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(C20, C40, C60, C90) TC4.2.1 and above See issues with endpoints running TC version 5.x or earlier.
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See issues with endpoints running TC version 5.x or earlier.
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We strongly recommend using the latest publicly-released version (i.e. "stable version" or "supported release") of a browser.
RTMP media streaming is also supported in all browsers.
Instant Messaging to and from Skype for Business / Lync clients is supported in all browsers.


So, how is it going? Are you all having fun "stalking" your partners? Have you figured out what you are making? Oh, it is fun, isn't it?
this is sew much fun -- I have the initial stages of the project ready and got the materials for completing part one -- I sure hope my swapper likes this little cutie because it's becoming harder not to keep it for myself.


text:
Jesús Pareja Mayo, né le  à Guadalajara, est un pilote automobile espagnol sur circuits à bord de voitures de sport type Tourisme, Grand Tourisme et Sport-prototypes, spécialiste ibérique de courses d'endurance.

Biographie
Sa carrière de compétiteur automobile se déroule entre 1983 (Coupe d'Europe Alfasprint) et 1998.

Il dispute une soixantaine de course en championnat du monde des voitures de sport (WSC, ou WSPC) entre 1985 et 1992, accomplissant sa dernière saison chez Euro Racing ( Donington et  à Suzuka, pour la dernière année d'existence du championnat).

Il participe treize fois consécutivement aux 24 Heures du Mans entre 1985 et 1997, se classant cinq fois dans les dix premiers. Il finit deuxième en 1986 sur Porsche 962C de l'écurie suisse Brun Motorsport avec, entre autres, le Français Joël Gouhier, puis il remporte la catégorie GT2 en 1994, après avoir fini deuxième en GT la saison précédente, sur des Porsche 911 Carrera (dont une RSR).

En WSPC il gagne les  de Jerez en 1986 avec la 962 ( à Monza durant la même saison), et finit dixième du championnat pilotes avec l'écurie Brun Motorsport. L'année suivante il est deuxième des 200 Meilen de Nuremberg au Norisring, et troisième des 1 000 kilomètres de Monza encore avec Brun. Son dernier podium en mondial SP/endurance a lieu en 1989 à l'issue des 480 kilomètres de Jarama, troisième sur une 962 de Brun.

Lors des 480 kilomètres de Montréal sur le Circuit Gilles-Villeneuve en Championnat du monde des voitures de sport 1990 (WSPC), sa Porsche 962C partagée avec le constructeur Walter Brun s'embrase après avoir heurté un fragment de plaque d'égout arraché par un concurrent précédent, devant la vie aux commissaires de piste proches.

Pour la première saison 1994 du Championnat BPR de Global GT Series, il remporte les 4 Heures du Paul-Ricard, les 4 Heures de Jarama, et les 1 000 kilomètres de Suzuka avec Jean-Pierre Jarier et Bob Wollek sur une Porsche 911 Turbo S LM du team Larbre Compétition (avec aussi Dominique Dupuy à Jarama), finissant deuxième en début d'année aux 24 Heures de Daytona (et  au Mans). Malheureusement dans ce championnat international naissant il n'existe pas encore de classement pilotes.

De 1994 à 1996 il passe aussi trois saisons en Championnat d'Espagne de Tourisme (1 victoire en 1993 sur Ford Escort Cosworth officielle). Il dispute encore plusieurs courses entre 2000 et 2001 dans les championnat espagnol de Grand Tourisme et de Formule 3.

En 1998 il obtient un dernier podium aux 4 Heures de Jarama, avec les français Chéreau et Leconte.

Notes et références

Liens externes
  Jesús Pareja, sur HistoricRacing (biogtraphie);
  Jesús Pareja, sur RacingSportsCars;
  Jesús Pareja, sur Driverdb:
 Jesús Pareja, sur Les24Heures;
 Jesús Pareja, sur 24HeuresenPiste;
 .

Pilote automobile espagnol
Pilote des 24 Heures du Mans
Naissance en mars 1955
Naissance à Guadalajara (Espagne)

redpajama_set_name: RedPajamaWikipedia


The park is situated in a beautiful place - stunning views across the Bay, sandy beach and wonderful sea views are just right on your doorstep. The wildlife is also impressive here.
By clicking "Submit" you certify that this review is based on your own experience and is your genuine opinion of "Cooper Angus Park" and that you have no personal or business relationship with "Cooper Angus Park" and have not been offered any incentive or payment originating from "Cooper Angus Park" to write this review.


text:
Q: Are there smooth functions that in their limit can perform ceiling and floor operations? Preamble

*

*There is a motivation section at the bottom which explains where this arose from -- might be helpful or of interest

*There is a set of ideal criteria which if met would define the ideal solution

*There a follow on set of less than criteria which relax the ideal criteria -- some readers pointed out that the original criteria are unnecessarily restrictive

Do we have
Ideal Criteria
$1.$ functions like $f(x,\theta)$ and $g(x,\theta)$
$2.$ are defined where $\theta \in {\rm I\!R}^1$ and $x \in {\rm I\!R}^1$
$3.$ are smooth and continuous where $ \left| \theta \right| \lt C$ where $C$ is some constant
$4.$ $f$ and $g$ themselves cannot be defined (make use of) the floor or ceiling functions
$5.$ $f$ and $g$ cannot be defined as different functions over subsets over their domain for example: (,)=0 for ||< and (,)=⌊⌋
$6.$ $f$ and $g$ can make use of $\Sigma$ and $\Pi$ operators
$7.$ $f$ and $g$ can make use of frequency type decomposition
Less than Ideal Criteria -- which may involve relaxing some of the Ideal Criteria
$8.$ a less than ideal solution would allow $\theta$ to be $\in \mathbb{Z}$
$9.$ a less than ideal solution can allow $f$ and $g$ to make of differentiation and integration
$10.$ a borderline admissible solution would allow $f$ and $g$ to a composition of different functions over disjoint subsets over their domain -- in other word relaxing condition $4.$
that we get
$$
\lim_{\theta \to \infty} f(x, \theta) = \lfloor x \rfloor
$$
and
$$
\lim_{\theta \to \infty} g(x, \theta) = \lceil x \rceil
$$
Motivation

*

*The question really comes from can we implement something in terms of something else -- kinda like how can we use deterministic logic to generate random numbers, or how can we implement a Turing machine using NAND logic

*Additionally, more mental itch -- would be great to see floor and ceiling implementations using middle-school or say high-school math

*I want a representation off floor and ceiling that is does not make use of the if-then -- say we were to implement floor and ceiling in terms of electrical or mechanical machinery, if-then machinery is complex and expensive

*Say we were in a world where analog computers existed where we had black-boxes that did addition, multiplication, power, division, log, but no memory and no if-then/jump type stuff -- could we implement floor and ceiling

*Allowing direct memory components such as accumulators or delay operators would not be allowed

A: For continuous functions, we can take
$$
f(x,\theta) = \lfloor x \rfloor + \big( x - \lfloor x \rfloor \big)^\theta.
$$
It's easy to convert this to smooth functions, since there is always a smooth function $\tilde f(x,\theta)$ uniformly satisfying $\big| \tilde f(x,\theta) - f(x,\theta) \big| < \frac1\theta$.
In any case, we can take $g(x,\theta) = -f(-x,\theta)$, since $-\lfloor-x\rfloor = \lceil x\rceil$.

A: Here's one way of building these functions.
Throughout most of this, I'll be discussing functions with a domain where $\theta > 0$. But at the end, there's a way to fix that up if desired.
First, to get a non-smooth "sharpness", approximate $|x|$ by hyperbolae with $y=\pm x$ as asymptotes:
$$ f_1(x,\theta) = \sqrt{x^2 + \frac{1}{\theta}} $$
$$ \lim_{\theta \to \infty} f_1(x,\theta) = |x| $$
The derivative of this function with respect to $x$ will have a discontinuity in the $\theta \to \infty$ limit, without explicitly being defined with an "if-else", and remaining smooth at all $\theta>0$:
$$ f_2(x,\theta) = \frac{\partial f_1}{\partial x}(x,\theta) = x \left(x^2 + \frac{1}{\theta}\right)^{-1/2} $$
$$ \lim_{\theta \to \infty} f_2(x,\theta) = \begin{cases}
-1 & x<0 \\
0 & x=0 \\
1 & x>0 \end{cases} $$
Also notice that $|f_2(x,\theta)| < 1$ for all real $x$ and all positive $\theta$.
The "fractional part" function $\{x\} = x - \lfloor x \rfloor$ is periodic, so to work in some periodicity the natural choice is trigonometric functions. One slight catch is that we need the function to be one-to-one on the period between discontinuities, but $\sin$ and $\cos$ are not one-to-one in their periods. But this use of $f_2$ solves that nicely by using half-periods of the trig functions:
$$ f_3(x,\theta) = \cos(\pi x) \, f_2 \big(\!\sin(\pi x), \theta \big) $$
$$ \lim_{\theta \to \infty} f_3(x,\theta) = \begin{cases} 0 & x \in \mathbb{Z} \\
\cos\!\big[\pi (x- \lfloor x \rfloor) \big] & x \notin \mathbb{Z} \end{cases} $$
(If $2n < x < 2n+1$ for some integer $n$, then $\cos(\pi x) = \cos\!\big[\pi(x - 2n) + 2n \pi\big] = \cos\!\big[\pi(x - \lfloor x \rfloor)\big]$, and $f_2$ approaches $+1$ in the limit. If $2n+1 < x < 2n+2$, then $\cos(\pi x) = \cos\!\big[\pi(x - 2n-1) + (2n+1)\pi\big] = -\cos\!\big[\pi(x - \lfloor x \rfloor)\big]$, and $f_2$ approaches $-1$ in the limit.)
Since $|\cos| \leq 1$ and $|f_2| < 1$, $|f_3(x,\theta)| < 1$ on the domain, which means the arccosine is defined. So the next simple step:
$$ f_4(x,\theta) = x - \frac{1}{\pi}\, \cos^{-1}\! \big[ f_3(x,\theta) \big] $$
$$ \lim_{\theta \to \infty} f_4(x,\theta) = \begin{cases}
\frac{1}{2} & x \in \mathbb{Z} \\
\lfloor x \rfloor & x \notin \mathbb{Z} \end{cases} $$
@GregMartin mentioned in a comment a way to fix up singleton points, like these at the discontinuities:
$$ f_5(x,\theta) = (\cos^2 \pi x)^\theta $$
$$ \lim_{\theta \to \infty} f_5(x,\theta) = \begin{cases}
1 & x \in \mathbb{Z} \\
0 & x \notin \mathbb{Z} \end{cases} $$
$$ f_6(x,\theta) = f_4(x,\theta) + \frac{1}{2} f_5(x,\theta) $$
$$ \lim_{\theta \to \infty} f_6(x,\theta) = \lfloor x \rfloor $$
Or written all the way out,
$$ f_6(x,\theta) =  x - \frac{1}{\pi} \cos^{-1} \left[
\cos(\pi x) \sin(\pi x) \left(\sin^2(\pi x) + \frac{1}{\theta}\right)^{-1/2}
\right]
+ \frac{1}{2} (\cos^2 \pi x)^\theta $$
This function is smooth everywhere, but its limit at large $\theta$ is not. See a graph of $f_6(x,5)$ on Wolfram Alpha.
If definition on all real $\theta$ is important, instead of just on positive $\theta$, you could take $f_7(x,\theta) = f_6(x,e^\theta)$.
Since $\lceil x \rceil = - \lfloor -x \rfloor$, a similar function approaching $\lceil \cdot \rceil$ is just
$$ g(x,\theta) = -f_6(-x,\theta) $$
[or use $f_7$ in place of $f_6$.]

redpajama_set_name: RedPajamaStackExchange


text:
Q: How to enable OpenGL 2.x+ on Windows 7 guest on Virtualbox? This question has been asked before here but with no answers, so I'm going to ask it again.
How do I enable OpenGL version 2.x+ on VirtualBox? I've installed all guest additions. I'm on an Ubuntu 16.10 host.
Thanks!


text:
Towns > Kilmarnock (and Riccarton) > 1868, 1872 - Post Office Kilmarnock directory > 1868
‹‹‹ prev (77)
(79) next ›››
B&W composite text file (pdf, 8295kb)
Search within: 18681868, 1872 - Post Office Kilmarnock directoryKilmarnock (and Riccarton)TownsScottish Post Office Directories
Select a page: (1) (2) (3) (4) (5) (6) (7) Title page (8) (9) (10) (11) (12) (13) Index (14) (15) (16) (17) (18) (19) (20) (21) (22) (23) (24) (25) (26) (27) (28) (29) (30) (31) (32) (33) (34) (35) (36) (37) (38) (39) (40) (41) (42) (43) (44) (45) (46) (47) (48) (49) (50) (51) (52) (53) (54) (55) (56) (57) (58) (59) (60) (61) (62) (63) (64) (65) (66) (67) (68) (69) (70) (71) (72) (73) (74) (75) (76) (77) (78) (79) (80) (81) (82) (83) (84) (85) (86) (87) (88) (89) (90) (91) (92) (93) (94) (95) (96) (97) (98) (99) (100) (101) (102) (103) (104) (105) (106) (107) (108) (109) (110) (111) (112) (113) (114) (115) (116) (117) (118) (119) (120) (121) (122) (123) (124) (125) (126) (127) (128) (129) (130) (131) (132) (133) (134) (135) (136) (137) (138) (139) (140) (141) (142) (143) (144) (145) (146) (147) (148) (149) (150) (151) (152) (153) (154) (155) (156) (157) (158) (159) (160) (161) (162) (163) (164) (165) (166) (167) (168) (169) (170) (171) (172) (173) (174)
STAIR. trades' directory. ^TIN.
Walker, Andrew, George Hotel
Wallace, William, 8 London road
Watson, Robert, 4 St. Marnock street
Wilson, Alexander, 3 Market lane
Wilson, James, 1 Mill lane
Wilson, Mrs. Robert, 118 King street
Young, John, Royal Hotel, King street
STAIR RAILERS.
Alexander, A., & Sons, Mill lane
Craig, Robert. 80 King street
Cunningham, A., & Son, 8 Duke street
TAILORS AND CLOTHIERS.
Those marked t are Tailors only.
Agnew, Robert, 24 Bank street
Aird, Charles, 32 Boyd street t
Blain, John, 48 Robertson place t
Bunten, James, 12 Portland street
Cameron, Nicol B , 56 King street
Campbell, Thomas, 44 Titchfield street t
Craig, John, 1 Grange street
Dufif, William, 1 Bank street
Dunlop, Alexander, & Son, 1 1 King st.
Dunlop, Huizh, 38 King street
Ferguson, Edward, 3 Croft street
Ferguson, Jno., & Son, 68 and 70 King st.
Foster, George, 93 King street
Foster. Robt., Victoria place, 19 King st.
Fraser, W. M., St. Marnock corner,
Garven, Alexander, 20 King street
Gordon, William, 20 West George street
Kerr, John, 22 Regent street
Leiper, R. & J., 28 Portland street
Maekay & Son, 85 King street
Hanson, John, 92 Titchfield street t
Mitchell, Wm., & Son, 13 Douglas st. t
M'Cracken, Andrew, 37 Portland street
M'Gary, John, Cheapside street
Paterson, James, 13 Douglas street t
Rae, David, 18 Cheapside street
Runcie, Samuel, 7 Portland street
Smith, James, 32 King street
Stewart Brothers, 31 and 33 King street
Stewart, Andrew, St. Marnock street
Tannahill, Robert, 16 Low Glencairn st. t
Taylor, James, 54 King street
Turnbull & M'Kenzie, 61 King street
Wiecht & Sawer, 10 Queen street
Wyllie, James, 16 Douglas street
TALLOW CHANDLERS.
Crooks Brothers & Co. , Ladeside
TANNERS.
SEE ALSO CURRIERS.
Crooks Brothers & Co., Ladeside
TEACHERS.
Anderson, Peter, Free School, Dundonald
Black, Francis M., School of Art, Corn
Exchange Buildings, Green street
Boyle, Rose, St. Joseph's Catholic School,
Low Church lane,
Crawford, John S., George Hotel Assem-
bly Rooms (dancing and calisthenics)
Dodds, James, Nelson Street School
Ferguson, Donald, Townhead District
Frazer, William, East Shaw street
Grant, Misses, Allanhill, London road
(ladies)
Gunnyon, William, classical and com-
mercial. New Academy, Princes st.
Henderson, Diana, South Hamilton st.
Lee,Thos., commercial and mathematical
teacher, Kilmarnock Academy
Logan, William C, English teacher, Kil-
marnock Academy
MacGlashan, Misses, Springvale Semi-
nary, Dundonald road (ladies)
Miller, Annie C, Female School of In-
dustry, West Netherton street
Moodie, Agnes, Beansburn
Patrick, Misses, Ladies' Seminary, John
Finnic street
Rose, James, Langlands street
Roxburgh, Miss, Female School of In-
Russell, James, West Shaw street
Stevenson, James, New Public School,
Fowlds street
Stewart, James, Clark Street School
Taylor, R. W., Ragged Industrial School,
Kilmarnock House
Thomson, M., Corn Exchange (dancing
and calisthenics)
Wyllie, Daniel, East George street
THATCHER.
M'Quade, Peter, Low Church lane
TIN PLATE WORKERS.
Bicket, John, & Son, 92 King street
Brodie, Neil, 33 Portland street
Scottish Post Office Directories > Towns > Kilmarnock (and Riccarton) > Post Office Kilmarnock directory > 1868 > (78)

redpajama_set_name: RedPajamaCommonCrawl


text:
And Jethro said, "Blessed be the Lord, who hath delivered you out of the hand of the Egyptians and out of the hand of Pharaoh, who hath delivered the people from under the hand of the Egyptians.
And Jethro said, Blessed be Jehovah, who hath delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh; who hath delivered the people from under the hand of the Egyptians.
Jethro said, "Blessed be the Lord, who has rescued you from the hand of the Egyptians and from the hand of Pharaoh, and who has rescued the people from under the hand of the Egyptians.
Jethro said, Blessed be the Lord, Who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh, Who has delivered the people [Israel] from under the hand of the Egyptians.
And Jethro said, Blessed be the Lord, who hath delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh, who hath delivered the people from under the hand of the Egyptians.
"Blessed be the Lord," Jethro exclaimed, "who rescued you from the power of Egypt and from the power of Pharaoh. He has rescued the people from under the power of Egypt!
Jethro said, "Bless the Lord who rescued you from the Egyptians' power and from Pharaoh's power, who rescued the people from Egypt's oppressive power.
Yitro said, "Blessed be Adonai, who has rescued you from the Egyptians and from Pharaoh, who has rescued the people from the harsh hand of the Egyptians.
that he shouted, "Praise the Lord! He rescued you and the Israelites from the Egyptians and their king.
And Jethro said, Blessed be Jehovah, who has delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh; who has delivered the people from under the hand of the Egyptians.
And he said: Blessed is the Lord, who hath delivered you out of the hand of Pharao, and out of the hand of the Egyptians, who hath delivered his people out of the hand of Egypt.
He said, "Praise the Lord! He freed you from the power of Egypt. He saved you from Pharaoh.
Jethro said, "Blessed be the Lord, who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh and has delivered the people from under the hand of the Egyptians.
He said, "·Praise [Blessed be] the Lord. He has saved you from the [L hand of the] Egyptians and [L the hand of] ·their king [L Pharaoh], and he has saved the people from the ·power [L hand] of the Egyptians.
Therefore Jethro said, Blessed be the Lord who hath delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh: who hath also delivered the people from under the hand of the Egyptians.
He said, "Thank the Lord! He rescued you from the Egyptians and their Pharaoh and rescued these people from the control of the Egyptians,
and said, "Praise the Lord, who saved you from the king and the people of Egypt! Praise the Lord, who saved his people from slavery!
"Praise the Lord," Jethro exclaimed, "who rescued you from Pharaoh and the power of the Egyptians and snatched the people from the power of the Egyptians.
Jethro said, "Praise the Lord. He has saved all of you from the Egyptians and their king. He has saved the people from the power of the Egyptians.
Jethro said, "Blessed be the Lord, who delivered you from the hand of the Egyptians and from the hand of Pharaoh, and who delivered the people from the oppression of the Egyptians.
And Jethro said, Blessed be the LORD, who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh, who has delivered the people from under the hand of the Egyptians.
And Jethro said, "Blessed be Yahweh, who has delivered you from the hand of Egypt and from the hand of Pharaoh—who has delivered the people from under the hand of Egypt.
"Bless the Lord," Jethro said, "for he has saved you from the Egyptians and from Pharaoh, and has rescued Israel.
Jethro was delighted in all the good that God had done for Israel in delivering them from Egyptian oppression. Jethro said, "Blessed be God who has delivered you from the power of Egypt and Pharaoh, who has delivered his people from the oppression of Egypt. Now I know that God is greater than all gods because he's done this to all those who treated Israel arrogantly."
Jethro said, "The Lord be blessed, who has delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh, who has delivered the people from under the hand of the Egyptians.
He said, "Thank Yahweh! He rescued you from the Egyptians and their Pharaoh and rescued these people from the control of the Egyptians,
"Blessed be the Lord," he said, "who has rescued you from the power of the Egyptians and of Pharaoh.
So Jethro said, "Blessed be the Lord who delivered you from the hand of the Egyptians and from the hand of Pharaoh, and who delivered the people from under the hand of the Egyptians.
He said, "Praise the Lord. He has saved you from the Egyptians and their king, and he has saved the people from the power of the Egyptians.
Jethro said, "Blessed be the Lord who has delivered you from the hand of Egypt, and from the hand of Pharaoh, who has delivered the people from the Egyptians' control!
He said, "I praise the Lord. He saved you and your people from the power of the Egyptians and of Pharaoh.
He said, "Praise be to the Lord, who rescued you from the hand of the Egyptians and of Pharaoh, and who rescued the people from the hand of the Egyptians.
He said, 'Praise be to the Lord, who rescued you from the hand of the Egyptians and of Pharaoh, and who rescued the people from the hand of the Egyptians.
And Jethro said, "Blessed be the Lord, who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh, and who has delivered the people from under the hand of the Egyptians.
So Jethro said, "Honor and thanks be to the Lord, Who saved you from the hand of the Egyptians and from the hand of Pharaoh, and Who made you free from the power of Egypt.
"Praise the Lord," Jethro said, "for he has rescued you from the Egyptians and from Pharaoh. Yes, he has rescued Israel from the powerful hand of Egypt!
Jethro said, "Blessed be the Lord, who has delivered you from the Egyptians and from Pharaoh.
Jethro said, 'Blessed be the Lord, who has delivered you from the Egyptians and from Pharaoh.
And Yitro said, Baruch Hashem, Who hath rescued you out of the hand of the Egyptians, and out of the hand of Pharaoh, and Who hath delivered HaAm from under the hand of the Egyptians.
And Jethro said, "Blessed be the Lord, who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh.
Jethro said, "Blessed be Adonai, who has delivered you out of the hand of the Egyptians and out of the hand of Pharaoh, and has delivered the people from under the hand of the Egyptians.
Jethro: Praise to the Eternal, for He rescued you from the powerful hand of the Egyptians, from the cruel grip of Pharaoh. He has liberated His people from beneath the harsh hand of their Egyptian masters.
Jethro said, "Blessed be Yahweh, who has delivered you out of the hand of the Egyptians, and out of the hand of Pharaoh; who has delivered the people from under the hand of the Egyptians.
And Jethro said, Blessed be the Lord, that delivered you from the hand(s) of the Egyptians, and from the hand of Pharaoh, the which Lord delivered his people from (being under) the hand, (or the power,) of Egypt;
and Jethro saith, `Blessed [is] Jehovah, who hath delivered you from the hand of the Egyptians, and from the hand of Pharaoh -- who hath delivered this people from under the hand of the Egyptians;
Exodus 18:9Exodus 18:11


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text:
Home › News › On weirdos
On weirdos
Posted by Amanda Woade on June 16, 2019
I was thinking about my mission statement the other day. I came up with "To inspire weirdos to be comfortable with themselves at every age". I feel really good about it.
A lot of people probably think of the term "weirdo" as derogatory. People think it's an insult to be called a weirdo. But I disagree. It's a great term that encompasses all kinds of people outside the "norm", and it should be appreciated and loved as such.
I think it's a treat and an honor to be weird. Just think of Weird Al, he's an inspiration to me in his endless goofiness, wit, talent, and desire to spread the joy of accordions to the world. He's not everyone's favorite artist, but he brings something different than everyone else to the table. That's what it is to be weird, to be a weirdo - to bring something uniquely you to whatever you do. To not hold back and let yourself shine through.
I've been a weirdo my whole life. While I haven't always embraced the term, I have always been different and I've never fit neatly into a box. I was never popular growing up, and I always pushed the boundaries of what was expected in unusual ways. (Some of the outfits I wore...!) My parents not only allowed my weirdness, but fostered it and nurtured it. I was always allowed to make my own weird decisions to do my own weird stuff. It's given me a lot of self-confidence, and it's all done without a second thought. It helps that they were weirdos themselves, and that my brother was another weirdo before me. But we stand out, make changes, and inspire people in unexpected ways.
So let yourself be a weirdo. Show off that interest you know that no one else shares - you'd be surprised who else has been hiding it. Put on that outfit that makes you feel great, without a thought of other people's opinions. Make a strange joke, ask a different question, try something new. It might feel uncomfortable at first, but trust me - it'll feel amazing soon.
Hello-ween!
It's almost Halloween?
A grand reopening celebration
Starting off summer
banyan
copurrnicus
makrs society
nice things handmade


text:
Cirrhosis leading to hepatocellular carcinoma (autopsy specimen).
K70.3, K71.7, K74.
med/3183 radio/175
Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrotic scar tissue as well as regenerative nodules, leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism and hepatitis C, but has many other possible causes.
Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible once it occurs, and treatment generally focuses on preventing progression and complications. In advanced stages of cirrhosis the only option is a liver transplant.
The word "cirrhosis" is a neologism that derives from Greek kirrhos, meaning "tawny" (the orange-yellow colour of the diseased liver). While the clinical entity was known before, it was René Laennec who gave it the name "cirrhosis" in his 1819 work in which he also describes the stethoscope.[1]
Safe Weighing Range Ensures Accurate Results
1 Symptoms and signs
4.1 Lab findings
4.2 Imaging
4.3 Endoscopy
4.4 Pathology
5 Grading
6 Pathophysiology
7.1 Treating underlying causes
7.2 Preventing further liver damage
7.3 Preventing complications
7.3.1 Ascites
7.3.2 Esophageal variceal bleeding
7.3.3 Hepatic encephalopathy
7.3.4 Hepatorenal syndrome
7.3.5 Spontaneous bacterial peritonitis
7.4 Transplantation
7.5 Decompensated cirrhosis
Symptoms and signs
The following signs and symptoms may occur in the presence of cirrhosis or as a result of the complications of cirrhosis. Many are nonspecific and may occur in other diseases and do not necessarily point to cirrhosis. Likewise, the absence of any does not rule out the possibility of cirrhosis.
Spider angiomata or spider nevi. Vascular lesions consisting of central arteriole surrounded by many smaller vessels due to an increase in estradiol. These occur in about 33% of cases.[2]
Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism.
Nail changes.
Muehrcke's nails - paired horizontal bands separated by normal color due to hypoalbuminemia (low production of albumin).
Terry's nails - proximal two thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia
Clubbing - angle between the nail plate and proximal nail fold > 180 degrees
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain.
Dupuytren's contracture. Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be due to fibroblastic proliferation and disorderly collagen deposition. It is relatively common (33% of patients).
Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples. This is due to increased estradiol and can occur in up to 66% of patients.
Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
Liver size. Can be enlarged, normal, or shrunken.
Splenomegaly. Due to congestion of the red pulp as a result of portal hypertension.
Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 mL to detect flank dullness). It may be associated with hydrocele and penile flomation (swelling of the penile shaft) in men.
Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, manifesting as caput medusa.
Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region due to collateral connections between portal system and the remnant of the umbilical vein in portal hypertension.
Fetor hepaticus. Musty odor in breath due to increased dimethyl sulfide.
Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least 2-3 mg/dL or 30 mmol/L). Urine may also appear dark.
Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
Other. Weakness, fatigue, anorexia, weight loss.
As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.
Bruising and bleeding due to decreased production of coagulation factors.
Jaundice due to decreased processing of bilirubin.
Itching (pruritus) due to bile products deposited in the skin.
Hepatic encephalopathy - the liver does not clear ammonia and related nitrogenous substances from the blood, which are carried to the brain, affecting cerebral functioning: neglect of personal appearance, unresponsiveness, forgetfulness, trouble concentrating, or changes in sleep habits.
Sensitivity to medication due to decreased metabolism of the active compounds.
Hepatocellular carcinoma is primary liver cancer, a frequent complication of cirrhosis. It has a high mortality rate.
Portal hypertension - blood normally carried from the intestines and spleen through the hepatic portal vein flows more slowly and the pressure increases; this leads to the following complications:
Ascites - fluid leaks through the vasculature into the abdominal cavity.
Esophageal varices - collateral portal blood flow through vessels in the stomach and esophagus. These blood vessels may become enlarged and are more likely to burst.
Problems in other organs.
Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be aspecific are more difficult to recognize (e.g. worsening encephalopathy but no fever).
Fluid in the abdomen (ascites) may become infected with bacteria normally present in the intestines (spontaneous bacterial peritonitis).
Hepatorenal syndrome - insufficient blood supply to the kidneys, causing acute renal failure. This complication has a very high mortality (over 50%).
Hepatopulmonary syndrome - blood bypassing the normal lung circulation (shunting), leading to cyanosis and dyspnea (shortness of breath), characteristically worse on sitting up.[3]
Portopulmonary hypertension - increased blood pressure over the lungs as a consequence of portal hypertension.[3]
Cirrhosis has many possible causes; sometimes more than one cause is present in the same patient. In the Western World, chronic alcoholism and hepatitis C are the most common causes.
Alcoholic liver disease (ALD). Alcoholic cirrhosis develops in 15% of individuals who drink heavily for more than a decade. There is great variability in the amount of alcohol needed to cause cirrhosis (as little as 3-4 drinks a day in some men and 2-3 in some women). Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.
Chronic hepatitis C. Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis. Can be diagnosed with serologic assays that detect hepatitis C antibody or viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used screening test in the US.
Chronic hepatitis B. The hepatitis B virus is probably the most common cause of cirrhosis worldwide, especially South-East Asia, but it is less common in the United States and the Western world. Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection. Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether patient will need antiviral therapy.
Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications. This disorder is similar to that of alcoholic liver disease but patient does not have an alcohol history. Biopsy is needed for diagnosis.
Primary biliary cirrhosis. May be asymptomatic or complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial antibodies with liver biopsy as confirmation if showing florid bile duct lesions. It is more common in women.
Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with contrast cholangiography showing diffuse, multifocal strictures and focal dilation of bile ducts, leading to a beaded appearance. Non-specific serum immunoglobulins may also be elevated.
Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins. Therapy with prednisone +/- azathioprine is beneficial. Cirrhosis due to autoimmune hepatitis still has 10-year survival of 90%+. There is no specific tool to diagnose autoimmune but it can be beneficial to initiate a trial of corticosteroids.
Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload. Labs will show fasting transferrin saturation of > 60% and ferritin > 300 ng/mL. Genetic testing may be used to identify HFE mutations. If these are present, biopsy may not need to be performed. Treatment is with phlebotomy to lower total body iron levels.
Wilson's disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and altered mental status.
Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD, especially if they have a history of tobacco smoking. Serum AAT levels are low. Recombinant AAT is used to prevent lung disease due to AAT deficiency.
Cardiac cirrhosis. Due to chronic right sided heart failure which leads to liver congestion.
Galactosemia
Glycogen storage disease type IV
Drugs or toxins
Certain parasitic infections (such as schistosomiasis)
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach. Histologically cirrhosis can be classified as micronodular, macronodular, or mixed, but this classification has been abandoned since it is nonspecific to the etiology, it may change as the disease progresses, and serological markers are much more specific. However, a biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications due to liver biopsy.[4]
Lab findings
The following findings are typical in cirrhosis:
Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.
Alkaline phosphatase - usually slightly elevated.
GGT -- correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
Bilirubin - may elevate as cirrhosis progresses.
Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
Prothrombin time - increases since the liver synthesizes clotting factors.
Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
Serum sodium - hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. However this rarely results in platelet count < 50,000/mL.
Leukopenia and neutropenia - due to splenomegaly with splenic margination.
Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
Other laboratory studies performed in newly diagnosed cirrhosis may include:
Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle, anti-mitochondria, anti-LKM)
Ferritin and transferrin saturation (markers of iron overload), copper and ceruloplasmin (markers of copper overload)
Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in distinguishing various causes
Cholesterol and glucose
Alpha 1-antitrypsin
Ultrasound is routinely used in the evaluation of cirrhosis, where it may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas. Ultrasound may also screen for hepatocellular carcinoma, portal hypertension and Budd-Chiari syndrome (by assessing flow in the hepatic vein).
A new type of device, the FibroScan (transient elastography), uses elastic waves to determine liver stiffness which theoretically can be converted into a liver score based on the METAVIR scale. The FibroScan produces an ultrasound image of the liver (from 20-80mm) along with a pressure reading (in kPa.) The test is much faster than a biopsy (usually last 2.5-5 minutes) and is completely painless. It shows reasonable corellation with the severity of cirrhosis.[5]
Other tests performed in particular circumstances include abdominal CT and liver/bile duct MRI (MRCP).
Gastroscopy (endoscopic examination of the esophagus, stomach and duodenum) is performed in patients with established cirrhosis to exclude the possibility of esophageal varices. If these are found, prophylactic local therapy may be applied (sclerotherapy or banding) and beta blocker treatment may be commenced.
Rarely diseases of the bile ducts, such as as primary sclerosing cholangitis, can be causes of cirrhosis. Imaging of the bile ducts, such as ERCP or MRCP (MRI of biliary tract and pancreas) can show abnormalities in these patients, and may aid in the diagnosis.
Macroscopically, the liver may be initially enlarged, but with progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm and the color is often yellow (if associates steatosis). Depending on the size of the nodules there are three macroscopic types: micronodular, macronodular and mixed cirrhosis. In micronodular form (Laennec's cirrhosis or portal cirrhosis) regenerating nodules are under 3 mm. In macronodular cirrhosis (post-necrotic cirrhosis), the nodules are larger than 3 mm. The mixed cirrhosis consists in a variety of nodules with different sizes.
Microscopically, cirrhosis is characterized by regeneration nodules, surrounded by fibrous septa. In these nodules, regenerating hepatocytes are disorderly disposed. Portal tracts, central veins and the radial pattern of hepatocytes are absent. Fibrous septa are important and may present inflammatory infiltrate (lymphocytes, macrophages) If it is a secondary biliary cirrhosis, biliary ducts are damaged, proliferated or distended - bile stasis. These dilated ducts contain inspissated bile which appear as bile casts or bile thrombi (brown-green, amorphous). Bile retention may be found also in the parenchyma, as the so called "bile lakes".[6]
The severity of cirrhosis is commonly classified with the Child-Pugh score. This score uses bilirubin, albumin, INR, presence and severity of ascites and encephalopathy to classify patients in class A, B or C; class A has a favourable prognosis, while class C is at high risk of death. It was devised in 1964 by Child and Turcotte and modified in 1973 by Pugh et al.[7]
More modern scores, used in the allocation of liver transplants but also in other contexts, are the Model for End-Stage Liver Disease (MELD) score and its pediatric counterpart, the Pediatric End-Stage Liver Disease (PELD) score.
The liver plays a vital role in synthesis of proteins (e.g. albumin, clotting factors and complement), detoxification and storage (e.g. vitamin A). In addition, it participates in the metabolism of lipids and carbohydrates.
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are still fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function. Recent research shows the pivotal role of stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the stellate cell, which becomes contractile (called myofibroblast) and obstructs blood flow in the circulation. In addition, it secretes TGF-β1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it disturbs the balance between matrix metalloproteinases and the naturally occurring inhibitors (TIMP 1 and 2), leading to matrix breakdown and replacement by connective tissue-secreted matrix.[8]
The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, which leads to hypersplenism and increased sequestration of platelets. Portal hypertension is responsible for most severe complications of cirrhosis.
Traditionally, liver damage from cirrhosis cannot be reversed, but treatment could stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process. Close follow-up is often necessary. Antibiotics will be prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose, decrease risk of constipation; their role in preventing encephalopathy is limited.
Treating underlying causes
Alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis. Cirrhosis caused by Wilson's disease, in which copper builds up in organs, is treated with chelation therapy (e.g. penicillamine) to remove the copper.
Preventing further liver damage
Regardless of underlying cause of cirrhosis, alcohol and acetaminophen, as well as other potentially damaging substances, are discouraged. Vaccination of susceptible patients should be considered for Hepatitis A and Hepatitis B.
Preventing complications
Main article: Ascites
Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). Diuretics may be necessary to suppress ascites.
Esophageal variceal bleeding
Main article: Esophageal varices
For portal hypertension, propranolol is a commonly used agent to lower blood pressure over the portal system. In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting is occasionally indicated to relieve pressure on the portal vein. As this can worsen encephalopathy, it is reserved for those at low risk of encephalopathy, and is generally regarded only as a bridge to liver transplantation or as a palliative measure.
Hepatic encephalopathy
Main article: Hepatic encephalopathy
High-protein food increases the nitrogen balance, and would theoretically increase encephalopathy; in the past, this was therefore eliminated as much as possible from the diet. Recent studies show that this assumption was incorrect, and high-protein foods are even encouraged to maintain adequate nutrition.
Main article: Hepatorenal syndrome
The hepatorenal syndrome is defined as a urine sodium less than 10 mmol/L and a serum creatinine > 1.5 mg/dl (or 24 hour creatinine clearance less than 40 ml/min) after a trial of volume expansion without diuretics.[9]
Spontaneous bacterial peritonitis
Main article: Spontaneous bacterial peritonitis
Cirrhotic patients with ascites are at risk of spontaneous bacterial peritonitis.
Main article: Liver transplantation
If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary. Survival from liver transplantation has been improving over the 1990s, and the five-year survival rate is now around 80%, depending largely on the severity of disease and other medical problems in the recipient.[10] In the United States, the MELD score (online calculator)[11] is used to prioritize patients for transplantation. Transplantation necessitates the use of immune suppressants (ciclosporin or tacrolimus).
Decompensated cirrhosis
In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation, infection (of any source), increased alcohol intake, medication, bleeding from esophageal varices or dehydration. It may take the form of any of the complications of cirrhosis listed above.
Patients with decompensated cirrhosis generally require admission to hospital, with close monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical treatment - often with diuretics, antibiotics, laxatives and/or enemas, thiamine and occasionally steroids, acetylcysteine and pentoxifylline. Administration of saline is generally avoided as it would add to the already high total body sodium content that typically occurs in cirrhosis.
Cirrhosis and chronic liver disease were the 10th leading cause of death for men and the 12th for women in the United States in 2001, killing about 27,000 people each year.[12] Also, the cost of cirrhosis in terms of human suffering, hospital costs, and lost productivity is high.
Established cirrhosis has a 10-year mortality of 34-66%, largely dependent on the cause of the cirrhosis; alcoholic cirrhosis has a worse prognosis than primary biliary cirrhosis and cirrhosis due to hepatitis. The risk of death due to all causes is increased twelvefold; if one excludes the direct consequences of the liver disease, there is still a fivefold increased risk of death in all disease categories.[13]
Little is known on modulators of cirrhosis risk, apart from other diseases that cause liver injury (such as the combination of alcoholic liver disease and chronic viral hepatitis, which may act synergistically in leading to cirrhosis). Studies have recently suggested that coffee consumption may protect against cirrhosis, especially alcoholic cirrhosis.[14]
^ Roguin A (2006). "Rene Theophile Hyacinthe Laënnec (1781-1826): the man behind the stethoscope". Clinical medicine & research 4 (3): 230–5. PMID 17048358.
^ Li CP, Lee FY, Hwang SJ, et al (1999). "Spider angiomas in patients with liver cirrhosis: role of alcoholism and impaired liver function". Scand. J. Gastroenterol. 34 (5): 520-3. PMID 10423070.
^ a b Rodriguez-Roisin R, Krowka MJ, Herve P, Fallon MB; ERS Task Force Pulmonary-Hepatic Vascular Disorders (PHD) Scientific Committee. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J 2004;24:861-80. PMID 15516683.
^ Grant, A; Neuberger J (1999). "Guidelines on the use of liver biopsy in clinical practice". Gut 45 (Suppl 4): 1-11. PMID 10485854. "The main cause of mortality after percutaneous liver biopsy is intraperitoneal haemorrhage as shown in a retrospective Italian study of 68,000 percutaneous liver biopsies in which all six patients who died did so from intraperitoneal haemorrhage. Three of these patients had had a laparotomy, and all had either cirrhosis or malignant disease, both of which are risk factors for bleeding."
^ Foucher J, Chanteloup E, Vergniol J, et al (2006). "Diagnosis of cirrhosis by transient elastography (FibroScan): a prospective study". Gut 55 (3): 403-8. doi:10.1136/gut.2005.069153. PMID 16020491.
^ Pathology atlas, "cirrhosis".
^ Pugh RN, Murray-Lyon IM, Dawson JL, Pietroni MC, Williams R. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973;60:646-9. PMID 4541913.
^ Iredale JP. Cirrhosis: new research provides a basis for rational and targeted treatments. BMJ 2003;327:143-7. Fulltext. PMID 12869458.
^ Ginés P, Arroyo V, Quintero E, et al (1987). "Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study". Gastroenterology 93 (2): 234-41. PMID 3297907.
^ E-medicine liver transplant outlook and survival rates
^ Cosby RL, Yee B, Schrier RW (1989). "New classification with prognostic value in cirrhotic patients". Mineral and electrolyte metabolism 15 (5): 261-6. PMID 2682175.
^ Anderson RN, Smith BL (2003). "Deaths: leading causes for 2001". National vital statistics reports : from the Centers for Disease Control and Prevention, National Center for Health Statistics, National Vital Statistics System 52 (9): 1–85. PMID 14626726.
^ Sørensen HT, Thulstrup AM, Mellemkjar L, et al (2003). "Long-term survival and cause-specific mortality in patients with cirrhosis of the liver: a nationwide cohort study in Denmark". Journal of clinical epidemiology 56 (1): 88–93. PMID 12589875.
^ Klatsky AL, Morton C, Udaltsova N, Friedman GD (2006). "Coffee, cirrhosis, and transaminase enzymes". Arch. Intern. Med. 166 (11): 1190–5. doi:10.1001/archinte.166.11.1190. PMID 16772246.
[1] at the National Library of Medicine and the National Institutes of Health. Medline Plus: Cirrhosis -- also called: Hepatic fibrosis
Categories: Gastroenterology | Hepatology
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Cirrhosis". A list of authors is available in Wikipedia.
https://www.bionity.com/en/encyclopedia/Cirrhosis.html


"Partnerships in Employment Brief: Influencing Changes in State Policy " by Evelyn Doxey, Leslie Jaehning et al.
Subminimum wage is a pervasive and controversial issue. In many states there are individuals with disabilities who earn as little as seven cents an hour and workers who do not earn any wages because they do not produce enough products to be paid wages for their work according to the 14(c) Certificate holder.
There are many ways that data on wages earned under Section 14(c) of the Fair Labor Standards Act, i.e., 14(c) Certificates can be used to influence changes in state policy and practice. This brief describes examples from Partnerships in Employment grantee states.
Doxey, Evelyn; Jaehning, Leslie; McMillan, Elise; Vandagriff, Kristin; and Winsor, Jean, "Partnerships in Employment Brief: Influencing Changes in State Policy and Practice with Data on Subminimum Wages" (2017). All Institute for Community Inclusion Publications. 40.


Gluesys is aiming to become Smart IT Solution Group that provides the competitive IT solutions.
Ever since its foundation in April, 2000, the Company has dedicated itself to the development of storage software and is now truly the only specialty NAS company in Korea.
Gluesys has expanded beyond the domestic market into foreign markets such as Singapore, Malaysia, and Vietnam with its corporate NAS solutions and shipped its personal NAS solutions to the USA, Europe, and Japan, gaining good reputation. Furthermore, it has made efforts to protect and manage personal and corporate data and assets through development and sales of various data management solutions such as personal file management devices, corporate file management solutions, enterprise security management solutions, and backup solutions.
Gluesys hopes that its customers keep their continued and attentive eyes on its leap forward to becoming one of the global smart IT solution providers.


No good deed goes unpunished. Mark Samuels, a somewhat seedy matrimonial lawyer, is dead from an overdose of suspiciously pure cocaine. Jane Larson, a hotshot litigator for a large law firm in New York City, is sucked into the world of divorce and child support when her friend Francine asks her to help out one of Mark's clients.Jane quickly learns that the case is a complete loser and that her new client, Gail, is a demanding and unscrupulous prima donna. However, through some skillful legal work and a tip-off from a mysterious informant, Jane uncovers a safe deposit box where the deadbeat husband has been hiding a large chunk of cash.
She also attracts the attention of a fellow lawyer (Bryan) who is handsome and successful and an excellent protector from the threats to her life that suddenly start popping up with alarming frequency, along with murders of people related to the case—among them the deadbeat dad and an undercover cop.
It soon becomes apparent that Jane's discovery of the cash has only started to unravel a web of lies, drugs, and criminal activity. Ultimately, she is involved in a race to recover a suitcase of money that Jane hopes will help police catch the murderer before she becomes the next victim.
A fast paced legal thriller.
Jane Larson takes on a divorce case at the request of a friend. She quickly discovers it is not only her client who is after her husband's assets and others are prepared to kill for them. With bodies dropping like flies around her, her own life is in danger as is the reputation of an ex-lover as she races against the police and an unknown killer to uncover the truth.
I've only visited New York once but this book brings to life the inhabitants along with the sights and sounds of the city exactly as I remember them. Jane Larson is a likeable if sometimes brash and prickly character who I could relate to. Suspense and intrigue builds but never at the expense of realism and the story and all the characters that play a part are totally believable.
Thank you for having Anne and I and our mystery on your blog today. We appreciate it.
It was a pleasure 🙂 Good luck with your book!


A few months ago I designed an Iraqi-inspired meal-kit delivery box with Out of the Box Collective that delivered within and beyond the greater Los Angeles area. The goal was to introduce people to Iraqi food in the hopes that they might think about Iraq in a new context and what that might mean. I wondered if people would actually take my message into consideration when making the meals or if they would simply eat the food and go on with their lives.
And then I received this incredible letter, which I'll leave you with.
Apologies that this email took so long. I wanted you to know that our "Add a Little Lemon" Iraqi box was extra special. During each night of cooking and eating we talked about how the food was from a far away country named Iraq. We loved every bite of it, and especially fun was the drama of sizzling turmeric oil and serving on giant platters and the funny instructions like "don't be lazy, tembal"Anyway, my 3 year old has recently taken a keen interest in maps and finding countries/states/etc. He showed me a doodle of a map he had drawn declaring, "This is Iraq!" So I just love love love that his first associations with Iraq - just as Sara was hoping - will not be violent or terrible, but delicious and wonderful instead.
November 28, 2017 by sara leana.
Add a Little Lemon is Saveur Awards Finalist: Best New Voice 2017!
When I started this blog it ended up being more of a vulnerability challenge than anything else really. I had been notoriously shy with my writing, afraid of revealing anything personal about myself and those close to me. Godfather status. Everything in my life was somehow a secret, always. And then that changed for me. I began learning how to be unapologetic about my own opinions and thoughts, something I labored over in a sort of self directed self-compassion training. I would practice saying what I believed in even if it often times upset others; and in a surprising effort to refrain from keeping the peace, I found that it wasn't actually so scary, after all. I was showing up for myself. Telling myself that it was okay, that I was safe, that I would take care of myself.
That's when I started opening up here.
It was uncomfortable, certainly. For a recovering people-pleaser most everything is uncomfortable. Yet being uncomfortable isn't so terrifying; and in fact, proves to be vital in the development of both integrity and authenticity.
Whenever I posted, I would call my brother and my oldest friend in a panic, afraid that I did something too bold, too opinionated, too unpleasant. And each time they assured me that my fears didn't actually come across in my writing, that what comes across is my integrity, not the trouble maker I imagined myself to be. It's uneasy for recovering people-pleasers.
And then something happened. One day I stopped worrying. I stopped making those late night panicked calls. I felt stronger, bolder, and more self-assured. The practice of coming here and writing for all of you has changed me incredibly and given me not only an opportunity to be more authentic and confident, but has also taught me how to recognize the bravery of being, as Brene Brown says, face down in the arena.
You have all been so kind and generous and brave. I've received so many messages letting me know that you identify with and appreciate my stories, recipes, and photos. It's been especially moving to hear from other Iraqis in diaspora, like myself, who have been wanting a space like this. Something that speaks to those growing up in the diaspora and who have struggled with identity, like myself. Many have sent me messages telling me how this space has inspired them to share their own Iraqi recipes and stories, too. When I first started here there were no other Iraqi food blogs in English. I, like others my age, worshiped Nawal Nasrallah and her cookbook because she gave me the gift of something comprehensive that I could actually read; she gave me a way to connect to Iraq that I desperately needed. Add a Little Lemon was something I was hungry for; and so I thought I'd just do it myself, for myself, showing up for myself with self-compassion. And I am so grateful for what it has given me. My voice feels new if only because this space has allowed me to grow into it.
August 9, 2017 by sara leana.


I grew up gathering apples from apple trees in my front yard. Picking the ones I could reach or picking up the good ones without too many bugs from the ground. I'd even climb the tree if there were some in reach. Child labor at its best.
After all the apples were gathered, we'd sit in my grandma's kitchen and eat parts of apples as she cleaned, cored, and prepped them to make applesauce. At least I think that is what we were doing with a small metal press that was probably as old as my grandma. The delicious applesauce was canned and lasted through the summer, winter, and spring until the apples started growing again.
To celebrate fall, our friends rented an apple press from local tool library and invited us over. It was simple, we were asked to bring apples and supplies (cutting boards, knives, and empty pitchers). Unsure on how many apples to buy, we bought 4.5 lbs.
Along with others invited to the party, we all took turns learning the simple process of making apple cider. Maybe next year we'll even host our own party.
1. Pick or buy apples.
Whether you picked your apples outside or bought them in the store, the apples should be at least rinsed as no preservatives are added.
For the apple press we were using, we quartered the apples. There's no need core the apples.
4. Add the mesh-lining to the bucket.
The mesh is used as a strainer to keep the apple pulp getting into the cider.
5. Add a catch pot or bucket for the juices.
The apple juice will drip out of the pomace, or apple mash, when grinding the apples. Make sure to catch all the juice by placing your catch container where the liquid will drain.
6. Add apples to the fruit grinder.
Toss the apples and turn the hand crank. The grinder will mash the apples into the mesh-lined bucket for pressing.
First, add the pressing lid to the top of the pomace.
Second, add the press mechanism to the lid and crank it until the juice stops draining into your catch container.
8. Empty the pomace into compost and repeat.
Divide the cider to growlers or bottles and share with friends. I suggest bringing a flask of whiskey to the party to spice up the cider.
Make your own apple press.


Fancy a Drink With Hello Kitty? Order a Beer!
Who says China isn't a capitalist wonderland? The latest weapon in the Chinese economic arsenal is Hello Kitty beer.
Yes, you read that correctly: Hello Kitty beer.
Officially licensed by Japanese company Sanrio, the elixir is brewed in Taiwan by Long Chuan, and it is only available in China (for now) . The brew comes in six fruity flavors, including lemon-lime, passion fruit, banana and peach, according to Geek Tyrant.
Could that "something" be the collective tears of millions of little Hello Kitty fans?


text:
Home Health and Beauty Top Docs Top Docs 2013-2014
Top Docs 2013-2014
View Annapolis / West County Top Docs
View Eastern Shore Top Docs
We take the peer review process very seriously here at What's Up?. Our Top Docs, Top Dentists, and Leading Lawyers surveys (produced every other year) require a surprising amount of time and energy to execute. The extent of this hands-on work might explain why so many publications (in our area and across the country) now subcontract their "Best of " issues for doctors, lawyers, and dentists. They let someone in another state entirely do "samplings" and "polling." We, on the other hand, make the effort to contact each professional personally. And we're proud of that fact.
The extent of the effort expended also explains why we are so gratified by and grateful for the enthusiastic support and response from Chesapeake region professionals. Our physicians, for instance, are very busy people. Yet many, many took the time to fill out a long survey form, which listed more than 40 areas of specialty. Doctors didn't have to fill in each category, of course, but a surprising number did. Some filled in particular specialties with which they deal most often. (No survey forms, by the way, were accepted which had only one specialty filled in.)
The Top Docs contained on these pages (listed in alphabetical order) represent the individuals who received the highest number of nominations from their peers. We have also vetted these names using the Maryland Board of Physicians to make certain that they are currently licensed professionals in good standing in the community.
Please note that many fine physicians who are either new to the area or affiliated with other medical institutions may not be included. Additionally, this list represents only those "winners" who received the most substantial number of votes, not everyone who was nominated.
Once again, we would like to thank all the busy doctors who took the time to respond to this important survey. Knowing who medical professionals consider the best in their respective fields is an invaluable asset. Many of our well-informed readers will keep this issue year-round for ready reference. What's Up? readers know the real thing when they see it.—Sarah Hagerty
Health and Beauty In Print The Look Top Docs Health Winners Top Docs Year Issued: 2013 Month Issued: 10


text:
using namespace IECoreGL;

TextureLoader::TextureLoader( const IECore::SearchPath &searchPaths )
	:	m_searchPaths( searchPaths )
{
}

TexturePtr TextureLoader::load( const std::string &name, int maximumResolution )
{
	TexturesMapKey key( name, maximumResolution );
	TexturesMap::const_iterator it = m_loadedTextures.find( key );
	if( it!=m_loadedTextures.end() )
	{
		return it->second;
	}

	boost::filesystem::path path = m_searchPaths.find( name );
	if( path.empty() )
	{
		IECore::msg( IECore::Msg::Error, "IECoreGL::TextureLoader::load", boost::format( "Couldn't find \"%s\"." ) % name );
		m_loadedTextures[key] = nullptr; // to save us trying over and over again
		return nullptr;
	}

	if( !IECoreImage::ImageReader::canRead( path.string() ) )
	{
		IECore::msg( IECore::Msg::Error, "IECoreGL::TextureLoader::load", boost::format( "Couldn't create an ImageReader for \"%s\"." ) % path.string() );
		m_loadedTextures[key] = nullptr; // to save us trying over and over again
		return nullptr;
	}
	IECoreImage::ImageReaderPtr imageReader = new IECoreImage::ImageReader( path.string() );

	// Set miplevel if texture resolution is limited
	if( maximumResolution < std::numeric_limits<int>::max() )
	{
		int miplevel = 0;

		Imath::V2i dataWindowSize = imageReader->dataWindow().size();
		int currentMax = std::max( dataWindowSize.x, dataWindowSize.y ) + 1;
		IECore::IntParameter *miplevelParameter = imageReader->mipLevelParameter();
		while( currentMax > maximumResolution )
		{
			miplevelParameter->setNumericValue( ++miplevel );

			dataWindowSize = imageReader->dataWindow().size();
			currentMax = std::max( dataWindowSize.x, dataWindowSize.y ) + 1;
		}
	}

	IECore::ObjectPtr o = imageReader->read();
	IECoreImage::ImagePrimitivePtr i = IECore::runTimeCast<IECoreImage::ImagePrimitive>( o.get() );
	if( !i )
	{
		IECore::msg( IECore::Msg::Error, "IECoreGL::TextureLoader::load", boost::format( "\"%s\" is not an image." ) % path.string() );
		m_loadedTextures[key] = nullptr; // to save us trying over and over again
		return nullptr;
	}

	TexturePtr t = nullptr;
	try
	{
		ToGLTextureConverterPtr converter = new ToGLTextureConverter( i );
		t = IECore::runTimeCast<Texture>( converter->convert() );
	}
	catch( const std::exception &e )
	{
		IECore::msg( IECore::Msg::Error, "IECoreGL::TextureLoader::load", boost::format( "Texture conversion failed for \"%s\" ( %s )." ) % path.string() % e.what() );
	}
	m_loadedTextures[key] = t;
	return t;
}

void TextureLoader::clear()
{
	m_loadedTextures.clear();
}

TextureLoader *TextureLoader::defaultTextureLoader()
{
	static TextureLoaderPtr t = nullptr;
	if( !t )
	{
		const char *e = getenv( "IECOREGL_TEXTURE_PATHS" );
		t = new TextureLoader( IECore::SearchPath( e ? e : "" ) );
	}
	return t.get();
}

redpajama_set_name: RedPajamaGithub


is it possible to change document ownership in alfresco share?
Consider the following: User A created a directory and a bunch of documents. Now User B takes over User A's duties, and thus should become the owner of these documents.
(1) Is it possible to take document ownership in Alfresco Share, if the User B that is trying to take the ownership is *not* site admin?
(2) Is it possible for the Site Manager to change document ownership (i.e., not take it, but change it from User A to User B)?
(3) If the answer to both is "no", is it possible for the Site Admin (or the admin in general) to change document ownership in Alfresco Explorer?
As far as I know it is not possible to change ownership through Share and by using Explorer admin can take the ownership over the document but cannot set someone else as document owner.
To solve your problem you will need to implement this functionality in Share (i.e. custom web script, using OwnableService and setOwner method).


Norway is the Country in Focus at the 2019 European Film Market (EFM). Here is the official programme for Feb. 8th-13th.
Gender, Genre & Big Budget. Press conference. Hollywood producer Gale Anne Hurd introduces WIFT seminar.
Nations without Borders. Indigenous people produce films worldwide.
International Sami Film Institute invites friends from around the world to a reception.
Presentation of 10 Norwegian Producers.
Film production and Creative Industries funding: finding the optimal business approach.
Discussion: Artificial Intelligence may be the most disruptive and far-reaching technology in the history of mankind. How can humanity maximise the benefits of Artifical Intelligence?
Stories from Norway. Pitches from talented filmmakers that are part of the UP Programme.
Norwegian Party, hosted by the Norwegian Film Institute, incl a miniconsert with an internationally known Norwegian artist.
Debate: Meet the censors: What are the obstacles that keep controversial content away from our screens and TVs? Is it self-censorship within the channels, or bad filmmaking? Is fact checking too expensive?
Work-In-Progress. Norwegian producers and directors present teasers and promos from upcoming feature films; take a look into the future of Norwegian film!
Books made for film. Norwegian literary agents meet German producers and Norwegian producers meet German publishers/ agents. In cooperation with Books at Berlinale.
Lillehammer Stories. In the recent years filmmakers in Lillehammer and its regional surroundings has produced a number of successful films and TV productions. We invite you to get to know this interesting film region of cold hearts and warm stories and meet decision makers.
Books at Berlinale. Presentation of Norway at Frankfurt 2019 and the Norwegian Book Keep Saying Their Names by Simon Stranger.
Speeddate a Nordic Composer. Each director/producer gets 9 minutes to meet each composer, then move on to the next meeting. Meet and greet afterwards.
Less is More: A New Generation of Screenwriting Workshops in Europe. New frame, new methodology, new perspectives: how to stimulate creativity in the writing process and have films reaching their audience?
Born 2 Drive Oliver Solberg has fast-driving cars in his blood and genes. Meet him and his famous father, World Rallycross and World Rally champion Petter Solberg, and see excerpts from the new documentary.
"Norway in Focus" is organized by the Norwegian Film Institute in cooperation with the EFM, and will offer a host of possibilities for networking with Norwegian producers, distributors, investors, and creative talents, as well as the chance to take a closer look at Norwegian productions.


Corporate offices and historic buildings, including City Hall, span across Logan Square. While this neighborhood is a corporate hub, its wide streets also attract city events such as the Philadelphia Marathon or Fourth of July concert.
It's not a bad neighborhood, but it can get deserted. It's a pretty corporate area. Coffee shops are closed on the weekend, that kind of thing. It's close enough to other neighborhoods though, so you don't feel super isolated.
It's not Rittenhouse, but it's not as pricey; it's not Washington, so it's not as oddly out of the way; and it's not Franklin, thank God. Logan is lots of families, a handful of schools, some great museums, a scattering of acceptable restaurants, a Whole Foods, an excellent running trail, and some of the most accessible transit options are found on Market as soon as you cross the river. Once you're off that, it's fairly quiet, and the parkway quiets down once commuting is over (unless, of course, a world-class concert or festival is taking place, and is that really that much of a problem?) and the walk from Logan into Center City is a breeze.
Great location for convenience - along the river, smack between Trader Joe's and Whole Foods (7-8 min walk to each). About 30 min walk to hospital or 10 min bike ride. Quiet neighborhood, not too many bars or restaurants nearby.
Originally was concerned it'd be too far from the "Rittenhouse Bubble" - in reality only 2 blocks away from great restaurant / bar scene. That 2 blocks provides a quieter atmosphere while still providing anything we need at our fingertips (convience store/deli, cleaners, nail salon, all in the building).
A bit north of the beaten path for Wharton, but it's actually only a 5 minute walk from Rittenhouse park. Really convenient for going to / from pub on Thursdays. Food options are not fantastic within a 2 block radius, but you have easy access to all the north-of-Rittenhouse options.
Cons: JFK and Market st. can be quite noisy with cars and fire engines from the nearby fire dept - some people may have difficulties sleeping at night due to that.
I think the Murano's location is unbeatable. Trader Joe's is across the alley, the liquor store is across the street, and the Septa stop (which is HUGE in inclement weather) is on the corner.
So many restaurants to try! Prime location- 1 block from Trader Joe's and right above a liquor store.


text:
The secret of R1218
It all depends on what's underneath. Wörwag's primer has been demonstrating its versatility for some 15 years. No one sees the primer, but everyone needs it. Prime stuff—a look at the recipe for success.
Thomas Stehle grabs a plastic plate. Fifteen centimeters long, ten centimeters wide. The expert from the primer development department at Wörwag paints countless plates like this almost daily.
Today he is applying a medium gray primer with a hydrobase and a clear lacquer in order to systematically destroy it later. To do so, he has used a knife to incise a check pattern into the plate. Now he pulls off the cross-hatching with tape. Some of the other plates he shoots with steel shot at a certain pressure from a controlled distance. In many places, the paint is all but gone. Peeled off. Disintegrated. Yet Stehle seems relaxed.
He had a hunch this would happen. This paint system was doomed to fail. "If the primer's not right, the paint can sparkle and shine all it wants; as soon as it goes through a car wash, it's finished." And that is precisely what this simulation was about. If it doesn't stick, it can't shine. Mishaps of this kind can be avoided with a primer designed to meet the requirements.
Stehle takes another plastic board from the test bench. The difference is evident. In spite of an identical load, the paint still stuck even where the cuts were made. It shows hardly any signs of its ordeal. This recipe works. The primer is the behind-the-scenes hero that keeps its word.
Article as PDF Send Article Zurück zur Heftübersicht
Ramona Baumgärtel, today the head of the technology development department for pastes and top coats, was the driving force behind the development of the primer 15 years ago. Together with Georg Bussmann, who is now responsible for international technology and know-how transfer, she got the successful Wörwag product off the ground. The primer is used on components such as plastic bumpers and mirror shells on cars. "At present, with this composition and with these characteristics, there's no one else who does it this way," says Bussmann.
Allow me to introduce R1218. This is no code for some android from the future, but the indispensable Wörwag product of today. An evergreen that's been impressing customers since its launch in 1999. Two thousand metric tons of it leave the plants in Zuffenhausen (Germany), Langfang (China), Lafayette (USA), Barcelona (Spain) and Cape Town (South Africa) every year—from five-kilo cans to containers weighing tons.
Many production locations, one recipe for success: R1218 is made to the same quality standards worldwide.
R1218 stands for the highest quality worldwide.
The primer's advantages are legion: it can be used on almost any system, adheres to most materials, and fulfills the specifications of the carmakers. It can be delivered in countless colors and settings. With this single primer, the user covers all coating processes, whether dry, wet-in-wet or electrostatic.
R1218 also has another ace up its sleeve. It is permitted in the spare parts service of every carmaker. Parts are put into storage primed and can be reliably finished even after lengthy periods. "Many people don't think of primers as sexy products because they don't shine," says Bussmann.
"You don't even see them. For a reliable coating system, however, the primer is absolutely indispensable", Georg Bussmann
Bussmann still clearly recalls the beginnings of the innovative primer system in the late '90s. It took about three years to reach the launch phase.
During the process, the developers had to learn to dispense with the old standards. If you want to make a single product out of six or seven primer variants with different characteristics and applications, you have to find new ways of thinking. You have to be bold, try things out—and keep learning from experience.
The persistence paid off. The result was a primer unlike any that came before. R1218 is especially unique in the combination of binding agents. But ingredients alone do not make a good primer. "The trick is in the production process," confides Bussmann.
Today R1218 is available in 130 recipes and color variants, from transparent to shiny, black to slate gray. Red, white, green, and beige are possible as well. For John Deere's tractors, a very special green primer was developed. Another company wanted a glossy primer to make it easier to identify impurities during inspections. For vehicle door handles, Wörwag has a transparent variant that makes scratches less apparent.
Beyond its vast spectrum of uses, the primer also demonstrates the highest reliability. Bussmann: "Many customers demand a system that can be implemented with less technologically advanced procedures. And whatever they do with our primer, it works." Particularly in markets like Brazil, Mexico, and China. In those countries, few factories are capable of combining the work steps in a coating system. That's one reason why R1218 is the top-selling product group in China.
Thomas Stehle and Georg Bussmann (right) are two of Wörwag's primer experts.
Wörwag offers custom solutions. That's what Stehle's coating tests are about as well. If the primer has to meet special requirements, the customer consultants are the first responders. They have the basic composition of R1218 and a modular system at their disposal.
This allows them to change parameters such as the viscosity of the application type. If the requirements are more complex, Stehle joins the fray. Reasons for altering the recipe might include substitution of raw materials to meet new environmental regulations or to avoid supply bottlenecks. And of course, that requires the entire testing program for the respective specification.
Extensive testing
New color tones and changes to the composition of the solvents require equally extensive testing. Depending on the intensity and complexity of the task, it can take up to six months for the modified primer to be ready. "Paint lives, and sometimes it behaves rather oddly," chuckles Stehle. Some things are a lot different in the chemistry books. But if you think your way into things, you always get to the bottom of it." That's why it doesn't bother him in his development lab when the paint goes missing from the test boards. Once in a blue moon.
Georg Bussmann,
today the head of International Technology Management (ITM), was involved in developing the primer 15 years ago. His motto: "Primers can be sexy too."
Thomas Stehle
has worked for Wörwag since 1991. The trained commercial vehicle painter and paint and plastics technician is responsible for continuous primer development. His motto: "You can't re-invent the wheel every day, but you have to keep it rolling."
Text: Michael Thiem
Photos: iStock, Boris Schmalenberger
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