book is very well develped already. MeMoria

Teaching Computer Literacy - From the Beginning
Support I think this book has a lot of potential and is a book that any editor should be able to help with. --Mattwj2002 05:03, 11 Jun 2005 (UTC)

Samba

 * 1) MeMoria 16:21, 28 Jun 2005 (UTC)

COMMENTS; Everyone can help with this one. Samba is an important technology, so let's get it some recognition!
 * Why don't you contribute something to it then?

--Robofrance 17:40, 15 Jun 2005 (UTC)
 * 1) Klingoncowboy4 03:13, 26 Jun 2005 (UTC)

Photoschule Großformat

 * 1) Support - This book, while it has a German title, and was written in German, already has a paragraph by paragraph translation of most or all of the text. What we really need to do here is clean it up, remove the German text, and move the book and chapters to English titles, and we'll have a very nice Wikibook to show off. Gentgeen 16:51, 14 Jun 2005 (UTC)

Introduction to Philosophy

 * 1) Support - This book is a little underdone and could be easily edited by many. As a major part of the humanities area it should be one of our larger books. Serge 07:44, 27 Jun 2005 (EST)
 * 2) Klingoncowboy4 03:16, 26 Jun 2005 (UTC)
 * 3) Support Much need be considered when building this book, much of which has been excluded from it. I would like to see more persons working on this collaboration. It is sad to see something that many people are trying to push fall short. I see this as a keystone to many young minds, and the way it is being formed is ridiculous. It needs much support from the WikiBooks community. Consequently, I am forced to vote for it as a collaboration of the month canidate, not for the fact that it is well-formed, but for the fact it need be seen and helped. Destrogal 18:48, 13 July 2005 (UTC)

London

 * 1) Charlie123 14:21, 23 Jun 2005 (UTC) (support). Following rejection of this book from "Book of the month", due to its lack of content, why not make it a collaboration and therefore solve this problem? This is also the first travel book for Wikibooks.
 * 2) Klingoncowboy4 03:21, 26 Jun 2005 (UTC)
 * 3) Grimm 18:01, 26 Jun 2005 (UTC)
 * 4) MeMoria 16:21, 28 Jun 2005 (UTC) Not a fan of the city, but a good book. MeMoria 16:21, 28 Jun 2005 (UTC)
 * 5) Gentgeen 20:17, 28 Jun 2005 (UTC)


text:
User talk:Erichmj~enwikibooks

[[Media:Example.mp3]]

Your account will be renamed
Hello,

The developer team at Wikimedia is making some changes to how accounts work, as part of our on-going efforts to provide new and better tools for our users like cross-wiki notifications. These changes will mean you have the same account name everywhere. This will let us give you new features that will help you edit and discuss better, and allow more flexible user permissions for tools. One of the side-effects of this is that user accounts will now have to be unique across all 900 Wikimedia wikis. See the announcement for more information.

Unfortunately, your account clashes with another account also called Erichmj. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Erichmj~enwikibooks that only you will have. If you like it, you don't have to do anything. If you do not like it, you can pick out a different name.

Your account will still work as before, and you will be credited for all your edits made so far, but you will have to use the new account name when you log in.

Sorry for the inconvenience.

Yours, Keegan Peterzell Community Liaison, Wikimedia Foundation 23:08, 17 March 2015 (UTC)

Renamed
 This account has been renamed as part of single-user login finalisation. If you own this account you can |log in using your previous username and password for more information. If you do not like this account's new name, you can choose your own using this form after logging in: . -- Keegan (WMF) (talk) 04:56, 19 April 2015 (UTC)

title: User talk:Erichmj~enwikibooks


text:
User talk:Name of Feather

Demystifying Depression

 * Hello, Name of Feather.
 * I believe I saw some articles that made up this book in Kuro5hin while I was looking around (or more properly, was referred).
 * This seems to be an informative and friendly book on an important subject.
 * Depression does need to be demystified. I fully understand that the moods/affective side is the tip of the iceberg.
 * How very true that it's chronic brain overload...
 * It would be easy to upload charts and graphs representing what you intended.

--EuropracBHIT 07:26, 2 Jun 2005 (UTC).

Don't forget to sign your comments
Hi N.O.F.,

It is standard practice to sign your comments when ever you make a change to a talk page. With out this it makes it hard to figure out who is adding what comments. You do this with 4 tilde like ~ and it looks like this: Triddle 01:35, 4 Jun 2005 (UTC)

Thanks for your contributions
Name of Feather, thanks for your work donating this information in your book to the site! I appreciate it and think that many other people will appreciate it and benefit from it as well. --Karl Wick 21:37, 6 Jun 2005 (UTC)

title: User talk:Name of Feather


text:
Portuguese/Contents/L1/Lesson Seven - What Time Is It?

Return to Portuguese – Return to Contents – Go to Lesson Eight

Here are the numbers 1-10 in Portuguese. It is essential that you learn these by heart. Next is a table with some other numbers in portuguese.

Now, to our usual dialogue.

In Portuguese, the way you tell the time is similar to English. You first say the hour number, then the word e and finally the minute number. Ex: São sete e vinte. - It's seven twenty. For half an hour, you say e meia in the place of "and a half" or e trinta as in thirty and in case the minute number is very close to the full hour (bigger than 30), it is more common to say the remaining time to the next hour, using the structure: São + remaining time in minutes + para a(s) + next hour. Ex: São duas e meia. - It's two and a half. São cinco para as quatro - It's five to four. Also, there are synonyms for midnight and midday in Portuguese: meia-noite and meio-dia, respectively. These words are used the same way. Ex: É meio-dia. - It's midday.

Now, let's do some exercises:

1)Tell the times below in Portuguese:

a)10:30 PM b)8:55 AM c)3:15 AM d)7:25 AM e)1:00 PM f)4:40 PM g)12:50 PM h)11:55 AM

Answers:

1) a)São dez e meia. b)São cinco para as nove. c)São três e quinze. d)São sete e vinte e cinco. e)É uma hora.* f)São vinte para as cinco. g)São dez para uma. h)São cinco para meio-dia.

 * Note that since one hour is singular, the verb ser is in the singular form.

de:Portugiesisch: Lektionen: Wieviel Uhr ist es?