text:
User talk:The wub

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Good luck! --Remi 21:23, 30 March 2007 (UTC)

title: User talk:The wub


text:
User talk:Asymptote~enwikibooks

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Good luck! --Remi 21:23, 30 March 2007 (UTC)

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 Asymptote. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Asymptote~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 22:57, 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) 04:35, 19 April 2015 (UTC)

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

title: User talk:Asymptote~enwikibooks


text:
User talk:Derae

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Good luck! --Remi 21:25, 30 March 2007 (UTC)

title: User talk:Derae


text:
User talk:Jfk55

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:25, 30 March 2007 (UTC)

title: User talk:Jfk55


text:
User talk:Joewambu

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Joewambu


text:
User talk:Muniganeshenoy

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Muniganeshenoy


text:
User talk:Lczernia

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

Copyright problem with Image:UC200.jpg

 * Hi Lczernia. The images you purchased can't be uploaded on Wikibooks unless they were released under a free license or are public domain. It's similar to when you buy music: you own that copy, but you don't have the right to make up copies of your copy and sell them, because you don't have control of the copyright (and thus can't release it under a free copyright). -- SB_Johnny | PA! 13:00, 26 September 2007 (UTC)

Cyber Guide to ODU Career Management/Get Up-to-Date/OCCS Footprints Problems Reported
I'm just wondering what this page is; I can't make heads nor tails of it. Thanks. – Mike.lifeguard  | talk 21:00, 28 November 2007 (UTC)

title: User talk:Lczernia


text:
User talk:Gam4me

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Gam4me


text:
User talk:Mavisvaldez

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Mavisvaldez


text:
User talk:Arq.Kim.Rod~enwikibooks

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

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 Arq.Kim.Rod. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Arq.Kim.Rod~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 22:59, 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) 04:34, 19 April 2015 (UTC)

title: User talk:Arq.Kim.Rod~enwikibooks


text:
User talk:Rob toran

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Rob toran


text:
User talk:Sir Drance

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:30, 30 March 2007 (UTC)

title: User talk:Sir Drance


text:
User talk:Shartec

Hello, and welcome to Wikibooks!

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Good luck! --Remi 21:31, 30 March 2007 (UTC)

title: User talk:Shartec


text:
Introduction to Chemical Engineering Processes/Numerical Root Finding Methods

Basics of Rootfinding
Rootfinding is the determination of solutions to single-variable equations or to systems of n equations in n unknowns (provided that such solutions exist). The basics of the method revolve around the determination of roots

A root of a function $$ F(x_1,x_2,...) $$ in any number of variables is defined as the solution to the equation $$ F(x_1,x_2,...) = 0 $$. In order to use any of the numerical methods in this section, the equation should be put in a specific form, and this is one of the more common ones, used for all methods except the iterative method.

However, it is easy to put a function into this form. If you start with an equation of the form:

$$ F_1(x_1,x_2,...) = F_2(x_1,x_2,...) $$

then subtracting $$ F_2 $$ will yield the required form. Do not forget to do this, even if there is only a constant on one side!

Since any equation can be put into this form, the methods can potentially be applied to any function, though they work better for some functions than others.

Analytical vs. Numerical Solutions
An analytical solution to an equation or system is a solution which can be arrived at exactly using some mathematical tools. For example, consider the function $$ y = ln(x) $$, graphed below.

The root of this function is, by convention, when $$ y = 0 $$, or when this function crosses the x-axis. Hence, the root will occur when $$ ln(x) = 0 \rightarrow x = e^0 = 1 $$

The answer x=1 is an analytical solution because through the use of algebra, we were able to come up with an exact answer.

On the other hand, attempting to solve an equation like:

$$ -x = ln(x) $$

analytically is sure to lead to frustration because it is not possible with elementary methods. In such a case it is necessary to seek a numerical solution, in which guesses are made until the answer is "close enough", but you'll never know what the exact answer is.

All that the numerical methods discussed below do is give you a systematic method of guessing solutions so that you'll be likely (and in some cases guaranteed) to get closer and closer to the true answer. The problem with numerical methods is that most are not guaranteed to work without a good enough initial guess. Therefore, it is valuable to try a few points until you get somewhere close and then start with the numerical algorithm to get a more accurate answer. They are roughly in order from the easiest to use to the more difficult but faster-converging algorithms.

Iterative solution
Iterative solutions in their purest form will solve the desired function so that it is in the form:

$$ x = f(x) $$

Then, a value for x is guessed, and f(x) is calculated. The new value of x is then re-inserted into f(x), and the process is repeated until the value of x changes very little.

The following example illustrates this procedure.

This method has some rather severe limitations as we'll see in this example:

This example shows that the success of the iteration method strongly depends on the properties of the function on the right-hand side. In particular, it has to do with how large the slope of the function is at the root. If the slope is too large, the method will not converge, and even if it is small the method converges slowly. Therefore, it is generally undesirable to use this method, though some more useful algorithms are based on it (which is why it is presented here).

Iterative Solution with Weights
Although the iterative solution method has its downfalls, it can be drastically improved through the use of averaging. In this method, the function is still solved for x in the form:

$$ x = f(x) $$

From the initial guess $$ x_0 $$, the function f(x) is used to generate the second guess $$ x_1 $$. However, rather than simply putting $$ x_1 $$ into f(x), a weighted average of $$ x_0 $$ and $$ x_1 $$ is made:

$$ x_1(New)= \alpha*x_0 + (1-\alpha)*x_1(old), 0 \le \alpha \le 1 $$

The term $$ \alpha $$ is called the weight. The most common value of the weight is one-half, in which case the next value to plug into f(x) is simply the average of $$ x_0 $$ and $$ x_1(old) $$:

This new value is then plugged into f(x), averaged with the result, and this is repeated until convergence.

The following examples show that this method converges faster and with more reliability than normal iterative solution.

The method is not only faster-converging but also more stable, so that it can actually be used solving the equation the other way too.

Notice that in this case, if we use regular iteration the result only converged if the equation was solved in a certain way. Using weighted iteration, it is possible to solve it either way and obtain a solution, but one way is clearly faster than the other. However, weighting will accelerate the algorithm in most cases and is relatively easy to implement, so it is a worthwhile method to use.

Bisection Method
Let us consider an alternative approach to rootfinding. Consider a function f(x) = 0 which we desire to find the roots of. If we let a second variable $$ y = f(x) $$, then y will (almost always) change sign between the left-hand side of the root and the right-hand side. This can be seen in the above picture of $$ y = ln(x) $$, which changes from negative to the left of the root $$ x = 1 $$ to positive to its right.

The bisection method works by taking the observation that a function changes sign between two points, and narrowing the interval in which the sign change occurs until the root contained within is tightly enclosed. This only works for a continuous function, in which there are no jumps or holes in the graph, but a large number of commonly-used functions are like this including logarithms (for positive numbers), sine and cosine, and polynomials.

As a more formalized explanation, consider a function $$ y = f(x) $$ that changes sign between $$ x = a $$ and $$ x = b $$ We can narrow the interval by:

 * 1) Evaluating the function at the midpoint
 * 2) Determining whether the function changes signs or not in each sub-interval
 * 3) If the continuous function changes sign in a sub-interval, that means it contains a root, so we keep the interval.
 * 4) If the function does not change sign, we discard it. This can potentially cause problems if there are two roots in the interval,so the bisection method is not guaranteed to find ALL of the roots.

Though the bisection method is not guaranteed to find all roots, it is guaranteed to find at least one if the original endpoints had opposite signs.

The process above is repeated until you're as close as you like to the root.

Note that convergence is slow but steady with this method. It is useful for refining crude approximations to something close enough to use a faster but non-guaranteed method such as weighted iteration.

Regula Falsi
The Regula Falsi method is similar the bisection method. You must again start with two x values between which the function f(x) you want to find the root of changes. However, this method attempts to find a better place than the midpoint of the interval to split it.It is based on the hypothesis that instead of arbitrarily using the midpoint of the interval as a guide, we should do one extra calculation to try and take into account the shape of the curve. This is done by finding the secant line between two endpoints and using the root of that line as the splitting point.

More formally:

 * Draw or calculate the equation for the line between the two endpoints (a,f(a)) and (b,f(b)).
 * Find where this line intersects the x-axis (or when y = 0), giving you x = c
 * Use this x value to evaluate the function, giving you f(c)
 * The sub-intervals are then treated as in the bisection method. If the sign changes between f(a) and f(c), keep the interval; otherwise, throw it away. Do the same between f(c) and f(b).
 * Repeat until you're at a desired accuracy.

Use these two formulas to solve for the secant line y = mx + B:

The regula falsi method is guaranteed to converge to a root, but it may or may not be faster than the bisection method, depending on how long it takes to calculate the slope of the line and the shape of the function.

In some cases, the regula falsi method will take longer than the bisection method, depending on the shape of the curve. However, it generally worth trying for a couple of iterations due to the drastic speed increases possible.

Tangent Method (Newton's Method)
In this method, we attempt to find the root of a function y = f(x) using the tangent lines to functions. This is similar to the secant method, except it "cuts loose" from the old point and only concentrates on the new one, thus hoping to avoid hang-ups such as the one experienced in the example.

Since this class assumes students have not taken calculus, the tangent will be approximated by finding the equation of a line between two very close points, which are denoted (x) and $$ (x+\delta x) $$. The method works as follows:

 * 1) Choose one initial guess, $$ x_1 $$
 * 2) Evaluate the function f(x) at $$ x = x_1 $$ and at $$ x = x_1 + \delta x $$ where $$ \delta x $$ is a small number. These yield two points on your (approximate) tangent line.
 * 3) Find the equation for the tangent line using the formulas given above.
 * 4) Find the root of this line. This is $$ x_2 $$
 * 5) Repeat steps 2-4 until you're as close as you like to the root.

This method is not guaranteed to converge unless you start off with a good enough first guess, which is why the guaranteed methods are useful for generating one. However, since this method, when it converges, is much faster than any of the others, it is preferable to use if a suitable guess is available.


text:
User:Whiteknight/Electrical Engineering

This book will be a non-technical look at the field of electrical engineering, including education, careers, trends, economics, etc. --Whiteknight (talk) (projects) 22:24, 30 March 2007 (UTC)

Introduction
It may come as a surprise to some readers that no company in this day and age will hire a person to analyze a circuit. In fact, few companies will hire people to design circuits composed of resistors, capacitors, and inductors, because all these tasks are handled automatically by Computer-Aided Design (CAD) tools. Also, even though electrical engineering students do spend a large amount of time doing math, solving integrals, and manipulating equations, nobody in the entire industry gets paid to solve math problems. Again, computer tools are used to solve these math problems quickly and cheaply. In fact, for less then $1000, a company can buy a set of software tools that can solve all the basic problems that most undergraduate Electrical Engineering students can solve, and in a fraction of the time.

This is all the more shock to people whose only experiance with the whole phenomina of electricity is the wires in the home, and the few circuit tutorials (and wikibooks!) found online. After all, what else is there to the field then the wires we see, and the funny circuit diagrams online? Electrical engineering students, and graduated engineers are asked very frequently for help in wiring houses, to which the most common response is "I don't know anything about wiring houses". How can a person go to college for 4 years or more studying electricity almost exclusively, and not know a thing about the wires that bring electricity to your house? An electrical engineer, unless he has had some special training cannot fix your car, your toaster, or your alarm clock. An electrical engineer will frequently (although not always) be unable to fix your computer.

So what then, if anything, does an electrical engineer do?

The field of Electrical Engineering focuses on 2 aspects: Analysis, and Synthesis. Certainly a computer program can solve nearly any problem, but somebody must be there to feed the problem information into the computer. Not only that, but somebody must be on the other end to interpret the results. Engineering in general is all about trade-offs. Gaining an advantage in one aspect means losing an advantage in another aspect. Gaining a faster data rate, for instance, comes at the cost of a wider bandwidth (and more expensive cables and receivers and transmitters). Transmitting data reliably requires a large amount of power, which can be costly and can produce heat. Where is the line drawn? Where does the computer say that one negative aspect is acceptable in the face of a positive aspect?

Once a physical system has been analyzed, that information must be modeled mathematically, and converted into a format that a CAD tool can use. Once the CAD tool is done grinding away at the math, the human reader then needs to verify the output (because computers can do some whacky things), and then convert that information back into a form for humans to read, understand, and ultimately implement.

If an engineer needs a wire, a transistor, a diode, or a switch, he can walk down to a circuit supply shop, and buy it. Few people, if any, are working to improve these basic parts. No sense reinventing the wheel, after all. Electrical engineers are always attempting to take the things they know, and create new and better things.

History

 * Study of electromagnetics
 * Early EE
 * Edison and Tesla
 * World War II
 * Bell Labs

Disciplines

 * Power
 * Control
 * Microelectronics
 * Signal Processing
 * Telecommunications
 * Instrumentation
 * Computers

Education

 * Accreditation
 * Engineering Degrees
 * Licensing
 * Research

Work and Careers

 * Professional Organizations
 * Job Types
 * Job Trends
 * Salary Information
 * Life-Long Learning

Existing Pages
Electrical Engineering =History =Disciplines =Education =Work and Careers
 * Study of Electromagnetics
 * Edison and Tesla
 * World War II
 * Bell Labs
 * Power
 * Control
 * Microelectronics
 * Signal Processing
 * Telecommunications
 * Instrumentation
 * Computers
 * Accreditation
 * Engineering Degrees
 * Professional Licenses
 * Research
 * Professional Organizations
 * Job Types
 * Job Trends
 * Salary Information
 * Life-Long Learning

title: User:Whiteknight/Electrical Engineering


text:
Proteomics/Protein Separations- Electrophoresis/Types of Gel Electrophoresis/Differential in Gel Electrophoresis

Differential in Gel Electrophoresis (DIGE) is a technique to monitor the differences in proteomic profile between cells in different functional states. This is done by fluorescent tagging of two samples with two different dyes, then they are run the same 2D- PAGE, after the run superimpose the two fluorescent images of the same gel to study proteins common in both samples and also proteins that are expressed differentially. This technology allows for simultaneous separation and comparison of up to three samples on one gel.

DIGE vs 2D- PAGE
In the traditional 2D-PAGE to compare differential expression of proteins, different samples are often separated in multiple gels and then overlapped in order to compare different spots or intensity of spot changes from one gel to another. Due to differences between gels in spatial resolution and spot intensities the overlaying of images and correct matching of proteins difficult. These are also gel-to-gel variations in protein uptake by the isoelectric focusing strips, incomplete protein transfer from the first to the second dimension gel and local in homogeneities in gel composition, field strength or pH gradients. These gel-to-gel variation are the experimental variations and that masks the biological variation between the samples. Thus quantitative comparisons of protein expression levels are difficult using 2D - PAGE.

In DIGE protein mixtures are pre-labelled with cyanine dyes that guarantee co- migration of proteins, prior to electrophoresis. This co-migration on the same gel eliminate running differences these samples. In addition, the samples are subjected to same environment and procedures throughout the experiment,so it minimizes the experimental variation in spot quantities. In DIGE, there is no need for post-processing of gel for visualization.

Dyes
The cyanine dyes (Cy2, Cy3 and Cy5) used for DIGE are N-hydroxy succinimidyl ester derivatives,are covalently tagged to the amino group of lysine residue of proteins and replaces the -amino group positive charge with the positive charge of the dye. The binding of the dyes introduce small but matched increase in molecular weight. Since these dyes are hydrophobic, to prevent precipitation of proteins only one lysine residue per protein is labelled (minimal labeling). Minimal labeling limits the fluorescence intensity and thus the sensitivity of the stain. The dyes are all charge-matched and molecular mass-matched to prevent alterations of pI, and minimize dye-induced shifting of labelled proteins during electrophoresis.

Another approach is to use cyanine dyes other than the previously described dyes, which saturate cysteine residues instead of minimally labelling lysine residues. Again these cyanine dyes used are mass and charged matched; but there is a smaller chance of protein modification and pI shift. Saturation cysteine dyes have superior sensitivity than minimal lysine labeling. As with the minimal lysine labelling cyanine dyes, if a cysteine amino acid is not present in a protein then the saturation dyes will not be able to label it, leaving the protein undetectable.

Experiment
Two protein samples are first labeled with propyl-Cy3 and methyl-Cy5. The labelled samples are then mixed and applied onto a single 2D-GE gel and after the run the corresponding protein spot patterns are visualized by successively illuminating the gel with the excitation wavelengths of each of the dyes.To view images click here[][] The resulting protein spots are analyzed using software. Differentially expressed protein spots are then excised from the gel and identified by mass spectrometry. Only a direct comparison of two different protein samples can be performed using two dyes. To study multiple samples, a large number of pair wise comparisons or analysis of samples run on different gels is needed. An important alternative is to use a third dye (Cy2) with similar characteristics as Cy3 and Cy5. Protein samples are labelled with either Cy3 or Cy5 and a pooled sample containing equal amounts of all samples in the experiment is labelled with Cy2. All samples are then applied on the same gel.The pooled sample acts as an internal standard for every protein spot on each of the gels and is then used for normalization of all spots, across all gels. This approach reduces the experimental variation and increases the accuracy of quantification and the statistical confidence of protein expression differences.
 * Using 2 dyes
 * Using 3dyes

Advantages
To study differential expression of proteins, no need to run multiple gels.Loss of proteins even in the low molecular weight range is reduced since no post-electrophoretic processing (fixation or destaining) is necessary.This method is more quantitative than the standard colorimetric staining methods, both with regard to sensitivity as well as linearity.Also differences in spot fluorescence intensity are purely attributable to biological and not experimental variation with increased confidence.

Resources

 * Mustafa Ünlü, Mary E. Morgan , Dr. Jonathan S. Minden:Difference Gel Electrophoresis: A single method for detecting changes in protein extracts;Electrophoresis(1997) 18:2071-2077
 * Gert Van den Bergh,Lutgarde Arckens:Fluorescent two-dimensional difference gel electrophoresis unveils the potential of gel-based proteomics ;Current Opinion in Biotechnology(2003) 15:38-43
 * http://dir.niehs.nih.gov/proteomics/emerging.htm
 * http://www.decodon.com/Solutions/Delta2D/digeAnalysis.html
 * http://www.asbmb.org.au/magazine-sample/2004-August_%20Issue35-2/Technical%20Feature%202%20-%20Attard.pdf
 * http://ajprenal.physiology.org/cgi/content/full/286/1/F170


text:
Field Guide/Reptiles

 * /Western US and Canada/
 * /Spain/
 * /Eastern US and Canada/
 * /Western Europe/
 * /British Isles/
 * /Eastern Europe/
 * /Alpine Region/
 * /Scandinavia/
 * /Australia/
 * /New Zealand/
 * /Mexico and Central America/
 * /Caribbean/
 * /Northern South America/
 * /Amazon Rain Forest/
 * /Southern South America/
 * /Andean Region/
 * /India/
 * /Japan/
 * /Indonesia and Malaysia/
 * /Middle East/
 * /North Africa/
 * /Southern Africa/
 * /West Africa/
 * /Horn of Africa/
 * /Siberia/
 * /Central Asia/
 * /Caucasus/

title: Field Guide/Reptiles


text:
Field Guide/Reptiles/Eastern US and Canada

This Field Guide to Reptiles covers the portion of the United States and Canada east of the Rocky Mountains.


text:
Adventist Youth Honors Answer Book/Outreach/Sign Language

1. Learn the manual alphabet used by the deaf.
The American Manual Alphabet is a manual alphabet that augments the vocabulary of American Sign Language when spelling individual letters of a word is the preferred or only option, such as with proper names or the titles of works. Letters should be signed with the dominant hand and in most cases, with palm facing the viewer.

To practice fingerspelling receptive skills try Dr. Bill Vicars website http://asl.ms/ or ASLpro's Quizme fingerspelling http://www.aslpro.com/cgi-bin/aslpro/fingerspell.cgi

Chart

The ASL alphabet is based on an the French manual alphabet from which much of American Sign Language is derived.

It is used with minor modification in Paraguay, the Philippines, Thailand, Malaysia, Hong Kong, Taiwan, and Singapore. The Asian countries just listed modify the T, for the ASL T is considered obscene. Instead, they use the T of the Irish manual alphabet, which is like an ASL X, but with the thumb tucked into the index finger (that is, the index finger wraps around the tip of the thumb). In Thailand, one indicates points on the left hand for the tone and vowel marks of the Thai alphabet, and aspiration is not indicated. The Paraguay alphabet is identical to ASL, except for the addition of the letter Ñ, which is an N swiveled at the wrist so that the fingers move side to side, and the letters LL and RR, which are L and R plus movement to the side.

It is also used in Germany, Austria, Norway, and Finland, again with a modification for the letter T. T is like G with the thumb placed atop the first knuckle of the index finger.

German Ä, Ö, Ü, and ß are signed like A, O, U, and S but with a downward motion, while SCH is a 5 hand (palm forward). In Norwegian and Finnish, the letters Ä, Å, Ö, Ø are derived by moving A and O (in the case of Å, in a small window-washing circular motion), and it is the Æ that gets the 5 hand (perhaps somewhat flexed).

Good form

 * The hand should either remain in place while fingerspelling, or more often, drift slightly away from the midline in the manner of text being written out in the air; although, this is a subtle movement and should not be exaggerated.
 * If fingerspelling multiple words or entire sentences, there should be a very brief pause between terms so as to signify the beginning and ending of individual words.
 * Long nails or excessive jewelry can be distracting when watching fingerspelling and for this reason people who regularly use sign language usually avoid them.
 * When fingerspelling acronyms in American Sign Language, such as with FBI, NASA, or RID (Registry of Interpreters for the Deaf), the letters are often moved in a small circle to emphasize that they should not be read together as a word.
 * Additionally, when fingerspelling the hand should not bounce between letters. An exception is the case of double letters as with the word carry in which the double R can be shown by slightly bouncing the corresponding handshape, or by dragging it, slightly, to the side. Either method is a correct way to show double letters. However, people who bounce between every letter produce fingerspelling that is very hard to watch or understand. Those who cannot overcome the habit of bouncing every letter may find it helpful to hold the wrist of the hand doing the fingerspelling with the free hand so that they are forced to keep the hand from moving up and down while fingerspelling. Usually, only a few hours or days of this is enough to break the habit of unnecessary bouncing while fingerspelling.

Common mistakes
Many mistakes made by beginning fingerspellers are directly attributable to how the manual alphabet is most often shown in graphics.

Letters
In most drawings or illustrations of the American Manual Alphabet, some of the letters are depicted from the side to better illustrate the desired handshape; however in practice, the hand should not be turned to the side when producing the letter. The letters C and O are two that are often mistakenly turned to the side by beginners who become used to seeing them from the side in illustrations. Important exceptions to the rule that the palm should always be facing the viewer are the letters G and H. These two letters should be made, not with the palm facing the viewer or the speaker, but with the palm facing sideways - the hand in an ergonomically neutral position.

Numbers
Another mistake made by people faithfully following the pictures in most illustrations of the ASL fingerspelling alphabet is the signing of the cardinal numbers 1 - 5 with the palm facing out. The cardinal numbers 1, 2, 3, 4, and 5 should be signed palm in (towards the signer). This is in contrast with the cardinal numbers 6-9 which should be produced with the palm turned to face the person being addressed.

As with the letter O, the zero should not be turned to the side, but shown palm facing forward.

This applies only to the cardinal numbers however. Using numbers in other situations, such as with for showing the digits of the time for example, has different rules. When signing the time, the numbers are always facing the person being addressed, even the numbers one through five. Other signing situations involving numbers have their own norms that must be learned on a case by case basis.

Rhythm, speed & movement
When fingerspelling, your hand should be at shoulder height, and should not 'bounce' with each letter. Your hand should stay in one place and only the handshape changes (and orientation for some letters). If you have trouble doing this, you might want to hold your forearm with your nondominant hand in order to force your spelling hand to stay still. 'Bouncing' the letters makes your fingerspelling difficult to read, even for native signers.

As well, clear handshapes are much easier to read than fast fingerspelling. Do not concentrate on speed, as fast fingerspelling with poorly formed handshapes will be difficult to read. Try to fingerspell the whole word at the same speed, not speeding up or slowing down. A pause indicates the beginning of a new word, so if you suddenly slow down because a letter combination is difficult, your reader may think you are starting a new word, leading to misunderstanding. An exception to this sometimes appears at the beginning of a word. The first letter may be held for the length of a letter extra as a cue that the signer is about to start fingerspelling.

2. Have a minimum of three hours of instruction in signing.
Where do you find a sign language instructor? First, if you know a deaf person or someone who knows how to sign, ask them for a referral. If that doesn't work out, check with a local high school guidance counselor. They may be able to direct you to either a free or for-pay program. You can also check into a local social services organization, as many offer sign language classes for free.

Ideally, you will have a volunteer instructor come to instruct your club, but you may need to be flexible. Your club may need to come to the instructor. If only a few people in your club are interested, you should join a class that meets outside of Pathfinder time. If you invite an instructor to teach at your club, be sure to tell her how many students to expect before you ask for a commitment.

Once you find a class and instruction begins, we highly recommend that you take five hours of instruction rather than just the three required. It will be a lot easier to continue instruction until you have all five hours as opposed to resuming classes sometime in the future.

Tips
When you are first learning to sign the letters, a good Bible text to practice with is Philippians 4:8, as it repeats the phrase "whatever is" several times. Since it is so repetitive, You should be able to quickly sign the "whatever is" portion to get your speed up. This verse contains all the letters of the alphabet except j, q, and z which can be learned afterwards. Learning a text such as this will also force you to learn each letter on its own (as opposed to always signing K after J). Once a text such as this one has been learned you may be surprised that you can finger spell just about anything.

Graphically
We present this Bible verse graphically here, showing the first 108 letters of the verse. If you can sign this in under 4 minutes 20, seconds, you will have achieved 5 words per minute (assuming an average of 5 letters per word).

4. Learn at least 100 signs from one or more of the below referenced books.

 * A Basic Course in Manual Communication, T.J. O'Rourke, National Association of the Deaf, 814 Thayer Avenue, Silver Spring, MD 20901.
 * Ameslan, An Introduction to American Sign Language, Louie Fant, Jr., Joyce Media, P.O. Box 458, Northridge, CA 91328. Play It By Sign, Ibid. (Joyce Media also has instructional films.)
 * Joy of Signing, Lottie, L. Riekehof, Gospel Publishing House, Springfield, MO.
 * Talk to the Deaf, Etc., Gallaudet College Press, Washington, D. C. 20002.
 * Expressive and Receptive Fingerspelling for Hearing Adults, La Vera M. Guillory, Claitor's Publishing Division, P.O. Box 3333, Baton Rouge, LA 70821.
 * An Introduction to Manual English, The Washington State School for the Deaf, Vancouver, WA 98661.

If you cannot find any of these books, substitute something equivalent.

 * http://www.aslpro.com, Contains three ASL dictionaries and study tools.
 * http://www.lifeprint.com, Also is an excellent source for learning ASL signs.

5. Learn and present in sign language (not finger spelling) at least two simple songs.
The titles suggested below are popular Christian songs with few words, or words that repeat (that is our definition of simple). Repetition is very useful when learning something new, especially a language.
 * God is so Good
 * This Little Light of Mine
 * I've Got the Joy in my Heart
 * Rejoice in the Lord, Always

 * First Noel. More challenging Christmas songs http://www.aslpro.com/poemsnsongs/firstnoel.html
 * Silent Night. More challenging Christmas songs http://www.aslpro.com/poemsnsongs/silentnight.html

a. Explain the difference between Ameslan and signed English, and demonstrate the use of both.
Ameslan, or American Sign Language, has little connection to English grammar. This language was developed by the deaf community as an efficient and expressive method of communication. Signed English, on the other hand, was designed with a more direct connection to English grammar, the theory being that knowing it would make reading and writing in English easier. Signed English follows the same word order and syntax as spoken English, while the word order in Ameslan is conceptually-based.

b. Read and give an oral or written report on a school in your country or state specializing in deaf education.
See the Wikipedia article Schools for the Deaf for a list.


text:
Paint.NET/Lightsaber

Here's how the pros make a lightsaber.

Step 1: The image
You need an image to edit, preferably of somebody holding something saber-ish, a sword, a stick. Or perhaps a fully-fledged lightsaber prop? Or something similar such as a Force-FX saber or just a hilt.

Google can do your thing, but watch out for copyrights.

Step 2: The core effect
Now that you have got your image, it's time to start the effect. We begin by painting the core. That's the white blade in the middle. If you have a stick or a prop, use the line tool to cover it with white, or if you are in a self-destructive mood or have drawing specialised input tools, use the paintbrush.

If you have no stick you can use the hilt or your empty hands as a guide, remember, lightsaber blades are roughly one meter long.

Make sure the line extends at least a little over the hilt or hands, then use the eraser to adjust it so it matches up with the emitter hole just nicely.

Then use the paintbrush to round the other end. A flat saber is simply so boring.

If the stick or imaginary so is obstructed by anything so should the core be, erase.

The core is more important than you might think, a well made core greatly contributes to the 3D-effect that makes the saber look like it's there.

Step 3: The glow
Now, for the thing that makes the saber look bright and deadly, the glow.

Duplicate the core thrice;

Set the layers to screen, I have found this looks very similar to real photographic glows;

Now use gaussian blur on each of the layers in incremental values. Like for example: 10, 20, 30. Or 10, 20, 40.

It depends on what kind of glow you want. The amount of blur also depends on the size of the image.

Now merge the layers.

Step 4: The colour
The saber needs colour now. A white saber is simply so boring. The choice of colour is a good start. Remember, canonically there's only four colours. Red = bad. Blue & green = good. And then purple, for awesome.

But the expanded universe gives you the option for any colour you like, be it hot pink or rainbow gradient. Although I won't detail how to do the latter here.

You can apply the colour in two ways. By using levels, and by using recolour.

Levels: Open levels and adjust the colour sliders for the glow layer until it has the hue you want, some interesting and glow-ish effects can be achieved with this.

Recolour: I like this because it gives me better control over the hue, and I can always use levels after that, but thats just me. Select the colour you want for primary, and white for secondary. Use 100 px brush to go over the entire glow.

You're pretty much done now. But there's some finishing, although optional touches that can really make the saber better.

Step 5: The light
Lightsabers, are as the name suggest, light sources. You may want to add "Interactive Lighting". Force FX sabers light up, so they pretty much do the job for you, but you may want to enhance the effect as it isn't quite bright enough for a lightsaber. Or you can add additional light when you take the photo with lamps.

For digitally making the effect:

Make a new layer, use a tinted brush to paint a not-too-thick line or dot on the surfaces you want lit. Use much Gaussian blur. you may want to make several layers for surfaces that aren't parallel or need different amounts of light. You may also want to expand the canvas considerably for the next procedure.

Make selection boxes around the entire blurred lines and dots and use rotate/zoom to give them proper perspective.

Then use the eraser to go over the places that wouldn't receive light, such as the background behind a person or object, or on the shadow side of things, or maybe some things are shaded by another object?

Merge your light layers.

Duplicate it, then set the lower layer to overlay, and the upper to reflect. Make the reflect layer of limited opacity.

If the image has very dark areas you may want to use yet another layer to make a light foundation with screen. Again, with limited opacity.

Step 6: The reflections
Now, bright stuff reflect very visibly. Your forceFX may have left guide reflections or maybe your stick blatantly shows up? Anyways paint reflections with a tinted brush, then a smaller white one. Set the layer to... you guessed it, reflect. Again, of limited opacity.

If there's a big mirror you may want to make an entirely new saber effect for it instead.

Step 7: The adjustments
The final touches.

Make yet another glow that is very small and completely white, and only one duplication. It gives the saber an extra sense of brightness.

Make sure the layers are layered like this:

 * 1) Small glow
 * 2) Glow
 * 3) Core
 * 4) Interactive light reflect
 * 5) Interactive light overlay
 * 6) Interactive light screen
 * 7) Reflections
 * 8) Background

You may also want to adjust all the layers opacity settings so everything looks exactly perfect.

The idea of a saber glow is usually that it's perfect, artifactless. But you may want to add artifacts anyways. Duplicate the glow several times and move the dupes along an imaginary 3d-line of varying sizes and intensity.

You could also duplicate the core and stretch it with motion blur, of limited opacity.

If the image is old or of low quality you may want to adjust your saber equally. say, the image lacks contrast? The core probably shouldn't be pure white. Find the image's pure white and apply it to the core.

Is it grainy? Saber not excused. Apply grain. Etc, etc.

Remember when you initially make your saber effect to take into account the lighting conditions of the image, if it's dark the saber should appear very bright, if the sun is in the shot... probably not quite so.

If you have followed all the steps, you are very dedicated and now should have a very fine saber effect.

But mostly you'll probably just want to stick with the first 4 steps. There's not many who cares for all the mostly unnecessary extra work. But if you do happen to care...

But remember, don't slavishly follow a tutorial, everybody has their own idea of lightsabers, find yours. Stick to it.

title: Paint.NET/Lightsaber


text:
User talk:Waitak

Hey Waitak,

I heard you were interested in a Mongolian wikibook? I'd be glad to help in this project, and actually have some recources that might be useful to you. Look here how I'm doing the Uzbek book. I also have the Peace Corps books in Mongolian, and can get you the pdf's if you'll make a commitment to do the same thing for them that I have been doing with Uzbek. It's quite a lot of work typing it in, you can't just copy and paste. --but you might learn some Mongolian in the process.

Let me know on my talk page if you are interested.

---Uzbekscholar 07:36, 31 March 2007 (UTC)

title: User talk:Waitak


text:
User:68.54.253.180

Moved conversation to your talk page where it belongs.

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French/Vocabulary

This list contains a list of common words in French with their English meanings.

Tip:- If you want to search for a particular word, use the Find feature in your browser (CTRL + F, or F5 in Internet Explorer).

title: French/Vocabulary


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Pathology/Cell and Tissue Damage

= Zell- und Gewebsschäden =

Schäden der Zellorganellen
Viele pathologische Prozesse führen zu mehr oder weniger spezifischen Veränderungen einzelner Zellorganellen in bestimmten Zellpopulationen. Diese sind neben der Histologie und anatomischen Pathologie vielfach wegweisend bei der Diagnose und Beurteilung von Erkrankungen.

Zellkern

 * Unspezifische Reaktionen des Zellkerns auf Noxen
 * Kernschwellung
 * Kernpyknose - Kernschrumpfung durch Kondensation des Chromatins
 * Karyorrhexis - Kernfragmentierung
 * Karyolyse - Kernzerfall
 * Apoptose - Suizidprogramm der Zelle, ausgelöst durch Aktivierung des Fas-Ligand-Rezeptor-Weges oder Freisetzung von Cytochrom C aus den Mitochondrien -> morphologisch: Apoptosekörperchen

 * Kerneinschlüsse
 * Glykogen („Lochkerne“) - Z.B. bei Diabetes mellitus
 * Zytoplasma („Milchglaskerne“) - Z.B. beim papillären Schilddrüsenkarzinom
 * Viren („Eulenaugen“) - Einschluss von Virusmaterial, z.B. bei CMV-Infektion

 * Mehrkernige Riesenzellen - Sie entstehen durch Verschmelzung mehrerer Zellen oder bei inhibierter Zellteilung und kommen sowohl physiologisch als auch im Rahmen pathologischer Prozesse vor.
 * Physiologisch: Skelettmuskelzellen, Megakaryozyten, Osteoklasten, Trophoblast
 * Pathologisch:
 * Histiozytäre Zellen:
 * Fremdkörper-Riesenzellen - Typisch in Fremdkörpergranulomen, die Zellkerne sind in einem Haufen zusammengelagert
 * L ANGHANS -Riesenzellen - In Tuberkulosegranulomen, die Kerne sind hufeisenförmig angeordnet
 * A NITSCHKOW -Riesenzellen - Bei rheumatischer Myokarditis
 * T OUTON -Riesenzelle - Schaumzellen, bei denen um eine kleine schaumfreie Insel mehrere Kerne ringförmig angeordnet sind, Vorkommen z.B. bei juveniler Xanthogranulomatose, siehe Abb.
 * Riesenzelle bei Epulis
 * Tumor-Riesenzellen:
 * R EED -S TERNBERG -Riesen-Zellen (Morbus H ODGKIN )
 * Karzinom/Sarkom-Riesenzellen
 * Polymorphie - Zeichen der Malignität

Nukleolus

 * Vergrößerung

Zeichen eines erhöhten RNA-Umsatzes und damit Indikator für Aktivität, Proliferation oder Malignität der Zelle.

 *  Veränderungen

Schalen-, Ring-, Schwammnukleolen

 * AgNOR - Versilberbare Nucleolus-Organisator-Regionen

Anzahl, Größe und Fläche geben Auskunft über Aktivität und Malignität

Glattes Endoplasmatisches Retikulum
Pathologische Veränderungen:
 * Feinvakuoläre Degeneration
 * Hyperplasie bei chronischer Detoxifikation, z.B. in der Leberzelle bei langjähriger Medikamenteneinnahme
 * Milchglaszellen bei Hepatitis B durch Ablagerung von HBs-Ag
 * Dilatation und Zisternenbildung bei zellulären Sekretionsstörungen

Rauhes Endoplasmatisches Retikulum
Vergrößerung bei gesteigerter und/oder gestörter Funktion (vakuoläre Degeneration), z.B. bei Fibroblastom (Fibroblastentumor) oder Osteogenesis imperfecta (Osteoblasten).

Golgi-Apparat

 * Sekretionsstörungen führen zu Dilatation und Einschlüssen
 * Verstärkte Sekretionsleistung führt zur Hyperplasie

Mitochondrien

 * Verkalkung (Mitochondrien sind Kalziumfänger)
 * Megamitochondrien bei chronisch-toxischen Einflüssen
 * Schwellung: Crista-Typ (reversibel) oder Matrixtyp (irreversibel)
 * Feingranuläre Degeneration, trübe Schwellung
 * Einschlüsse
 * In Onkozyten (geschwollene, eosinophile Zellen mit vergrößerten Mitochondrien)

Lysomen

 * Lysosomale Restkörperchen - Bestehen aus Ablagerungen von Lipofuszin (Alterspigment)
 * Lysosomale Defekte - C HEDIAK -H IGASHI, Morbus W HIPPLE
 * Lysosomale Speicherkrankheiten - Morbus P OMPE, Morbus G AUCHER , Morbus N IEMANN -P ICK

Zellmembran
Z.B. Verlust der Mikrovilli des Darmepithels bei Zöliakie.

Zytoplasma
Verschiedene Viren führen zu intrazytoplasmatischen Einschlusskörperchen, so z.B. Tollwutviren (Negri bodies).

Degeneration

 * Fettige Degeneration
 * Mukoide Verquellung
 * Chondroide Metaplasie
 * Dystrophische Verkalkung
 * Metaplastische Ossifikation
 * Entzündungsreaktion

Fettablagerung
Intrazelluläre Verfettung
 * Fettkörnchenzellen, Schaumzellen (lipidbeladene Phagozyten)
 * Fettleber (nutritiv, metabolisch, toxisch, hypoxisch)
 * Degenerative Herzmuskelverfettung (Makro: Tigerfellzeichnung)
 * Nierenverfettung
 * Skelettmuskelverfettung (Muskeldystrophie)
 * Xanthome
 * Xanthelasmen am Auge

Extrazelluläre Verfettung
 * Lipomatosis cordis (alter Infarkt, nutritiv)

Adipositas
 * Größenzunahme der Adipozyten bei Überernährung

Tumore des Fettgewebes
 * Lipom (benigne)
 * Liposarkom (maligne)

Eiweißablagerungen
Amyloid

Amyloid bedeutet stärkeähnlich. Wie Stärke färbt es sich schwarz, wenn es mit Jodlösung (Lugol'sche Lösung) behandelt wird.

Eigenschaften: Extrazellulär, homogen, spezifisch anfärbbar mit Kongorot, Doppelbrechung im Polarisationsmikroskop: Apfelgrün-gelb, irreversibel wasserunlöslich, immer pathologisch (von den Corpora amylacea der Prostata abgesehen).

Diagnose: Bioptisch mit Kongorot und Polarisation.

Formen:
 * Generalisiert
 * Amyloid A - ein alpha-Globulin. Vorkommen bei chronischen Entzündungen und Tumoren sowie beim autosomal-rezessiv erblichen Mittelmeerfieber.
 * Amyloid L - Leichtkettenamyloid (Lambda > Kappa), entspricht dem Bence-Jones-Protein im Harn. Vorkommen bei Ig-Ketten produzierenden Lymphomen wie dem Plasmozytom oder beim Morbus Waldenström.
 * Lokalisiert
 * Hämodialyse-Amyloid - ein beta-Globulin.
 * ZNS-Amyloid - Amyloid-β-Peptid. Vorkommen beim Morbus A LZHEIMER.

Fibrinoid

Eigenschaften: Extrazellulär, homogen, vorkommen bei Autoimmunerkrankungen (z.B. fibrinoide Nekrose in subkutanen Rheumaknötchen).

Hyalin

Eigenschaften: Milchglasartig, homogen, eosinophil, Protein und MPS.

Formen:
 * Intrazellulär
 * M ALLORY -bodies („Alkoholisches Hyalin“ in Hepatozyten bei alkoholischer Hepatitis, bestehend aus mehr oider weniger abgebauten Keratinfilamenten)
 * Russelkörperchen (Plasmazellen bei chronischer Entzündung)
 * Extrazellulär
 * Bindegewebiges H. : Zuckergußmilz, Leberkapsel, hyaline Pleuraplaques
 * Vaskuläres Hyalin : Diabetes mellitus, Hypertension
 * Councilman-bodies : Apoptotische Hepatozyten bei Virushepatitis
 * Pulmonale hyaline Membranen : ARDS, Beatmung, Frühgeborene
 * Hyaline Zylinder : Eiweißzylinder im Urin (T AM -H ORSFALL -Protein)
 * Hyaline Thromben : Endotoxinschock

Pigmentablagerungen
Exogene Pigmente

 * Tätowierungepigment (Kohle, Tusche)
 * Anthrakose der Lunge (Kohlenstaub, Ruß), unschädlich
 * Anthrakosilikose der Lunge (Quarzstaub/Siliziumoxid SiO2), toxisch
 * Saturnismus (chronische Bleivergiftung)
 * Argyrismus (chronische Silbervergiftung)

Endogene Pigmente

 * Häm- und Hämoglobinderivate
 * Hämosiderin - Vitale Reaktion, intrazytoplasmatisch, eisenhaltig, pyrrolfrei, gelbbraun, Vorkommen z.B.: in Herzfehlerzellen, bei Transfusions-Hämosiderose, Hämochromatose
 * Hämatin - Entstehung: Hb + HCl, schwarz-braun, Bsp.: Kaffeesatzerbrechen, Teerstuhl bei oberer GI-Blutung
 * Hämatoidin = Indirektes Bilirubin - Entsteht ohne vitale Reaktion, extrazellulär, eisenfrei, pyrrolhaltig, gelb-orange, Bsp.: Bluterguss, Ikterus, Kernikterus
 * Hämatozoidin - Malariapigment in Kupfer-Stern-Zellen, schwarz-braun-grau
 * Porphyrin (Häm-Vorstufen) - Einlagerung in Haut und innere Organe, Bsp.: Porphyrie
 * Hämoglobinzylinder im Urin - Bsp.: Transfusionszwischenfall
 * Myoglobinzylinder im Urin - Bsp.: Crash-Niere

 * Phenylalaninstoffwechsel

Überblick über die Biochemie des Phenylalanin- bzw. Tyrosinstoffwechsels:

.-> Homogentisat -3-> ... -> Acetoacetat + Fumarat | Phenylpyruvat <- Phenylalanin -1-> Tyrosin -2-> L-Dopa -> Dopamin -> Noradrenalin -> Adrenalin u.a. toxische                      |    | Metabolite                         V    V                                               T3/T4  Melanin 1.: Phenylalaninhydroxylase (PAH) 2.: Tyrosinase 3.: Homogentisatdioxidase

Melanozyten versorgen, stimuliert durch MSH, die Keratinozyten über ihre Fortsätze mit Melanin. UV-Licht oxidiert das Melanin und aktiviert die Tyrosinase.

 * Hypopigmentierung:
 * Phenylketonurie : Phenylalaninhydroxylase-Mangel
 * Albinismus : Tyrosinase-Defekt
 * Vitiligo : Fehlen von Melanozyten
 * Hyperpigmentierung:
 * Morbus A DDISON : Hyperpigmentierung (NNR↓ -> CRH↑ -> POMC↑ -> ACTH↑, α-MSH↑, β-Endorphin↑)
 * Chloasma uterinum : hormonell
 * Sommersprossen (Ephelides) : Melaninreiche Flecken

 * Sonstiges:
 * Alkaptonurie : Homogentisatdioxidase-Mangel (schwarz-brauner Urin, Einlagerung von schwarzem Homogentisat in Knorpel und Bindegewebe)

 * Tumoren:
 * Naevuszellnaevus
 * Malignes Melanom

Verkalkung
Physiologische Verkalkung

An der Knorpel-Knochen-Grenze

Dystrophische Verkalkung

Normaler Ca-P-Stoffwechsel, Zellschäden, Calcium reichert sich in saurem Gewebe an und fällt bei intermittierend besserer Durchblutung und pH-Anstieg aus. Z.T. ohne Einschaltung der Mitochondrien (degeneriertes Gewebe), z.T. mit (nekrotisches Gewebe mit Restdurchblutung).

Bsp.: Verkalkte Tuberkulome, Psammomkörperchen, Atherosklerose, Kalzium-Nierensteine.

Metastatische Verkalkung

Hyperkalzämie, keine Zellschäden (bzw. erst sekundär), Ablagerung in Säure-abgebenden Organen (Lunge H2CO3, Niere Harnsäure, Magen HCl).

Bsp.: Tuffsteinlunge, Nierenkalzinose

Idiopathische Verkalkung

 * Kalzium-Hydroxylapatit - Degenerativ, lokalisiert am geschädigten Bindegewebe, nicht doppelbrechend, Bsp.: Tendinosus calcanea des M. supraspinatus.

 * Kalzium-Pyrophosphat (Kalkgicht, Chondrokalzinose) - Bei Stoffwechselstörungen (Diabetes, Gicht), lokalisiert in bradytrophen Geweben (Menisken), doppelbrechend.

Kalkspritzer

Bei schwerer Pankreatitis: Freigesetzte Lipasen spalten Fette im Bauchraum in Glyzerin und Fettsäuren. Fettsäuren fangen Kalziumionen ein.

Kollagen
Kollagentypen:

 * I - Knochen, Sehnen, Muskel, Gefäße
 * II - Knorpel
 * III - Retikulin
 * IV - Basalmembran

I, II und III interstitielle Typen

Störung der Kollagensynthese
 * Skorbut
 * Osteogenesis imperfecta (Kollagen I)
 * E HLERS -D ANLOS -Syndrom (EDS)

Störung der Kollagenvernetzung
 * E HLERS -D ANLOS Typ V (Kollagen III)
 * Morbus W ILSON (Kupferspeicherkrankheit)

 * Dornenkollagen : Vermehrter Proteoglycananteil
 * Asbestfasern : Verminderter Proteoglycananteil, z.B. bei arthrotischem Gelenkknorpel (Demaskierung der Kollagenfasern)

Störung der Kollagenzusammensetzung
 * Kollagen I vermehrt : Atherosklerose, Sklerose, Fibrose

Störung des Kollagenabbaus
 * Hypertrophe Narben

Kollagenosen

Kollagenosen haben primär nichts mit Kollagenstoffwechsel zu tun, die Kollagenschäden entstehen erst sekundär.

Ursachen: Chronisch-rezidivierende Autoimmunerkrankungen (SLE, Dermatomyositis, Morbus W EGENER, CP).

Folgen: Generalisierte Bindegewebsveränderungen, fibrinoide Nekrose

Proteoglykane
Aufg.:
 * Organisation der Interzellularsubstanz des Bindegewebes
 * Gefäßpermeabilität
 * Mechanischer Schutz der Zelle vor Zerquetschung

Komplexierungsstörung

Mukoide Degeneration -> Wasserbindung -> Gewebsschwellung

Ursachen: M ARFAN -Syndrom, idiopathische Medianekrose E RDHEIM -G SELL

Synthesestörung

Erkrankungen: Multiple epiphysäre Dyplasie, Chondrodystrophie

Folge : Zwergwuchs

Sekretionsstörung

Erkrankung: Mukoviszidose (Chlorid-Kanal CFTR defekt)

Zelltod
Apoptose

„Programmierte Zelltod“

Ursachen:
 * Freisetzung von Cytochrom C aus Mitochondrien oder Bindung von Fas-Ligand an den Fas-Ligand-Rezeptor
 * Genetisch induzierter Zelltod
 * Aktiver, energieverbrauchender Prozess der Zelle („Suizidprogramm“).

Mikro: keine Entzündungsreaktion, Beginn mit Kernpyknose, später Apoptose-Körperchen

Bsp.: Abtötung autoreaktiver T-Lymphozyten im Thymus, i. R. d. Embryonalentwicklung

Nekrose

Nekrose ist das intravitale Absterben von Zellen

Mikro: (nach Ablauf der Manifestationszeit!)
 * Homogenisierung des Zytoplasmas
 * Azidophilie, Eosinophilie
 * Kernpyknose, -lyse, -rhexis
 * Verlust zellspezifischer Parameter (z.B. Querstreifung beim Herzinfarkt)
 * Entzündungsreaktion

Formen:

 * Gruppenzellnekrosen - Bsp.: Tubulusnekrosen bei der Schockniere

 * Koagulationsnekrose - Eiweißdenaturierung, Verfestigung, Narbenbildung, Bsp.: Anämische Infarkte in eiweißreichen Organen (Herz, Niere, Milz), Säureverätzungen

 * Kolliquationsnekrose - Verflüssigung, Pseudocysten statt Narben, Bsp.: Infarkt in eiweißarmen, fettreichen Organen (Gehirn), Laugenverätzungen

 * Enzymatische Fettgewebsnekrose - Bsp.: Pankreatitis: Die freigesetzten Lipasen setzten aus dem Fettgewebe z.B. des Mesenteriums Fettsäuren frei, die mit Calzium Kalkseifen bilden.

 * Traumatische Fettgewebsnekrose

 * Käsige Nekrose - Bsp.: Tbc (Epitheloidzelliges Granulom mit Langhans-Riesenzellen und zentraler käsiger Nekrose)

Makrophagenreaktion (Histiozyten), Bsp.: Autoimmunerkrankungen (CP, M. Wegener).
 * Fibrinoide Nekrose - Keine echte Nekrose, Entstehung im Bindegewebe oder in der glatten Muskulatur,

 * Gangränöse Nekrose
 * Trockene Gangrän - Oft oberflächlich
 * Feuchte Gangrän - Fäulniserreger (Anaerobier)

 * Hämorrhagische Nekrose - Nekrose mit Einblutung, Bsp.: Hämorrhagische Pankreatitis

Entzündungspathologie
Eine Entzündung ist eine Gewebsabwehrreaktion gegen lokale Schädigungen.

Einteilung:
 * Spezifische Entzündung - Entzündungsmanifestationen, die für eine Erkrankung typisch sind z.B. Tbc, Sarkoidose
 * Unspezifische Entzündung

Ursachen:
 * Mikroorganismen
 * Bakteriell -> Eher eitrige, d.h. granulozytäre Entzündung
 * Viral -> Eher seröse, lymphoplasmazelluläre Entzündung
 * Mechanisch
 * Thermisch
 * Chemisch
 * Ionisierende Strahlen

Ablauf:
 * Schädigung
 * Gefäßreaktion, erhöhte Gefäßpermeabilität (Schwellung), Thrombosierung (Auskopplung vom Blutkreislauf)
 * Granulo-monozytäre Reaktion
 * Lympho-plasmazelluläre Reaktion und Granulationsgewebe
 * Kollagenfaserbildung, Vernarbung

Formen:

 * Serös - Bsp.: Rhinitis, virale Infektionen
 * Fibrinös - Bsp.: Fibrinöse Perikarditis
 * Eitrig (purulent, granulozytär)
 * Infektiös - Meist bakteriell
 * Abszess - Abgekapselter Eiterherd in einem nicht präformierten Hohlraum
 * Empyem - Eiterherd in einer präformierten Körperhöhle
 * Phlegmone - Sich diffus ausbreitende eitrige Entzündung
 * Steril - z.B. Pyoderma gangraenosum, Psoriasis pustulosa
 * Hämorrhagisch - Bsp.: Hämorrhagische Enterokolitis
 * Nekrotisierend - Bsp.: Verätzung
 * Putride gangräneszierend - Bsp.: Gasbrand

Klassische Entzündungszeichen:
 * Dolor - Schmerz
 * Calor - Überwärmung
 * Rubor - Rötung
 * Tumor - Schwellung
 * Functio laesa - Funktionseinschränkung

Entzündungsmediatoren:
 * Chemotaxis - C5a, Leukotrien B4, Bakterienprodukte
 * Fieber - IL-1, TNF, PG
 * Gewebsschädigung - O2-Radikale, lysosomale Enzyme, Proteasen
 * Permeabilitätserhöhung - Histamin, C3a, C5a, Bradykinin, Leukotriene, PAF
 * Schmerz - PG, Bradykinin
 * Vasodilatation - PG

Systemische Entzündungsreaktion

 * Akute-Phase-Reaktion bzw. SIRS (systemic inflammatory response syndrome)
 * Sepsis = SIRS mit Nachweis einer Infektion

SIRS ist eine sterotype unspezifischen Immunreaktion des Organismus auf Gewebsschädigungen (Verletzungen, operative Eingriffe, Infektionen, Verbrennungen). Bei Dekompensation wird die inflammatorische Kaskade zum Selbstäufer und kann nicht mehr gestoppt werden (circulus vitiosus).

Enzündungsmediatoren

Endothelzellen, Fibroblasten und Gewebsmakrophagen im geschädigten Gewebe setzen Entzündungsmediatoren frei, z.B. IL 1, IL 6, TNF-α, Transforming Growth Factor-β (TGF-β), IF-γ, Epidermal Growth Factor (EGF), Leukozyten induzierender Faktor (LIF) u.a., die einerseits für lokalen Effekte verantwortlich sind und andererseits in Anwesenheit von Cortisol die Leber zur vermehrten Synthese der etwa 30 verschiedenen Akute-Phase-Proteine stimulieren, deren  Konzentration innerhalb von 6-48 Stunden nach dem schädigenden Ereignis auf das zwei- bis eintausendfache zunimmt.

Akute-Phase-Proteine

Aufgabe:
 * Lokalisierung der Entzündung
 * Verhinderung der Ausbreitung
 * Unterstützung des Immunsystems bei der Sanierung des Entzündungsherdes

Beispiele für Akute-Phase-Proteine:
 * Fibrinogen -> lokale Thrombusbildung im Entzündungsgebiet -> Erreger werden nicht weiter in die Blutbahn ausgeschwemmt.
 * α1-Antitrypsin und α-Antichymotrypsin -> reduzieren als Anti-Proteasen die Gewebsschädigung.
 * C-Reaktives-Protein -> Opsonierung
 * Saures Alpha1-Glykoprotein
 * Haptoglobin
 * Coeruloplasmin
 * Komplement-C3
 * Plasminogen
 * Transferrin

Stresshormone

Weiterhin werden die klassischen Stresshormone Adrenalin, Noradrenalin und Cortisol, sowie weitere Hormone (ADH, Aldosteron) freigesetzt. Diese Hormone dienen u.a. der Kreislaufstabilisierung durch Vasokonstriktion, Natrium- und Wasserretention (ggf. Zentralisation) und der Energiebereitstellung (Lipolyse, Glykogenolyse, Glukoneogenese).

Bakterielle Zellwandprodukte (bei Sepsis, bes. LPS gramneg. Keime)

bakterielle Zellwandprodukte ->

 * -> Komplementaktivierung und
 * -> primäre Mediatoren (TNF,IL1,IFN..) -> Leukozytenaktivierung -> sekundäre Mediatoren (PAF, Eicosanoide, IL)
 * => Aktivierung von PMN -> Kapillar- und Endothelschäden -> Volumenverlust ins Interstitium
 * -> ACTH/Endorphine -> Gerinnungsaktivierung -> Aktivierung d. Kallikrein-Kinin-Systems -> Vasdodilatation, Endothelschäden -> absoluter und relativer Volumenverlust
 * ==>> Schock, MOV, DIC
 * ===>>> Tod

Klinische Symptome:
 * Fieber > 38 °C oder < 36 °C
 * Herzfrequenz > 90/min
 * Tachypnoe > 20/min oder Hyperventilation mit pCO2 < 4,3 kPa (33 mmHg)
 * Leukozytose (> 12.000/μl) oder Leukopenie (< 4.000/μl) oder Linksverschiebung (d. h. > 10 % unreife Leukozytenformen)

bei Säuglingen oft unspezifisch!

Schock
Der Schock ist Ausdruck einer Systemerkrankung und definiert als ein Missverhältnis zwischen 02-Bedarf und 02-Angebot an die peripheren Gewebe.

Schockformen:

 * Kardiogener Schock - Ursachen: Herzinfarkt, Herzinsuffizienz, Herzrhythmusstörungen, hypertensive Krise

 * Hypovolämischer Schock (absoluter Blutvolumenmangel)
 * Flüssigkeitsverluste - Ursachen: Hitzekollaps, Verbrennungen, Diarrhoe und Erbreche.
 * Blutverluste
 * Distributiver Schock (relativer Blutvolumenmangel durch Vasodilatation)
 * Septischer Schock (Sepsis)
 * Anaphylaktischer Schock
 * Neurogener Schock - Ursachen: psychisch, Verletzungen, neurologische Erkrankungen, Vergiftungen
 * Spinaler Schock - SF des neurogenen Schocks bei Querschnittslähmung
 * Obstruktiver Schock - Störung der Blutzirkulation durch Verschluss von Innen oder Kompression von Außen. Ursachen: Perikardtamponade, Perikarderguss, Lungenembolie, Spannungspneumothorax, Vena-cava-Kompressionssyndrom, Thrombose

Allgemeine Entwicklungsstörungen
Gametopathien (siehe im Buch Klinische Humangenetik)
 * Autosomale Trisomien
 * Trisomie 13 - Pätau-Syndrom
 * Trisomie 18 - Edwards-Syndrom
 * Trisomie 21 - Down-Syndrom
 * Gonosomale Trisomien
 * XXY - Klinefelter-Syndrom
 * Monosomien
 * X0 - Ullrich-Turner-Syndrom
 * Triploidien

Blastopathien

 * Doppelmißbildungen
 * Symmetrisch: Siamesische Zwillinge
 * Assymetrisch: Autosit und Parasit (z.B. Steißbeinparasit)

Embryopathien

Entscheidend ist der Zeitpunkt und das Ausmaß des Schädigung, die Art der Noxe ist weniger bedeutsam.

 * Fetales Alkoholsyndrom (FAS, Alkoholembryopathie) - Weblink: Fasworld.de
 * Rötelnembryopathie
 * Strahlenembryopathie
 * Thalidomidembryopathie

Fetopathien
 * Alkohol
 * Röteln, Listerien, CMV, Lues, Toxoplasmose
 * Diabetes der Mutter
 * Morbus haemolyticus neonatorum (Kernikterus, Hydrops congenitus)

Minderwuchs

 * Genetische Variante
 * Proportioniert
 * Z.B. Pygmäen

 * Kongenitale Skelettdysplasien (meist dysproportioniert)
 * Osteogenesis imperfecta (Kollagen I)
 * Achondroplasie (aut.-dom., Neumut., enchondrale Ossifikation)
 * Thanatophore Dysplasie (enchondrale Ossifikation, letal)
 * Achondrogenesis I und II (aut.-rez., letal)

 * Erworben
 * Rachitis (Vitamin D-Mangel)

Riesenwuchs

 * Hypophysärer Riesenwuchs (STH-produzierendes Adenom bei noch offenen Epiphysenfugen)
 * Akromegalie (nach Epiphysenschluss)

Regeneration
Die Regenerationsfähigkeit verhält sich reziprok zur Gewebedifferenzierung.

 * Physiologische Regeneration
 * Einmalig: Milchgebiss
 * Zyklisch: Endometrium
 * Dauernd: „Mausergewebe“, z.B. Endothel, Epidermis, hämatopoetisches System, Spermatogenese

 * Pathologische bzw. reparative Regeneration
 * Vollständig: Restitutio ad integrum.
 * Unvollständig: Defektheilung mit Bildung von Ersatzgewebe (Narbe).

Wundheilung

Phasen:
 * Exsudationsphase (seröses Exsudat, Antikörper, Fibrin, Plasmafaktoren)
 * Resorptionsphase (Immunzellen)
 * Proliferationsphase (Fibroblasten, Myofibroblasten, Kapillareinsprossung (Granulationsgewebe), Epithelialisierung)
 * Reparationsphase (Bildung extrazellulärer Matrix, Kollagen) -> Narbe (nach 3 Monaten volle Belastbarkeit)

Formen der Wundheilung:
 * Primäre Wundheilung (per primam, p.p.) - Frische, saubere Wunde, adaptierte Wundränder - rasche Heilung, geringe Narbenbildung
 * Sekundäre Wundheilung (per secundam, p.s.) - Ältere, offene, infizierte Wunden - Heilung aus der Tiefe, längere Heilungsdauer, Narbenbildung

Störungen:
 * „Wildes“ Fleisch : Überschießendes Granulationsgewebe
 * Narben-Keloid : Hypertrophische Narbe bei überschießender Bindegewebsbildung

Knochenheilung nach Frakturen

Arten der Knochenheilung:
 * Primäre/direkte Knochenheilung (nur bei anatomischer Reposition und Ruhigstellung, Osteosynthese) : direkte knöcherne Überbrückung des Frakturspalts (Osteoklasten bohren sich in den gegenüberliegenden Knochen, Osteblasten füllen die verbindenden Kanälchen wieder auf).
 * Sekundäre/indirekte Knochenheilung (bei konservativer Frakturbehandlung) : Frakturhämatom -> Kallusbildung (bindegewebige Organisation) -> Faserknochen -> Lamellenknochen

Störungen:
 * Pseudarthrose - Bindegewebige Überbrückung des Frakturspalts. Hypertrophe Pseudarthrose durch mangelnde Ruhigstellung, atrophe Pseudarthrose durch mangelnde Versorgung.
 * Frakturkrankheit, S UDECK -Dystrophie - Lokale Atrophie und Schrumpfung von Muskeln, Knorpel, Knochen, Gelenkkapsel und Bandapparat in der Nähe der Fraktur durch chronische Störungen der Trophik (Mikrozirkulation, Innervation).
 * V OLKMANN -Kontraktur - Ischämische und/oder neurogene Kontraktur der Armmuskulatur nach inadäquat versorgter Humerusfraktur mit Kompression der A. brachialis, des N. ulnaris, des N. medianus oder anderer Strukturen. Nekrose und Atrophie der Unterarmmuskulatur, besonders der Flexoren, die Hand befindet sich häufig in Krallenhandstellung.
 * Osteomyelitis - Bakterielle Entzündung des Knochenmarks, insbesondere bei offenen Frakturen zu erwarten.

Nervenheilung

Periphere Nerven können heilen, da sich jede Schwannsche Gliazelle in zahlreichen Windungen um jeweils nur ein Axon wickelt und nach Absterben des Axons die Axonhülle stehen bleibt. Im ZNS isolieren Oligodendrozyten gleichzeitig zahlreiche Axone, hier ist keine Heilung möglich.

Verletzung mit Durchtrennung des Axons -> W ALLER 'sche Degeneration des peripheren Axonteils -> proximales Axon wächst wieder in die stehengebliebende periphere Axonhülle (ca. 1mm/Tag). Voraussetzung: Genaue Adaptation, z.B. durch Nervennaht.

Störungen:
 * Neurom - Bei Amputationsverletzungen oder nicht adaptierten durchtrennten Nerven wachsen die Axone unkontrolliert aus und bilden schmerzempfindliche Nervenfaserknoten.

Tumorpathologie
Gutartige und bösartige (Krebs) Tumoren sind quasi der Preis für die Regenerationsfähigkeit der Gewebe. Es handelt sich dabei um Ansammlungen von Zellen mit überschießendem und unkontrollierten Wachstum.

Tumorklassifikation
 * Typing : Histologischer Typ (welches Ursprungsgewebe ahmt der Tumor nach)
 * Grading : 3 Malignitätsgrade (gegenläufig zum Differenzierungsgrad)
 * Staging : Ausbreitung (TNM-Schema)

Einteilung der Tumoren nach Dignität

 * Benigne - Verdrängend wachsend, langsam wachsend, oft abgekapselt, Organgrenzen respektierend, Ausdifferenzierung der Zellen, keine Metastasenbildung.
 * Maligne - Infiltrativ-invasiv wachsend, rasch wachsend -> Nekrosen, unreife, atypische Zellen, Metastasen.
 * Semimaligne - Lokal destruierend, selten Metastasen bildend.

Kriterien der Malignität

 * Makroskopisch: Infiltrierend/diffus wachsend
 * Histologisch: Nekrosen, Kapillarisierung (Neoangiogenese), Aufhebung der normalen Histologie.
 * Zytologisch: Polymorphie, basophiles Cytoplasma, erhöhte Kern/Plasmarelation
 * Nukleär: Polymorphie, Polychromasie, Hyperchromasie, Aneuploidie, (vergrößerte) Nukleolen, vermehrt Mitosen, atypische Mitosen, erhöhter Proliferationsindex (Ki-67 = MIB-1).

Kanzerogenese

Mutagene:
 * Chemikalien
 * Aromatische polyzyklische Kohlenwasserstoffe: Benzpyren, Anthrazen, Tabakrauch, Abgase
 * Aromatische Amine: Anilin, Aflatoxin (Aspergillus flavus), Benzidin, Benzol, Epoxide, Nitrosamine
 * Pharmaka (Zytostatika)
 * Viren: Virale Onkogene v-onc (Physiologische Protoonkogene (c-onc), zB. c-erb oder Bcl2, die durch Virus-DNA-Insertion verändert werden), Bsp.: HPV 16, 18 Zervixkarzinom
 * Ionisierende Strahlung
 * Chronische Entzündungen (Colitis ulcerosa)
 * Präkanzeröse Konditionen (XP, FAP, HNPCC u.a.)

Synkanzerogenese: Mutagene können sich bezüglich einer bestimmten Tumorentität additiv, überadditiv oder multiplikativ zueinander verhalten. Bsp.: Das Risiko für ein Bronchialkarzinom wird durch Asbestexposition 5x erhöht, durch Rauchen 10x. Asbest und Rauchen verhalten sich beim BC multiplikativ, das Risiko für einen Asbestexponierten Raucher ein BC zu entwickeln liegt also 50fach höher als beim nicht-rauchenden Bevölkerungsdurchschnitt!

Durch genetische Mutationen (ein Allel betroffen) kann die individuelle Anfälligkeit erhöht sein!

Wichtige Mutagene und Risikofaktoren nach Organsystemen:
 * Atemwege:
 * Nasen und NNH: Eichen- und Buchenholzstäube, Nickelverbindungen, Zinkchromat
 * Rachen: HPV, Rauchen, Alkohol
 * Larynx: HPV, Asbest, polyzyklische aromatische Kohlenwasserstoffe (PAH)
 * Lunge: Rauchen, Passivrauchen, Radon, aromatische Amine, Arsen, Asbest, Beryllium, Bischlordimethylether, Cadmiumverbindungen, chromhaltiger Staub, Hartmetalle (Wolframkarbid, Cobalt), Faserstäube, ionisierende Strahlen, Monochlordimethylether, Nickelverbindungen, Nitrosamine, PAH, Teer, Zinkchromat, Quarzstaub, Senfgas, Thorium, Uran
 * Pleura: Asbest
 * Seröse Häute (Pleura, Peritoneum, Tuncica vaginalis, Perikard): Asbest
 * MDT:
 * Magen: Helicobacter pylori, Nitrosamine
 * Darm: Faserarme Ernährung, Nitrosamine, Adipositas
 * Leber: Arsen, Vinylchlorid, chronische Hepatitis B und C
 * Gallengänge: Leberegel (Clonorchis, Opisthorchis)
 * Harnwege: 4-Aminodiphenyl, Benzidin, 4-Chlor-o-Toluidin, 2-Naphthylamin, Azofarbstoffe, Bilharziose, Arsen, Nitrosamine
 * Haematopoetisches System: Benzol, ionisierende Strahlen, Trisomie 21
 * Haut: UV-Licht, Arsen, Teer, ionisierende Strahlen

Genotoxine erhöhen die Inzidenz maligner Tumoren, sie vorverlagern den Erkrankungszeitpunkt (= Verkürzung der Latenzzeit) und sie erweitern das Tumorspektrum in einem Gewebe.

Mechanismen:
 * Punktmutationen: Basenaustausch, Addition, Deletion
 * Translokation (zB. t9/22 -> Philadelphia-Chromosom Bcr-Abl)
 * Amplifikation

Folgen:
 * Aktivierung von Protoonkogenen c-onc, die physiologisch vorkommen und für an der Proliferation beteiligte Gene kodieren, zB. Wachstumsfaktoren, Wachstumsfaktorrezeptoren, Tyrosinkinasen u.a.
 * Abschaltung von Tumorsupressorgenen, zB. DNA-Reparaturgene, Cycline

Formale Pathogenese:
 * Initiation - Initialer DNA-Schaden, Mutation
 * Latenz - Bis zu Jahrzehnten!
 * Promotion - Weitere Mutationen, Hormonwirkung
 * Progression - Entartung

Letztlich entsteht ein Tumor nicht von heute auf morgen, sondern die Zellen entarten über zahlreiche Zwischenschritte, bei denen diverse Gene an- und abgeschaltet werden. Bsp.: Adenom-Karzinom-Sequenz bei Darmkrebs unter Beteilung des Oncogens c-Ki-ras und der Tumorsupressorgene p53, APC, DCC u.a.m. Betroffen sind besonders Gewebe mit hoher regeneratorischer Aktivität (Epithel -> Karzinom, Knochenmark/Immunsystem -> Leukämie, Lymphome). Die Zunahme der Zellteilungen durch die Entartung beschleunigt dabei die Anhäufung von Mutationen im Sinne eines Circulus vitiosus und die Entstehung verschieden gut angepasster Zellklone, was den Tumorzellen einen Selektions- und Wachstumsvorteil gegenüber den körpereigenen Abwehrmechanismen und Geweben beschert.

Invasion

Abfolge:
 * Orientierung (Lamininrezeptoren)
 * Lokale Proteolyse (Cathepsin D, Kollagenasen)
 * Dissoziation - Die Krebszelle zieht die Adhäsionsmoleküle ein, kann den Zellverband verlassen, Verlust der Kontaktinhibition)
 * Lokomotion (Migration)

Metastasierung

Abfolge:
 * Infiltration - Einwachsen in umliegende Gewebe
 * Invasion - Eindringen in Blut- und Lymphwege
 * Disseminierung (lymphogen, hämatogen) - Verteilung im Organismus
 * Arrest im Zielorgan - Adhäsion an Rezeptoren oder Oberflächenmoleküle oder Steckenbleiben von Tumorzellemboli im Kapillarbett.
 * Reinvasion - Einwachsen ins Zielorgan
 * Angiogenese - Der Tumor bildet angiogenetische Wachstumsfaktoren, die das Wachstum neuer Gefäße stimulieren.
 * Anschluß an Arteriolen
 * Arterialisierung des Tumors (keine Venenbildung!)

Metastasierungswege:
 * Lymphogen - Über die Lymphwege
 * Hämatogen - Über den Blutweg (direkt oder erst lymphogen und dann über den Angulus venosus Eintritt in die Zirkulation)
 * Kanalikulär - Entlang seröser Häute
 * Per continuitatem - Direkt durchwachsend

Metastasierungstypen:
 * Cava-Typ : Organ -> Lunge
 * Arterieller Typ : Lunge -> Körper
 * Pfortadertyp : GIT -> Leber
 * Paravertebraler Venenplexus-Typ : Organ -> Wirbelsäule (Mamma-, Prostata-, Ovarial-Ca)
 * Cavitär : Organ -> Pleura, Peritoneum, Pericard
 * Lymphogen-hämatogen : Lymphgefäß -> Ductus thoracicus -> Venewinkel -> Blutbahn

Folgen der Tumorerkrankung
 * Kompression umliegender Strukturen
 * Stenosierung
 * Ulzeration
 * Gefäßarrosion
 * Fistelung
 * Nekrose
 * Abflussstörungen
 * Anämie (Ursachen: Chronische Blutung, Hämatopoesehemmung durch Tumorfaktoren, Knochenmarksverdrängung durch Metastasen, AIHA)
 * Gewichtsverlust
 * Paraneoplastische Syndrome (U: Entstehen indirekt durch vom Tumor freigesetzte Zerfallsprodukte und hormonähnliche Substanzen an primär nicht betroffenen Organen und Autoimmunphänomene (Kreuzantigenität)) Bsp.:
 * Hautveränderungen (Akanthose, Acanthosis nigricans maligna, Hyperkeratose, Dermatomyositis, Bullöses Pemphigoid)
 * Hämatologische Veränderungen (Anämie, leukämoide Reaktionen, Polyzythämie, Thrombosen, Nichtbakterielle thrombotische Endokarditis NBTE)
 * Endokrinopathien (M. Cushing (ACTH), Schwartz-Bartter-Syndrom (SIADH), Hyperkalzämie (PTH), Hypoglykämien (Insulin), Karzinoidsyndrom (5-HT, Histamin, Bradykinin), Polyzythämie (EPO))
 * Myasthenia gravis (bei Thymomen)
 * Paraneoplastische Kleinhirnatrophie, Polyneuritis
 * Glomerulonephritis

Spontane Tumorregression

Zerstörung von Tumorgewebe durch Makrophagen, NK, CD8-Zellen, AK (durch Kreuzantigenität auch Autoaggressionserkrankungen)

Spontanremission

Vollständige oder teilweise, vorübergehende oder dauerhafte Rückbildung sämtlicher oder einiger Aktivitätsmerkmale einer bösartigen Erkrankung, ohne Behandlung oder unter einer Behandlung, wo dies nicht zu erwarten gewesen wäre. Nicht unbedingt gleichbedeutend mit Heilung (Spontanheilung)!

Häufigkeit: 1:60.000 bis 1:100.000, Dunkelziffer!

In mehr als der Hälfte der Fälle betrifft die Spontanremission folgende Tumore: Malignes Melanom, malignen Lymphom, kindliche Neuroblastome, Nierenzellkarzinom

Tumormarker

Dienen hauptsächlich der Verlaufskontrolle und Rezidivfrüherkennung., einige auch zum Screening (PSA) und zur histopathologischen Diagnose (Immunhistochemie).

 * Onkofetal
 * AFP
 * CEA
 * Hormone
 * HCG (Trophoblasttumor)
 * Kalzitonin (C-Zell-Karzinom)
 * Katecholamine (Phäochromozytom)
 * Isoenzyme
 * Saure Prostataphosphatase
 * Neuronen spezifische Enolase (NSE)
 * Glykoproteine
 * CA 125
 * CA 19-9
 * CA 15-3
 * Intermediärfilamente
 * Keratin (Epithel)
 * Vimentin (Bindegewebe)
 * Neurofilamente (Nervenzelle)
 * Desmin (Muskel)
 * Aktin
 * Leukozytenantigen
 * Spezifische (Glyko)Proteine
 * Ig (Plasmazelltumoren)
 * PSA (Prostatakarzinom)
 * Thyreoglobulin (Schildrüsenkarzinom)

Weblinks

 * http://focosi.altervista.org/pathohomoprocess_regressive.html#degenerations

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