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February 06, 2007

Self-Fulfilling Prophecy?!

Our home school verse for this week is Philippians 2:14, "Do everything without complaining and arguing." (Rule 12: When we have work to do, we do it without complaining.) As I wrote the verse and rule on the white board Monday morning, I thought how appropriate it was that we're looking at this topic this week, because it seems that the complaining around here has escalated greatly. And, as any adult who has ever watched more than one child play knows, arguing is a fact of life amongst siblings and friends.

Little did I know that I'd soon be dealing with one of my children arguing with ME every time I asked him to do something! I told Ted this evening that I don't really recall this being much of an issue, but truly, the last two days, just about ANYTHING I have asked or told Tobin to do, the response is some kind of argument as to why he shouldn't do whatever it is.

"Tobin, you're my lunch helper this week. Please come help me set the table for lunch."

"Well, I just need to finish coloring this picture."
"I don't want to be lunch helper. I decided I want to be dinner helper instead." (What do you think he would say at dinner time if I asked him to help then?!)
"I'm making a house right now. I'll do it later."

And so on.

It makes no difference what the task is...it could be as simple as "Please take your dirty shoes off the counter" or "Let's get in the van and buckle up." EVERY time he has a come-back. For quite awhile he was doing a fabulous job of saying "Yes, Mommy," and obeying, if not immediately, at least somewhat in the vicinity of the time I asked.

So, I ask you: Did I bring this on by asking my children to memorize a verse and a rule against complaining and arguing?! Thank heavens I'm not having any major "issues" with Charis and Arden right now! I don't think I could handle training more than one child in more than one area at this time in my life!! Not that it will get any easier after the baby arrives, but my life is so full of distractions now as it is...I need help focusing.

Sigh. I guess no one ever said parenting would be easy...

Megan said...

Sela is full of excuses for why she can't help with certain things lately, too. And it's usually because she's "too tired" or her "legs are hurting." It doesn't help that she sees Daddy stretched out on the couch at least once a day to give his aching legs a rest. His excuse is legitimate, but maybe she thinks he's making it up, I don't know. If she complains that she can't help because she's feeling unwell, I send her to bed for a little bit. If she's too unwell to pick up toys, she's too unwell to play with them either. ;)

Sarah said...

Oh yes, I know Hannah and Kenzie both go through those phases. You KNOW they know how to obey nicely... that makes it even more frustrating when they don't!

Ski said...

Whew! It is nice to hear other moms have these issues with their children. Meghan in the last week is either arguing about doing something or is asking why about EVERYTHING even if I've explained it to her already. Thank you Sarah for giving me hope that my daughter hasn't turned into a monster but that this is a phase and it to shall pass.

Tina said...

At the beginning of your post I was thinking "Oh, that is a verse we need to start learning". By the end, I wasn't so sure. ;-) Actually, it is because I am tired of every requst being met with "Why?". I've struggled to balance the need to understand/logic with the "Obey Mommy".


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Tuesday, January 25, 2011

So this is the sampler I made for my Mum for Christmas. Thankfully, I had an extra few weeks before seeing her.

So it started out as a review of my year (one thing of each month), and then I found this cute owl on etsy by Michelle Palmer, and bought this cute stitching template of a turtle by Charlotte Lyons (funds raised to help Gulf wildlife), and acute mini fabric collage by Pam Garrison.

I got things back on the rails, though, and then filled the gaps with flowers and stars....

My "suzi blu" La Sirena mermaid. (I took this before I was finished, so her mouth isn't there.)

A lace scrap to symbolize my mori girl interest:

From my November vacation:

Charlotte's turtle:

V is for the Young Victoria project from the start of last year.

Thursday, January 20, 2011

One last look at #reverb10

One of the prompts was to share a favorite photo. I chose the top one of this strip from Photobooth (a cool iPhone app that Hope turned me onto!).

Just a bit of silliness.

Sunday, January 16, 2011

a couple of vintage finds...

Mary medals (and a brooch from Karla Nathan's shop).

These would be perfect strung with some twisted and knotted seam binding, wouldn't they?

Tuesday, January 11, 2011

La Sirena progress...

This is taking much longer than I planned.

I posted the background earlier.

This is my colored in sketch of my mermaid, using one of Suzi's templates:

And this is where she was at as of Saturday morning...

I tinkered some more Sunday after church ... hopefully I will be able to show you the finished painting soon....

Friday, January 7, 2011

To the Rescue!

Last week, my planned workday went to h*** in a handbasket (hey, I work in a church, remember?). The priest's vesting room stunk to high heaven of mold/mildew from the recent downpours, the carpet had been soaked in one place, and my hubby recommended we get the vestments outta there before the mold/mildew spores transferred as we knew the smell was coming from somewhere.

So we start hauling out vestments and transferring them to a couple of other closets....they were dry and untouched (and not smelly, apparently I have a nose for it) ....

But found that we had a pile of mildewy clothes on the floor of one of the closets, and the wet had wicked up from these.... Alas, two gorgeous black wool cassocks were completely ruined with mildew up to the knees. I have a bad feeling that can't have occurred in just the last couple of weeks and that this has been an undiagnosed problem...

Fortunately, the vestments currently in use were spared and weren't even damp, but there were some old red child-sized choir robes (that hadn't been used in 15-20 years) and a few Christmas pageant (we think) costumes. We didn't look too closely as most of them were the items on the floor, except for 3 pieces that were still hanging.

One of the mystery items was a floor-length under-petticoat which had gathered ivory lace starting at the knees. It came with this absurd pink satin and lace giant bow, so I suspect someone, sometime, had been an adult-sized Little Bo Peep. Or something.

As it's without the rest of its costume and we didn't otherwise have a use for it at church, I've taken it home, had it washed, and hung in the downstairs bathroom for "observation". I waited until after the second rain storm to do another check of it, and as it smells okay and there's no "bloom", I've just gained myself an underskirt to wear with some of my shorter skirts, like the dirndl underskirt I bought in Munich.

Wednesday, January 5, 2011

#reverb10 finished; goals set

I wasn't planning to share any pages from the #reverb series, but I thought I would share a couple that I don't mind, well, sharing! I filled up this entire notebook, mainly because I chose to glue pages together to prevent leak-through. The cool this is there are 2-3 more in this set that I can use in upcoming years for the same/similar purpose.

I don't remember which two days these were. I decided not to date them as I went. I'm sharing this one because of the right-hand side page. That, my friends, is what the salt and pepper comes in when you fly United. So it's this cool little double-sided window! (great for a subpage, but I didn't think that one ahead)

I kept it pretty simple. It was more important to me to respond honestly to the prompts (ok, am not sure about the jumping jacks part below) than to go all out with prettiness. But the Pitt artist pens did the job pretty well, I think.

I still have one page left of the #reverb10 to finish, and that's the photo prompt. I'm planning to use a pic I took using the Photobooth app on my iPhone which is most awesome (the app, and the pic!). Just have to print it out!

At the end I listed my art goals and my faith goals for 2011. But I didn't scan those pages in, so here they are:

Art Goals for 2011:
  1. Finish all the "La Sirena" paintings. Even the massive one.
  2. Alter and create clothes, mori-style
  3. Tackle Madonna Montage wall-hanging
  4. Define my artistic style
  5. Devise an art series that shares hope/faith/love.
(They are probably all hairy audacious goals, but #5 would be quite the accomplishment if I got there.)

Faith Goals for 2011:
  1. Find time to be in silence with God and make it a new habit. (I've only been trying, and failing, to do this since June!)
  2. Go on retreat to St. Mary's at least twice...

Monday, January 3, 2011

Art and...

So for various reasons, I had put off making a sincere start on my first "La Sirena" painting for Suzi Blu's La Petit Academy class (which was supposed to end December 31, but we all got an extension!). Last weekend, I really got started.

I drew and colored in my mermaid, sent her off to Suzi for a critique ... and then started on the background. The pictures are a bit blurry because it was a race between me and the dying camera battery....

Spraying paint christened the easel well and truly....

Oh, I also managed to spray my iPhone which was sitting to the far left of the easel. Really fine spray, so I'm going to have to be a little more careful next time. Don't worry, it survived.

So that was the weekend of Christmas' work. This weekend just gone, I've added my mermaid and done some more painting, and the goal today is to fix the fix from Saturday (my shadows were a wee bit too red, so I managed to use acrylic glazing medium to blend it more and take some off, unfortunately, off means "back to the wood" in a couple of places. I like it, but I did it a little too much and want to restore some color.) Anywho.

As well as add more layers, plus some dimension to the painting and figure out what to do with her bodice area as that's the most incomplete looking part of the painting thus far. And maybe mess with the tail some more....

This is fun!

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It's no secret that we at GameSpy love the Rock Band. Intrepid PC Editor-in-Chief Sal "Sluggo" Accardo jumps on a capture station each week to show you what's new in Harmonix's weekly updates. We inevitably chat about what's fresh in the Rock Band store during our Podcast. And after setting a standard for downloadable content that's been tough for other games in the music game genre to match, Harmonix will hit a new milestone this week: downloadable albums. First up to bat is Judas Priest's 1982 classic "Screaming for Vengeance." We tag-teamed a few songs on the eve of the album's release on Xbox Live Marketplace tomorrow. It'll be coming to PS3 on Thursday as part of the PlayStation Store's weekly update.

The demand for more metal has been high, and although these tracks aren't quite as brutal as "Metallica Track Pack 1," "Screaming for Vengeance" isn't a walk in the park for casual players. The likes of "Take These Chains," "Bloodstone," and "You've Got Another Thing Comin'" are set to "Moderate" within the multiplayer menu, while other songs like "Fever," "Devil's Child," and "Pain & Pleasure" fall into "Skilled." The album's title track joins the annals of "Blistering" songs.

We didn't get to see how the songs' difficulty is measured on an instrument-by-instrument basis, since the Rock Band Store wasn't available in our offline content demo. Even so, Rob Halford's shrill vocals looked pretty tough to emulate, and the drumming certainly isn't simple, either. Alongside some of our cohorts at sister sites IGN and Team Xbox, we huddled into a room, cranked up the volume, and jumped into five of the nine tracks. We suggest you send those "Say It Ain't So" devotees on a snack run while the rest of the band gets a workout. Our time on drums with "Devil's Child" and "Riding on the Wind" was appropriately metal.

If you're interested in picking up the album, it's $14.99, which translates to 1200 Microsoft Points. Each individual track will cost the usual $1.99, or 180 Microsoft Points. Also, as a result of the release, the "Albums" section of the Rock Band Store will be unlocked with this release.

Keep an eye out for our video footage of "Screaming for Vengeance" this week!


text:
Well The thing is i’m pretty sure i should probably go see a professional about it, but i would really prefer not to. But to sum up the last few years of whats been going on. 2 friends died by being hit by cars ( they were walking ) both at different times, my parents got a divorce in 2008 both remarried in 2009… Both divorced again in 2011.. and they are getting back together now.. I was constantyl in the middle, i was loaning my father money to pay
his bills and same for my mother. In the last 3 months i have been laid off of my job, and now i’m in threat of loosing everything i have worked for. Although i have a really crappy job offering which i’m going to take to pay the bills. Now let me explain the recent problems..

Starting about 2-3 days ago i have been getting extremely mad at my wife and children for no reason. I don’t know why.. I get to the point where i’m afraid to get near my girls i’m afraid i’ll hurt them, so instead i have them go play outside. My wife is usually at work so i’m acting as stay at home dad right now, Occasionally and including right now, it seems like i can’t get enough oxygen into my system no matter how deep i breath or how much i try. I personally love my wife and children to death, i dislike society and humanity as a whole so i don’t have friends and don’t want them ( i also have no interest in seeing a therapist although it’s probably for the best ) I do not talk to most of my family only my father and mother, and thats only becuase i have to i would prefer if they would stay out of my life..

I absolutely hate myself and constantly think of suicide. Of course i would never act on it, but it doesn’t stop me from day dreaming about it. Also at nights, almost every night i have nightmares, they are never plesent in any way. Usually my kids or wife dying. I’m not happy with my life for sure, i want much more out of my life. I’m not afraid of dying, only of being forgotten.. I want to do something to be remembered..

I know this isn’t much of a question, but i’m seeking advice, i want to make the best of myself and such for my wife and kids, so i’m considering seeing a therapist, but i think it will be a waste of time. I’m not really addicted to games and such, i mean i do play on the computer but i don’t mind getting off to play with my kids or spend time with my wife, even if i don’t want to get off i dont’ get mad about it i just do it. And through the day i’m not really on much, only at night..

The other problem is my wife is being bothered by my sleeping habits. I usually go to sleep about 10-11AM and wake at about 2-3PM about 2-3 times a month i’ll go 24-36 hours without sleep altogether, i’m not forcing myself i just don’t feel tired.. i’ve tried sleeping pills and they have done nothing. My father had prescription sleeping pills i tried and still nothing ( i know it’s wrong )

umm, other than that i’m sorta addicted to sex.. I mean i want sex every single night.. of course the wife isn’t always int he mood which is understandable. But in the past when she denied me for whatever reason, i would just cuddle with her then go watch tv or play a game, but in the last couple of days, i have gotten so mad at her i wanted to kill myself.. It almost feels like i’m being denied love. I’m honestly not sure wtf is going on.. I’m assuming depression, and maybe a bit of anxiety.. But i’m no therapist. Any way Yeah what do you think.

A: What I think is what you think. Follow your own good instincts. You need the support and advice of a therapist who can give you more than what we’re able to do through a letter. For starters, it sounds to me that you are still grieving your friends and your parents’ unstable relationship and that you have a serious sleep disorder (that, btw, could contribute to your depression and your episodes of rage). You may be feeling even more upset about being unemployed than you are letting yourself acknowledge. Losing a job and feeling forced to take a “crappy” one is a major hit on most adults’ self-esteem. You are wise enough not to take your feelings out on the family who loves you but you do think about taking it out on yourself — which of course would do unestimable damage to the wife and children you leave behind. I wonder if you want sex so much because it is the only way you’ve found to truly relax.

As you can see, your letter left me with more questions than answers – except one: Do see a therapist and go into the project with as much courage, openness, and honesty as you can. Your family deserves it. So do you.

I wish you well.
Dr. Marie


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File:DSC 4050-MR-Braille.jpg

The braille system, devised in 1821 by Frenchman Louis Braille, is a method that is widely used by blind people to read and write. Each braille character or cell is made up of six dot positions, arranged in a rectangle containing two columns of three dots each. A dot may be raised at any of the six positions to form sixty-four (26) permutations, including the arrangement in which no dots are raised. For reference purposes, a particular permutation may be described by naming the positions where dots are raised, the positions being universally numbered 1 to 3, from top to bottom, on the left, and 4 to 6, from top to bottom, on the right. For example, dots 1-3-4 would describe a cell with three dots raised, at the top and bottom in the left column and on top of the right column, i.e., the letter m. In braille, pages are separated by a line so that you can feel going across the page.

The braille system was based on a method of communication originally developed by Charles Barbier in response to Napoleon's demand for a code that soldiers could use to communicate silently and without light at night called night writing. Barbier's system was too complex for soldiers to learn, and was rejected by the military; in 1821 he visited the National Institute for the Blind in Paris, France, where he met Louis Braille. Braille identified the major failing of the code, which was that the human finger could not encompass the whole symbol without moving, and so could not move rapidly from one symbol to another. His modification was to use a 6 dot cell — the braille system — which revolutionized written communication for the blind.

The Braille alphabet

Braille can be seen as the world's first binary encoding scheme for representing the characters of a writing system. The system as originally invented by Braille consists of two parts:

  1. A character encoding for mapping characters of the French language to tuples of six bits or dots.
  2. A way of representing six-bit characters as raised dots in a Braille cell.

Today different braille codes (or code pages) are used to map character sets of different languages to the six bit cells. Different braille codes are also used for different uses like mathematics and music. However, because the six-dot Braille cell only offers 64 possible combinations, of which some are omitted because they feel the same (having the same dots pattern in a different position), many Braille characters have different meanings based on their context. Therefore, character mapping is not one-to-one.

In addition to simple encoding, modern braille transcription uses contractions to increase reading speed. (See: Grade 2 Braille)

The Braille cell

File:Braille cell.svg

Braille generally consists of cells of 6 raised dots arranged in a grid of two dots horizontally by three dots vertically. The dots are conventionally numbered 1, 2, and 3 from the top of the leftward column and 4, 5, and 6 from the top of the rightward column.

The presence or absence of dots gives the coding for the symbol. Dot height is approximately 0.02 inches (0.5 mm); the horizontal and vertical spacing between dot centers within a braille cell is approximately 0.1 inches (2.5 mm); the blank space between dots on adjacent cells is approximately 0.15 inches (3.75 mm) horizontally and 0.2 inches (5.0 mm) vertically. A standard braille page is 11 inches by 11.5 inches and typically has a maximum of 40 to 43 braille cells per line and 25 lines.

As originally conceived by Louis Braille, a sequence of characters, using the top 4 dots of the braille cell, represents letters a through j. Dot 3 is added to each of the a through j symbols to give letters k through t. Both of the bottom dots (dots 3 and 6) are added to the symbols for "a" through e to give letters u, v, x, y, and z. The letter w is an exception to the pattern because French did not make use of the letter "w" at the time Louis Braille devised his alphabet, and thus he had no need to encode the letter "w".

English braille codes the letters and punctuation, and some double letter signs and word signs directly, but capitalization and numbers are dealt with by using a prefix symbol. In practice, braille produced in the United Kingdom does not have capital letters.

There are braille codes for representing shorthand (produced on a machine which embosses a paper tape) and for representing mathematics (Method Braille) and musical notation (braille music).

Writing braille

Braille may be produced using a slate and a stylus in which each dot is created from the back of the page, writing in mirror image, by hand, or it may be produced on a braille typewriter or Perkins Brailler, or produced by a braille embosser attached to a computer. It may also be rendered using a refreshable braille display.

Braille has been extended to an 8-dot code, particularly for use with braille embossers and refreshable braille displays. In 8-dot braille the additional dots are added at the bottom of the cell, giving a matrix 4 dots high by 2 dots wide. The additional dots are given the numbers 7 (for the lower-left dot) and 8 (for the lower-right dot). 8-dot braille has the advantages that the case of an individual letter is directly coded in the cell containing the letter and that all the printable ASCII characters can be represented in a single cell. All 256 (28) possible combinations of 8 dots are encoded by the Unicode standard. Braille with six dots is frequently stored as braille ASCII.

Letters and numbers

Other symbols

The question mark is dots 2,3,6 which you may notice is the same as the opening quotation mark. Therefore the placement of the dots -before a word or after a word- will determine which symbol it is.

Opening and closing parentheses are shown with the same symbol. Therefore, the placement context will determine whether the parentheses is opening or closing.

Grade 2 Braille Contractions

This is just a small sample of some of the contractions that are used in Grade 2 Braille. More information about Grade 2 Braille is below in the section on Braille transcription.

Unicode rendering table

Because of technical limitations, some web browsers may not display some special characters in this article.</small>

The Unicode standard encodes 8-dot Braille glyphs according to their binary appearance, rather than following the alphabetic order of any particular convention. Unicode defines the "Braille Patterns" character block in the hex codepoint range from 2800 to 28FF.

Braille Letter        Braille Letter
Template:CT-7 | ⠁ A 1 Template:CT-7 | ⠞ T
Template:CT-7 | ⠃ B 2 Template:CT-7 | ⠥ U
Template:CT-7 | ⠉ C 3 Template:CT-7 | ⠧ V
Template:CT-7 | ⠙ D 4 Template:CT-7 | ⠺ W
Template:CT-7 | ⠑ E 5 Template:CT-7 | ⠭ X
Template:CT-7 | ⠋ F 6 Template:CT-7 | ⠽ Y
Template:CT-7 | ⠛ G 7 Template:CT-7 | ⠵ Z
Template:CT-7 | ⠓ H 8 Template:CT-7 | ⠠ Capital sign
Template:CT-7 | ⠊ I 9 Template:CT-7 | ⠼ Number sign
Template:CT-7 | ⠚ J 0 Template:CT-7 | ⠲ Period
Template:CT-7 | ⠅ K Template:CT-7 | ⠂ Comma
Template:CT-7 | ⠇ L Template:CT-7 | ⠦ Question mark
Template:CT-7 | ⠍ M Template:CT-7 | ⠆ Semicolon
Template:CT-7 | ⠝ N Template:CT-7 | ⠖ Exclamation mark
Template:CT-7 | ⠕ O Template:CT-7 | ⠦ Opening quote
Template:CT-7 | ⠏ P Template:CT-7 | ⠴ Closing quote
Template:CT-7 | ⠟ Q Template:CT-7 | ⠶ Bracket
Template:CT-7 | ⠗ R Template:CT-7 | ⠤ Hyphen
Template:CT-7 | ⠎ S Template:CT-7 |

Braille transcription

File:Braille Writer.jpg
File:Braille on tablet box.JPG

Although it is possible to transcribe braille by simply substituting the equivalent braille character for its printed equivalent, such a character-by-character transcription (known as Grade 1 Braille) is used only by beginners.

Braille characters are much larger than their printed equivalents, and the standard 11" by 11.5" (28 cm × 30 cm) page has room for only 25 lines of 43 characters. To reduce space and increase reading speed, virtually all braille books are transcribed in what is known as Grade 2 Braille, which uses a system of contractions to reduce space and speed the process of reading. As with most human linguistic activities, Grade 2 Braille embodies a complex system of customs, styles, and practices. The Library of Congress's Instruction Manual for Braille Transcribing runs to nearly 200 pages. Braille transcription is skilled work, and braille transcribers need to pass certification tests.

In English, the system of Grade 2 Braille contractions begins with a set of 23 words which are contracted to single characters. Thus the word but is contracted to the single letter b, can to c, do to d, and so on. Even this simple rule creates issues requiring special cases; for example, d is, specifically, an abbreviation of the verb do; the noun do representing the note of the musical scale is a different word, and must be spelled out.

Portions of words may be contracted, and many rules govern this process. For example, the character with dots 2-3-5 (the letter "f" lowered in the braille cell) stands for "ff" when used in the middle of a word. At the beginning of a word, this same character stands for the word "to" although the character is written in braille with no space following it. At the end of a word, the same character represents an exclamation point.

The contraction rules take into account the linguistic structure of the word; thus, contractions are not to be used when their use would alter the usual braille form of a base word to which a prefix or suffix has been added. And some portions of the transcription rules are not fully codified and rely on the judgement of the transcriber. Thus, when the contraction rules permit the same word in more than one way, preference is given to "the contraction that more nearly approximates correct pronunciation."

Grade 3 Braille is a system that includes many additional contractions, almost a shorthand; it is not used for publication, but is used mostly for individuals for their personal convenience.

The current series of Canadian banknotes have raised dots on the banknotes that indicate the denomination and can be easily identified by visually impaired people; this 'tactile feature' does not use standard braille but, instead, a system developed in consultation with blind and visually impaired Canadians after research indicated that not all potential users read braille.

Though braille is thought to be the main way blind people read and write, in Britain (for example) out of the reported 2 million visually impaired population, it is estimated that only around 15-20 thousand people use Braille. Younger people are turning to electronic text on computers instead; a more portable communication method that they can also use with their friends. A debate has started on how to make braille more attractive and for more teachers to be available to teach it.

In India there are instances where the parliament acts have been published in Braille too. For example 'The Right to Information Act'

Braille for other scripts

See main articles: Hebrew braille, Japanese braille, Korean braille, Vietnamese braille and Tibetan braille, Chinese braille.
File:Braille notice board.JPG
File:Safdarjungtomb notice.jpg

There are many extensions of Braille for additional letters with diacritics, such as ç, ô, é.

When braille is adapted to languages which do not use the Latin alphabet, the blocks are generally assigned to the new alphabet according to how it is transliterated into the Latin alphabet, and the alphabetic order of the national script (and therefore the natural order of Latin braille) is disregarded. Such is the case with Russian, Greek, Hebrew, Arabic, and Chinese. In Greek, for example, gamma is written as Latin g, despite the fact that it has the alphabetic position of c; Hebrew bet, the second letter of the alphabet and cognate with the Latin letter b, is sometimes pronounced /b/ and sometimes /v/, and is written b or v accordingly; Russian ts is written as c, which is the usual letter for /ts/ in those Slavic languages that use the Latin alphabet; and Arabic f is written as f, despite being historically p, and occurring in that part of the Arabic alphabet (between historic o and q). Esperanto letters with circumflexes, ĉ, ĝ, ĥ, ĵ and ŝ, are written as those letters without circumflexes with a filled sixth dot. Therefore the letter ĵ has the same representation as the English w and to write a w in Esperanto, the dot 3 is filled (dots 2-3-4-5-6 are used for w instead of dots 2-4-5-6) The ŭ, used in Esperanto also, is as the u but the first dot is moved to the fourth place.

Greater differences occur in Chinese braille. In the case of Mandarin Braille, which is based on Zhuyin rather than the Latin Pinyin alphabet, the traditional Latin braille values are used for initial consonants and the simple vowels. However, there are additional blocks for the tones, diphthongs, and vowel + consonant combinations. Cantonese Braille is also based on Latin braille for many of the initial consonants and simple vowels (based on romanizations of a century ago), but the blocks pull double duty, with different values depending on whether they're placed in syllable-initial or syllable-final position. For instance, the block for Latin k represents old-style Cantonese k (g in Yale and other modern romanizations) when initial, but aak when final, while Latin j represents Cantonese initial j but final oei.

However, at least three adaptations of Braille have completely reassigned the Latin sound values of the blocks. These are, Japanese braille, Korean braille, and Tibetan braille.

In Japanese Braille, alphabetic signs for a consonant and vowel are combined into a single syllabic block; in Korean Braille, the consonants have different syllable-initial and syllable-final forms. These modifications made Braille much more compatible with Japanese kana and Korean hangul, but meant that the Latin sound values could not be maintained.

In French Braille, because of the letters not in the English alphabet, those extra letters are assigned cells which are used for contractions in English Braille. Because of this, grade 2 Braille cannot be used and therefor French Braille is in uncontracted Braille (or grade 1 Braille) only.

See also

External links

Language Specific Resources

Computer Resources

Template:Writing systems

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text:
Top Definition
Drunk. Very drunk. No longer functional in any meaningful way.
Del was so boiled, he yacked in the taxi.
por redheadbass 22 de Janeiro de 2011
4 more definitions
The equivalent of being baked but through means of boiling marijuana into a tea and drinking the contents to get high, apposed to smoking or eating the cannabis.
"Awe dude, after that cup of dank bud chai i got sooo boiled!
por shakamaster 01 de Maio de 2012
Extremely High
Darrel:Just Boiled er what?
Larry:Duuuuu jer.
por Scrub pup 10 de Julho de 2008
The exact point when a combination of things (Hangover, Tiredness, Girlfriends/Boyfriends, Heat, Noises) culminate to produce the biggest stress head you have ever had.

Normally signalled by a large release of breath follwed by the exclamation "Booooiiillllleeeedd" in a high pitched tone.

A boiled head can be cured by beer, sleep or a "reflection hour" where the topics that have boiled your head are discussed with friends

See also cooked ,stressed.
Dude 1: Maan, Mike had a crazy night last night, he was in the club and about 5 of his ex girlfriends were there. He got home at 5am and had work at 8am! I hear his ex has been on to him all day too

Dude 2: Isn't he working duty til 10pm?

Dude 1: Oh man he must be BOILED!

*Mike walks in*

Mike: Boooooiiiiiillled!
por ManChild1984 13 de Junho de 2011
Getting high or drunk. Then smoking and getting high or getting drunk. Therefor getting totally boiled. Being High And Drunk.
Dude im so boiled. Yeah i got high then got drunk.
por Imacreeper 03 de Agosto de 2010

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Infect Immun. 2010 January; 78(1): 32–38.
Published online 2009 November 9. doi:  10.1128/IAI.00929-09
PMCID: PMC2798221

Precarious Balance: Th17 Cells in Host Defense [down-pointing small open triangle]

Lineage-specific responses from the effector T-cell repertoire form a critical component of adaptive immunity. The recent identification of Th17 cells—a third, distinct lineage of helper T cells—collapses the long-accepted paradigm in which Th1 and Th2 cells distinctly mediate cellular and humoral immunity, respectively. In this minireview, we discuss the involvement of the Th17 lineage during infection by extracellular bacteria, intracellular bacteria, and fungi. Emerging trends suggest that the Th17 population bridges innate and adaptive immunity to produce a robust antimicrobial inflammatory response. However, because Th17 cells mediate both host defense and pathological inflammation, elucidation of mechanisms that attenuate but do not completely abolish the Th17 response may have powerful implications for therapy.

Different classes of microbes elicit lineage-specific responses from the effector T-cell repertoire. Whereas helper T1 (Th1) cells are involved in cellular immunity against intracellular bacteria and viruses, Th2 cells mediate the humoral response to parasitic infection. Regulating the activation and expansion of these lineages are regulatory T cells (Tregs), a third subset of CD4+ T cells that holds the inflammatory response in check. Recently, the identification of a novel lineage of helper T cells, Th17, has collapsed the long-held paradigm that three lineages (Th1, Th2, and Treg) derive from naïve CD4+ T cells (Thp). Distinguished by the production of interleukin-17 (IL-17), these Th17 cells develop from Thp progenitors along a fourth distinct pathway under the influence of a network of inflammatory cytokines, including IL-1, IL-6, and transforming growth factor beta (TGF-β), which support commitment to this lineage, and IL-23, which stabilizes the phenotype of differentiated Th17 cells (27, 46, 70, 94). Studies of infectious disease highlight the critical role of the Th17 response in host defense against extracellular pathogens, particularly Gram-negative bacteria that colonize mucosal surfaces. More recent observations implicate Th17 cells in the immune response to facultative and obligate intracellular pathogens, including intracellular bacteria and fungi. However, whether Th17 cells mediate essential antimicrobial mechanisms or drive tissue destruction in these contexts remains unclear. This minireview will focus first on the general mechanistic paradigm associated with IL-17-mediated host defense and then discuss findings on the involvement of the Th17 response during infection by extracellular and intracellular bacteria and fungi. Emerging trends highlight the capacity of Th17 cells to bridge innate and adaptive immunity, while balancing the host on the precarious precipice between protective immunity and pathological inflammation.

Seminal studies linked increased morbidity during mucosal infection to dysfunctional IL-17 signaling (22, 61, 99). Consequently, interest grew in the protective mechanisms that characterize the Th17 response (Fig. (Fig.1).1). Production of IL-17 by CD4+ T cells has been demonstrated during the first 24 h of infection with extracellular bacteria (12, 26). Such activity is consistent with peripheral populations of constitutively activated IL-17-producing T cells observed in uninfected mice and implicates Th17 cells in immune surveillance and the first line of host defense (74). Additionally, IL-17 production has been observed from CD4+ T cells during a later time frame that coincides with the elaboration of adaptive immunity (89, 105). Evidence suggests that efficient Th17 differentiation requires high-dose antigen (Ag) stimulation through the T-cell receptor and additional stimulation through the costimulatory surface receptor CD40. (36, 73) Stimuli associated with severe infection—like coincidental activation of complement and Toll-like receptors (TLRs) or significant apoptosis in the intestinal epithelium—favor Th17 differentiation at the expense of the Th1 lineage (21, 89). Such stimuli promote proinflammatory cytokine release from antigen-presenting cells: of these, dendritic cell (DC)-derived IL-6 is critical for Th17 differentiation in murine models (21, 73, 90). In addition to traditional Th17 cells, CD8+ T cells (26), activated memory γδ T cells (66, 81, 85), and invariant natural killer T cells (19, 56) have been identified as IL-17 producers during the early response to extracellular infection. However, the extent to which IL-17 production from these alternative sources is crucial, compensatory, or redundant likely varies with each infection (26, 81).

FIG. 1.
Mucosal infection engages the Th17 axis of host defense. (A) Peripheral dendritic cells activated by pathogens produce IL-23, which upregulates IL-17 and IL-22 production from resident memory Th17 cells. (B) Synergy between IL-17 and IL-22 induces secretion ...

The near-ubiquitous expression of the IL-17 receptor facilitates the pleiotropic effector mechanisms of IL-17. Alone or in synergy, the Th17 effector cytokines IL-17 and IL-22 induce an array of antimicrobial peptides, including β-defensin-2, lipocalin 2, and members of the S100 family from colonic, skin, and airway epithelia (4, 11, 41, 50, 105, 106). Cytokines involved in the Th17 response, IL-1 and IL-6, are implicated in protecting the integrity of the colonic epithelium during bacterial infection (17, 48). IL-17 also induces chemokine expression in nonimmune cells. Upregulation of neutrophil-chemotactic IL-8 (CXCL8), macrophage inflammatory proteins 1 and 2 (MIP-1 and -2), and macrophage/monocyte-chemotactic protein 1 (MCP-1) (CCL20) by IL-17 turns infected sites into an innate immune cell sink (45, 61, 99, 105). IL-17 enhances the function and survival of recruited macrophages (80), and its effects on granulocytes appear even more pronounced. In addition to mediating neutrophil recruitment, IL-17 promotes granulopoiesis via the induction of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) and potentiates neutrophilic cytotoxicity and phagocytosis (32, 53, 99). It is tempting to speculate that this neutrophil influx reinforces the involvement of the IL-17 axis by providing stimuli involved in Th17 differentiation. As recruited neutrophils apoptose and are phagocytosed by resident activated antigen-presenting cells, naïve-T-cell fate may be further biased toward the Th17 lineage (89), thus giving rise to Th17-associated adaptive immunity. Although IL-17 primarily galvanizes the innate branch of host defense, recent evidence suggests a role for this cytokine in initiating the B-cell response, an aspect of immunity typically associated with Th2-related follicular T cells and Th2 cytokines (75, 101). In an ovalbumin-induced murine model of airway inflammation, adoptive transfer of Th17 clones leads to the induction of IgA and IgM and the recruitment of B cells (38), a function that may be supported by the preferential expression of B-cell chemoattractant CXCL13 on Th17 cells (88, 101).

The mechanisms by which the Th17 response is attenuated postinfection remain ill defined. Binding of IL-17 to its receptor has been proposed to play a role in clearance of this cytokine (85), and the induction of Th17 cells that coexpress the anti-inflammatory cytokine IL-10 may lead to a subsequent stage of dampened inflammation (89). As bacterial burden decreases, phagocytosis of apoptotic but increasingly uninfected neutrophils by DCs may downregulate the Th17-stabilizing cytokine IL-23 (86). Notably, the vaccine-induced kinetics of Th1 and Th17 populations suggest that activation of the IL-17 axis may partially induce a subsequent Th1 response that then attenuates IL-17 production through inhibitory effects of the Th1-produced cytokine gamma interferon (IFN-γ) (43, 65, 74). On the other hand, abundance of the antiapoptotic protein c-FLIP in Th17 cells decreases their susceptibility to activation-induced cell death, a known mechanism of clearance of Th1 cells (100). The Th17 subset also appears to subvert Treg-driven immunosuppression; unlike IFN-γ, Th17-associated IL-6 inhibits rather than enhances tryptophan catabolism, which is a process associated with Treg induction (18). In the absence of attenuation, Th17-associated effector mechanisms can mediate tissue injury through protracted local inflammation, a feature of certain chronic biofilm infections (20, 29, 78, 84).

According to the Th1/Th2 paradigm, different subsets of helper T cells protect against distinct types of infections; while Th1 cells primarily respond to intracellular pathogens, Th2 cells are principally associated with humoral immunity. Similarly, Th17 cells are thought to mediate immunity against another class of pathogen: extracellular bacteria, particularly those that colonize exposed surfaces like the airways, skin, and intestinal lumen. Mice infected by Klebsiella pneumoniae (25, 99), Bordetella pertussis (30), or Streptococcus pneumoniae (53, 105), for example, mount a Th17 response, and disruption of IL-17 signaling increases susceptibility in these models. Intact signaling appears particularly critical for the induction of a chemokine gradient that facilitates the recruitment of innate immune cells to the site of infection; however, the extent to which monocytes/macrophages or neutrophils account for the bulk of the IL-17-mediated cellular infiltrate varies with the infection (81, 98, 99, 105). Deficiency in IL-23, a cytokine that induces IL-17 production from memory cells and stabilizes the Th17 phenotype in effector cells (2, 87), also exacerbates pathology, but at least in the case of K. pneumoniae infection, exogenous IL-17 can compensate for the absence of IL-23 (25, 81). A critical role for the IL-23-IL-17 axis in these infectious models is supported by vaccination studies; activation of the Th17 lineage by pertussis toxin and pneumococcal antigen is required to confer full protection against subsequent infection (30, 53, 55).

Although host defense against extracellular bacteria is widely considered the Th17 domain, some evidence indicates that efficient protection requires synergy between the Th1 and Th17 lineages. For example, challenge by Bordetella pertussis induces both transient IFN-γ production that coincides with the peak phase of infection and extended IL-17 production that precedes the Th1 response and persists until clearance. Continuous neutralization of IL-17 modestly increases early bacterial load, but neither delays nor impedes ultimate resolution (3). This finding supports other work that suggests a role for the Th1 response in clearance (3, 57). Similarly, IL-12- and IL-23-deficient mice have targeted defects in the Th1 and Th17 networks, respectively, but both experience increased though comparable susceptibility to Klebsiella pneumoniae. Administration of IL-17 more effectively attenuates pathology in IL-23-deficient than in IL-23-/IL-12-deficient mice, suggesting a unique protective role for the Th1 axis (25). Thus, whether it would be more accurate to classify extracellular bacterial pathogens under a shared Th1/Th17 domain of host defense remains to be elucidated. Further contributing to this uncertainty are indications of the potentially detrimental nature of the Th17 response elicited by certain extracellular pathogens. Th17 cell infiltrates contribute to pathological abscess formation in response to Bacteroides fragilis (12), and modulation of macrophage function toward a Th17-conducive phenotype may facilitate persistent colonization by Bordetella bronchiseptica (82).

Chronic microbial infections in the setting of human disease underscore the precarious balance between inadequate host defense and unregulated inflammation. Immunocompromised hosts with defects in Th17 expansion, including HIV/AIDS patients and individuals with hyperimmunoglobulin E syndrome (HIES, or Job's syndrome), are susceptible to opportunistic infections by Staphylococcus aureus, Haemophilus influenzae, and Streptococcus pneumoniae, among others (15, 31, 59, 72). In HIV infection, Th17 cells are preferentially depleted from the gastrointestinal lymphocyte compartment, despite the unresponsiveness of this subset to viral antigens (9). Because the Th17 lineage is critical for mucosal homeostasis, their selective depletion compromises intestinal integrity and facilitates the translocation of microbial products across the epithelial barrier during progressive disease (10). However, there is some indication that infection does not similarly deplete the bronchoalveolar Th17 population (9), so the precise link between defects in the IL-17 axis and the high incidence of pneumonia remains unclear. In the case of HIES, mutations in the signal transducer and activator of transcription-3 (STAT3) gene preclude the generation observed in healthy patients of Th17 memory cells against common microbes, such as Staphylococcus aureus and Candida albicans (54, 58). Although HIES is characterized by a systemic deficiency in IL-17 production, recurrent staphylococcal infections are typically confined to the skin and lung. However, the bronchial and dermal epithelium appears particularly sensitive to synergy between IL-17 and classical proinflammatory cytokines, and such dependence may account for this apparent contradiction (59).

Excessive activation of the Th17 lineage may help precipitate and sustain inflammatory diseases in which microbial antigens contribute to disease etiology and/or pathogenesis. For example, deficiency in IL-17 inhibits the development of a canonical form of hypersensitivity pneumonitis (40, 84), a set of pulmonary disorders that results from chronic exposure to inhaled antigen, including Saccharopolyspora rectivirgula and other pathogenic bacteria (5). Likewise, animal models of allergen-induced airway and contact hypersensitivity suggest that the hyperreactivity of the Th17 lineage toward microbial antigens and homologous endogenous ligands contributes to pathology (64, 71, 92, 96). This has potential implications for our understanding of their human counterparts—severe asthma and allergen contact dermatitis, in which elevated levels of IL-17 have been observed (39, 47, 52, 62). Thus, establishing the mechanisms that regulate the Th17 response without entirely abolishing it will have important implications for therapy development.

Studies examining T-cell polarization in response to pathogen-associated molecular patterns (PAMPs) have identified an array of fungal components that preferentially induce the Th17 lineage (1, 9), suggesting a role for Th17 cells in fungus-induced host defense. Interestingly, recognition of these fungal PAMPs can occur independently of signaling by Toll-like receptors (TLRs), the primary but not exclusive receptors for PAMPs (93). For example, deficiency in the adaptor TRIF (TIR domain-containing adapter-inducing IFN-β), a downstream mediator of TLR signaling, does not preclude Th17 development in response to infection by Candida albicans (18). Indeed, under certain conditions, TRIF deficiency even enhances IL-17 production by dampening signals from the Th1 and Treg lineages that inhibit Th17 development (6, 18). Accordingly, alternative pathogen recognition receptors have been identified that bypass TLR signaling to activate the Th17 lineage. One such cascade engages dectin-1, a β-glucan receptor on antigen-presenting cells that can signal in concert with or independently of TLR2. In response to certain fungal glucans, dectin-1 sidesteps synergy with TLR2 and activates DCs by engaging the kinase Syk and adaptor CARD9, ultimately resulting in the induction of Th17 cells (49). In another example, monocytes activated through the mannose receptor by C. albicans mannan drive IL-17 production during coculture with human memory T cells (93). Such findings may have important implications not only for understanding the host response to fungal pathogens, but also in the context of autoimmunity. Further studies of these alternative PAMP receptors may suggest new targets for adjuvants that preferentially skew the T-cell repertoire toward certain lineages and may also reveal homologous endogenous ligands that drive autoimmune pathology (7).

Consistent with the ability of fungal components to drive IL-17 production, some animal models of opportunistic fungal infections suggest a positive, and in some cases essential, role for Th17 cells. Neutralization of or deficiency in IL-23 or IL-17 during disseminated and oral candidiasis and pulmonary aspergillus, among others, exacerbates pathology characterized by inadequate neutrophil recruitment, increased fungal burden, and reduced chemokine and antimicrobial expression (13, 35, 77, 95). In support of these findings, reexposure to antigen drives IL-17 production by human memory T cells specific for C. albicans antigen (1, 93, 95). However, vaccination models of Ag-induced protection and infection by C. albicans in TRIF−/− mice have linked the Th17 lineage to deleterious inflammation rather than protective immunity and buttress the prior emphasis on the Th1 lineage for host defense (7, 18, 68). Several of the fungal antigens identified as nonprotective in vaccine drive DCs toward an alternative activation state characterized by IL-23 rather than IL-12 production, thus supporting the expansion of the Th17 (sometimes concomitantly with the Th2) lineage at the expense of the Th1 and Treg lineages (18). Such bias results in tissue injury and reduced fungal clearance, in part by impairing the killing activity while extending the viability of recruited neutrophils (8, 102). Furthermore, expansion of the Th17 subset establishes a positive feedback loop that favors the Th17 response (18, 102) and inhibits the induction of Tregs required for homeostatic tolerance to commensal but opportunistic fungal pathogens (6, 63).

Infection by intracellular bacteria is classically considered the Th1 domain of host defense. However, current knowledge of the immune response during listeriosis illustrates the degree of uncertainty that remains about the role of IL-17 in host defense against this class of pathogen. A facultative intracellular bacterium, Listeria monocytogenes, tends to colonize phagocytes and induces a robust response associated with the prototypical Th1 cytokine IFN-γ (23, 33, 34). However, the essential role of IFN-γ has been called into question by studies demonstrating that IFN-γ deficiency does not preclude the generation of Ag-specific CD4+ T cells (28). Indeed, additional factors unassociated with the Th1 lineage, including IL-1 and IL-6, have been increasingly recognized for their protective role (37, 51, 67, 76). Additionally, production of IL-6 is linked to early neutrophilia, a phenomenon required for resolution of L. monocytogenes infection (16).

At the time of these studies, Th17 cells had not yet been distinguished as a distinct subset of helper T cells. Given that IL-6 and IL-1 are cytokines intimately associated with the Th17 lineage, which is known to mediate granulopoeisis and neutrophil chemotaxis, the possibility emerges that the Th17 lineage may be critical for the early host response to L. monocytogenes. Recent studies verify this link, with some evidence arguing for an essential role for IL-17. IL-17 production is localized to a third of hepatic γδ T cells and increases during the first 5 days of L. monocytogenes infection (24). IL-17A−/− mice experience higher morbidity than their wild-type counterparts, and infection in knockouts is characterized by increased bacterial burden, decreased neutrophilic induction, and malformed granulomatous lesions (24, 60). However, other evidence suggests that the contribution of IL-17 may serve a more compensatory function under unfavorable conditions. The absence of type I and II interferon signaling abrogates the Th1 response; in this situation, a low-magnitude Th17 response to Listeria is observed. This shift in CD4+ T-cell lineage commitment does not preclude resolution of infection (69). Cross-protection may be another method by which the Th17 lineage is recruited for anti-L. monocytogenes responses. Mice infected with Mycoplasma pulmonis exhibit enhanced protection against secondary infection with L. monocytogenes resulting from IL-17-induced neutrophil mobilization (83).

The lingering doubt about the role of IL-17 during L. monocytogenes infection reflects our generally incomplete picture of the Th17 lineage during host defense against intracellular bacteria. Studies of other intracellular infections, such as Salmonella enterica serovar Enteritidis (79), Toxoplasma gondii (42), and Chlamydia trachomatis (103), indicate a nonredundant role for IL-17 in complete bacterial clearance. Synergy between the Th1 and Th17 lineages has also been observed in response to postvaccination Mycobacterium tuberculosis challenge and Chlamydia muridarum, with some suggestion that deficiency in IL-17 impairs the expansion of antigen-specific Th1 cells (43, 91). Additionally, studies of primary infection by Mycobacterium tuberculosis indicate that the IL-23/IL-17 axis accounts for the modest protective response observed in the absence of Th1-associated IL-12 (14, 44). However, others suggest that the induction of a robust Th17 response is a detrimental supplement or even a malignant subversion of the protective Th1 response (97, 107). Another important consideration in evaluating the protection afforded by the Th17 lineage is the stage of infection. Some reports identify IL-17 function as part of the innate γδ T-cell response and neutrophil induction during the early response to intracellular bacteria (24, 79). However, findings diverge on the involvement of classical CD4+ Th17 cells and the Th17 adaptive immune response to these infections (79, 104). Some evidence indicates that IL-17 may bridge the innate and adaptive immune responses by supporting the generation of Th1 adaptive immunity; indeed, a murine model of vaccination against Mycobacterium tuberculosis suggests that IL-17 may play a crucial albeit indirect role in the recruitment of the Th1 cells required for efficient recall responses (43). It will be interesting to see whether underlying these diverging observations there are as yet undiscovered mechanisms that dictate the role of the IL-17 axis during infection by intracellular pathogens.

A population that bridges innate and adaptive immunity, Th17 cells are uniquely primed to mediate surveillance and early defense during mucosal infections by extracellular bacteria. However, the intensity of IL-17-driven inflammation may undermine the Th1 lineage and subvert more sustainable antimicrobial responses during intracellular infection by certain bacterial and fungal pathogens. Thus, elucidation of mechanisms that govern the amplification and attenuation of the Th17 lineage will have important implications for therapy. Particularly in the context of chronic infectious diseases that afflict both immune-compromised and immunocompetent hosts, strategies that restrain but do not entirely abolish the Th17 response will likely be critical to avoid magnifying susceptibility or pathological inflammation.

Editor: J. B. Kaper

[down-pointing small open triangle]Published ahead of print on 9 November 2009.

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Tuesday, November 8, 2011

My C-Cups Nay Runneth Over

You can laugh all you like Madonna, but I still want to squeeze that almost non-existent arse of yours.
Coz when I returned from the Melbourne Cup Day vintage fashion parade last Tuesday, you were my inspiration to strip down and don my 1970s le smoking-style wool suit.
I couldn't help it - the voices were screaming your name and I caved.

I snaffled this original 1970s suit, complete with satin collar and trouser side-stripes, from eBay a few months ago.
I'm pretty sure the seller had a bad case of "oh no what the feck have I done?" after I bought it coz she turned out to be a bit of a biatch.
But ya know, I think you've gotta be a god damn, fecking awesome bitch to wear this suit and if my prosti La Dama could do my eye make up for me, I reckon I could melt anyone into soup with my stink-eye look.

Except for one (or two) things.
I bought a 34C cup 1950s longline cotton bra from eBay thinking I could wear it as a top all this summer, but there's this one problem of a sad lack of boobage.
What the hell?
How come I fit all my other modern bras in that size?
Am I missing something?
Well yes, I know that quite clearly I'm missing some titties to fill the cups, but did they measure lingerie differently 50 years ago?
I mean a 34C is a 34C right?

I still reckon it's a feck-off awesome suit tho' and I can always wear my 1950s strapless black lace bustier.

Never mind all that boobage bollocks, I'm still going to wear it as a top and all those other bitches can go stick it.
See what happens when you channel Madonna?
All the swearing and attitude comes out.
God I love her.

An' I love all you gorgeous biatches!!!
Desiree xoxoxoxo

Miss Tallulah Porkchop said...

I have some great Madge bras. Modern sizing, retro look. What Katie Did makes bras that shape your boobs into perfect cones! :)

That necklace is fantastic! I'm drooling a little.

Madame G said...

You look Smokin' in that suit! I've got a bullet bra too that's supposed to fit me. It doesn't. But I did get a nice wee pair of cone-shaped fillers to sort the problem! x

Lakota [Faith Hope and Charity Shopping] said...

You make a better Madonna than Madonna does these days! It's a beautiful beautiful suit, you look GAW-JUS!

Kitty said...

And I love YOU right back, too bad that sexy man snapped you up, or there could be some serious frottage of the sapphic variety goin' on around here!!!! I always find vintage bras are smaller than their modern equivalents. Have you got your hot sticks yet??

Psycho Sue- Sew Misunderstood said...

you are fucking HOT as HELL! I would shake in my panties if you walked up to me!

VainGlorySinner said...

You make a wonderful Madonna!

Love the suit! I used to have a pair of trousers almost exactly like them when I was younger! They had the shiny satin black stripe down the side of the legs too. I always thought they reminded me of geeky band trousers but they look excellent on you!

I think everyone in the 50s must have either stuffed their bullet bras or had super pointy boobs! x

Style Sud-Est said...

Hey, Hey, hey, you look, how do you say it... fecking hot in this suit! God you are smokinnnnn in that frock girl, ouh, ouh! forget the booby thing who cares!

Desiree, I love your feature on Miss P's blog, love your attitude and love what you said to your colleague about getting old, bastard he was!
I would have said the same to the fecker!

Thanks for your comment on my blog!

Love you ! Ariane xxxx

sylvia @ 40PlusStyle said...

This is so good. Love the attitude, love the suit! And yes, I'm a Madonna fan as well...

Mrs. D said...

Great outfit and even better attitude!
Thank you for following me back, I'm really flattered!

Glee said...

You look so hot and stylish in this killer all black outfit. I like it. :)

delia hornbook said...

ha ha ha ha ha ha i love you so much you have an amazing sense of style and sense of humour ;-)) You rock the suit loving your shoes. dee xx

tralala said...

And you could also swap out those suit trousers for the green lurex ones ...

Madonna who?

La Dama said...

Te amo Desireesita..I love your Marlene Diedrich suit amor!
I would love to paint your beautiful big eyes. you did a great job, smokey eyeshadow is my fave. forget Madonna has shit on you. the bra needed those bra pads that make your chi chis pointy. I need to get me some too for my bullet bra. I adorar your curly gorgeous locks.

Krista said...

FRIGGIN BAM BADA BOOM, dang mama you are looking FIERCE in this suit. I mean I'm kinda cowering at your command of the suit, and your body is BANGIN!!!!!! Madonna has nada on you!

Pointy banana boobs meh, never did much for me, I prefer my boobs a bit smooched and overflowing :)

I love the curls in your hair and the second to the last photo is so sexy smug ~ I want you on my FRIG so I can look at that face every morning as I stumble around my kitchen in the dark cursing to the world making coffee.

You are gorgeous. I hope married life is treating you well and that you guys are "spending lots of quality time together" :) Ya gotta love love baby!

pastcaring said...

You look so hot, who cares whether the C cups are full or not?!
That suit is fabulous, I adore the necklace, and as always you are the BEST poser! I agree with Krista, that second to last pic of you is a stunner.
I know you were channelling Madonna, but it makes me think of Bianca Jagger's white trouser suit and Studio 54. Show us your moves, Desiree!! xxxxxxxxxxxxxxxxxx

Catherine said...

You are very beautiful! much better than Madonna)

Tomye said...

You are a trip Desiree! I love this look and am looking for something myself only with tails. You can always buy some boobs to fill out that sweet little cami. You are class and style squared! -T

Vix said...

You're dressed so much like my Mum used to when she went to posh do's it's uncanny. She much preferred a man's dinner suit, skimpy top and a velvet cummerbund & bow tie.
I love it, those trousers fit you like a freaking dream and you could always pad out those cups with chicken fillets, you gorgeous creature. xxx

Fashionistable said...

Have just read Sacramento's post about and had to come over and say hello, You are amazing. Xxxx

sacramento said...

People love your feature, but I am not surprised. Your absolutely Rock, my dearest friend.
Yeahhhhhhh Madona and you for ever

Vintage Coconut said...

*MmmeeeoooW* Des you are looking SMOKING hot!

pinktutu72 said...

Woooo weeee hot mama! You're tons sexier than The Material Girl. I love the way that suit looks on you. What a sexy bitch!

Thick Threads said...

you are so gorgeous! just saw you on mispapelicos blog and thought wow! what a gorgeous woman with amazing timeless style! love the blog and love this outfit! you look better than madonna :)

Susan Tiner said...

You totally crack me up :).

I love the Le Smoking suit. Very chic, and the big bra cups make it just a wee bit naughty.

LA Lynn's said...

I saw your feature on Sacramento Blog & now I am a new STALKER/FOLLOWER!!!! I absolutely ADORE your sense of style & humor... I think I will be reading your blog for the rest of the night! :))

Heather Fonseca said...

Clothing sizes have changed dramaticly over the decades. In vintage clothing I wear like a size 20. In today's clothing I'm about a 10 or a 12 (American). It would make sense that bras have changed too, and then there's the fact that bra sizing is not consistent anyway. I'm a "G" cup in some French brands, a "DDD" in some English brands, and I shrink down to "DD" or "D" in American brands. Go figure.

Vintage Sweetheart said...

Seriously what can't you wear??? Your suit looks amazing and you definitely have the attitude to pull it off!

Dash said...

Desiree you rock that suit girl, I love 'Le Smoking'.

Apologies for being such a terrible blogger, I have just been through your previous posts...you got MARRIED!

Many congratulations to you and your gorgeous man, you were a stunning bride I adored your wedding outfit.

joshylola said...

Amazing shoes.I follow your blog.Regards

RETRO REVA said...

Me thinks your cup(s) runneth over!
I cannot fit vintage either. The slips usually are more 'generous' in the cup for some reason, but in orfer to fit a skirt or dress of vintage, I must buy a size 16 usually to go round my belly!
Gorgeous suit my love!!!!!

Helga! said...

The Style Crone said...

How amazing you are! Pure glamour!

triskelos said...

Such a bummer - I have some troubles with vintage sizing too. I'm Brittish size 10-12, but I know for sure that when it comes to vintage dresses, 14 can be a bit tight.
But that bra still looks great. I'd love to have one of my own - it makes one pretty and really sexy top)

Tallulah May Vintage Socialite. said...

You look amazing in this suit and you are amazing everyone girl needs a girlfriend like you.

Love Flow said...

We love u 2

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1. Facile
a. Having an artificial or deceptive front.
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d. Done with little effort or difficulty.

2. Fastidious
a. Moving quickly and efficiently.
b. Displaying careful attention to detail.
c. Abstaining from eating.
d. Being firmly fixed or fastened.

a. Containing solidified animal or vegetable oil.
b. Obesity; corpulence.
c. Inspired with unreasoning love or attachment.
d. Ridiculous; smugly foolish.

4. Fettle
a. Proper or sound condition.
b. Courage and fortitude; spirit.
c. One of various stinging plants.
d. A chain or shackle for the ankles.

5. Filch
a. A small paint brush.
b. To tell on; betray.
c. To steal or take in a furtive manner.
d. Debris which collects in an irrigation ditch.

6. Florid
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b. In a watery state; liquid.
c. Very ornate; flowery.
d. Any of several gold coins formerly used in Europe.

7. Folly
a. A lack of good sense or understanding.
b. A large sheet of paper.
c. A shrub having glossy, evergreen leaves.
d. A young female horse.

8. Fulsome
a. Healthily plump and ample of figure.
b. Promoting the growth of; inciting.
c. Being full of things; abounding.
d. Offensively flattering or insincere.

9. Funicular
a. Operated or moved by a cable.
b. A sombre dance performed at certain funerals.
c. Pertaining to playful, often noisy, activity.
d. The lower wing segment of a moth.

10. Furlong
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