text:
Models of PNH development
PNH as a consequence of poor cell growth?
Commentary Free access | 10.1172/JCI11002
Genetic and environmental effects in paroxysmal nocturnal hemoglobinuria: this little PIG-A goes "Why? Why? Why?"
Neal S. Young and Jaroslaw P. Maciejewski
Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA
Address correspondence to: Neal S. Young, National Heart, Lung, and Blood Institute, NIH, Building 10, Room 7C-103, Bethesda, Maryland 20892-1652, USA. Phone: (301) 496-8396; Fax: (301) 496-8396; E-mail: youngn@gwgate.nhlbi.nih.gov.
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First published September 1, 2000 - More info
Published in Volume 106, Issue 5 on September 1, 2000
First published September 1, 2000 - Version history
Paroxysmal nocturnal hemoglobinuria (PNH) has been a medical curiosity since the description of the first case in the mid–19th century by the English physician Sir William Gull. (See Rosse [ref. 1] for an eloquent history of studies on this disease.) Gull's patient suffered morning crises of "intermittent hematinuria," which was later recognized as the destruction of red cells in circulation. Intravascular hemolysis is unusual, as erythrocyte destruction occurs in the reticuloendothelial system in most hemolytic anemias. PNH was puzzling in the laboratory as well: red cells were lysed in the presence of acidified serum by a factor that was not an antibody. When this property was utilized to formulate the diagnostic Ham's test, the symptoms and signs of the disease were broadened, and PNH was more fully characterized by a clinical triad of hemolysis, venous thrombosis, and marrow failure. Whereas thrombotic disease, which is often in unusual anatomical locations, recurrent, and resistant to therapy, is the major cause of death among Western patients, pancytopenia predominates as a manifestation of PNH in the Far East. PNH is closely related to aplastic anemia (AA), in which an autoimmune reaction leads to hematopoietic cell destruction and an empty bone marrow (2). AA usually responds to immunosuppressive therapies (3). Occasional patients who have been successfully treated with immunosuppressive drugs later manifest symptoms of PNH, evidently as a result of clonal expansion of cells prone to hemolysis and thrombosis. Furthermore, since PNH clones can be detected in as many as 25–35% of AA patients at presentation, the late outgrowth of these clones may not necessarily be seen as a complication of the immunosuppression, but rather as a consequence of persistent low-level PNH that predated and possibly contributed to the development of AA.
Despite its rarity, PNH has been studied by exceptional clinical and laboratory investigators, every era attracting a cohort of scientists to concentrate on a different aspect of the disease. Perhaps surprisingly, these often disparate lines of research led to the unraveling of many of PNH's mysteries (Figure 1) in logical sequence. The emphasis in the early 20th century was the mechanism for red cell lysis by treated sera, shown to be activation of the alternative pathway of complement (4). The erythrocyte defect was identified functionally as an inability to inactivate complement on the cell surface, in turn due to a deficit in specific membrane proteins (decay-accelerating factor [DAF, or CD55] and membrane inhibitor of reactive lysis [MIRL, or CD59]). Not only were these proteins absent, but PNH cells lacked a variety of others, including leukocyte alkaline phosphatase and erythrocyte acetylcholinesterase. Ultimately, demonstration of the enzymatic release of alkaline phosphatase by a specific phospholipase led to the identification of a structural feature common to this functionally diverse group of proteins: a distinctive biochemical linkage to the cell membrane, the glycosylphosphatidylinositol (GPI) anchor. Preformed GPI is attached covalently to proteins of appropriate carboxyl sequence and links them to the plasma membrane through the phosphatidylinositol moiety. GPI-anchored proteins thus lack the cytosolic tail of the more common transmembrane cell surface proteins, and they also appear to cluster on the cell surface in biophysically distinctive regions termed "rafts." Almost 100 different GPI-anchored proteins, including enzymes, adhesion molecules, receptors, and blood group antigens, have been identified to date in mammalian cells (5). The GPI anchor is evolutionarily conserved, and in parasites, GPI-anchored proteins predominate on the cell surface (6).
The pathophysiology of PNH. The genetic basis of the disease is diagrammed at upper left. Somatic mutations in the X-linked PIG-A gene occur in a hematopoietic stem cell. PIG-A consists of six exons with an open reading frame of 1455 bp; the putative protein product has 484 amino acids and an estimated molecular weight of 60 kDa. Small deletion and insertion mutations (dark triangles) are most common in PNH and are distributed throughout the coding sequence; missense mutations (dark circles) appear to cluster in exon 2, suggesting that this region encodes for a functionally crucial portion of the protein (see ref. 29 for details of the GPI-anchor chemical structure). At upper right, GPI-anchored proteins and conventional transmembrane proteins are contrasted, and the structure of the GPI anchor is shown in the inset. The anchor is a glycolipid composed of the lipid phosphatidylinositol, the sugars N-glucosamine and mannose, and ethanolamine. The acyl/alkyl-glycerol of the lipid anchors the structure in the bilayer of the cell membrane; an ethanolamine links the carboxyl terminal amino acid of the protein to the oligosaccharide portion of the anchor. The PIG-A gene product contributes to the N-acetyl-glucosaminyl transferase activity that adds this sugar to inositol, an early step in construction of the anchor; the entire anchor structure is preformed and then covalently bound to the protein in a transamidation reaction in the endoplasmic reticulum (not shown). Expansion of the PIG-A– clone is required for PNH (see text and Figure 2). Absence of GPI-anchored proteins, especially CD59 (MIRL), accounts for hemolysis; the inset shows the role of MIRL in blocking the late complement attack complex, by first binding to C8 and inhibiting spontaneous binding of C9 and then preventing C9 polymerization and subsequent red cell lysis. BM, bone marrow; RBCs, red blood cells; MAC, membrane attack complex.
The biosynthesis of the GPI anchor was determined for trypanosomes and later in deficient mammalian cell lines (7). The genetic defect in PNH, discovered by expression cloning and then phenotypic correction of mutant cell lines, was localized to the X-linked phosphatidylinositol glycan class A (PIG-A) gene (8), whose product is required for the transfer of N-acetylglucosamine to phosphatidylinositol, an early step in the synthesis of the GPI anchor (4). Immortalized cell lines from PNH patients all belong to the class A complementation group; the most frequent PIG-A alterations are small deletions that create stop codons or frameshifts, followed by missense mutations and small insertions.
PIG-A mutations in PNH are somatic, occurring in hematopoietic stem cells. Although there are germline polymorphisms in PIG-A, a constitutional form of PNH has not been described, and knockout animals have all been chimeras. Most likely, although the defect is compatible with survival and function of adult hematopoietic cells, embryonal development cannot proceed without GPI-anchored proteins. PIG-A mutations in all cases represent loss-of-function alleles and so would be expected to be recessive. Nevertheless, the disease phenotype is seen not only in men, who are hemizygous for the gene, but also, and with equal prevalence, in women. Due to random inactivation of the X-chromosome in the hematopoietic system, each blood cell in a female carries only a single transcriptionally active copy of PIG-A. A given stem cell and its progeny will express the PNH phenotype only if their active allele is mutated, but the hemolytic and thrombotic phenotype is evident despite the presence of some normal cells. The clonal origin of PNH cells was first inferred from G6PD enzyme analysis of circulating red cells in informative heterozygous females. All defective erythrocytes, leukocytes, and platelets are derived from a single affected hematopoietic progenitor cell carrying a particular PIG-A mutation. However, in some patients, genetic analysis reveals multiple PNH clones, which may persist for many years (9). Healthy individuals also harbor tiny PNH clones. Lymphocytes of PNH phenotype and PIG-A genotype have appeared in lymphoma patients treated with Campath-1, a monoclonal antibody that coincidentally recognizes a GPI-anchored protein (10), and very small numbers (20–60 per million) of GPI-anchored protein–deficient, PIG-A– granulocytes have been detected in the blood of normal persons (11).
The simplest model to explain how somatic mutations in PIG-A account for the development of PNH predicts that PIG-A– cells enjoy an intrinsic advantage over PIG-A+ cells, resulting in expansion of the defective clone (Figure 2a). Surprisingly, however, clinical observations and much experimental data do not support this hypothesis. Most obviously, PNH does not behave like a leukemia, with inexorable proliferation of abnormal cells. Rather, in most patients, the proportion of PNH cells is stable over years and their differentiation is normal. The presence of PIG-A– cells in normal adults is also difficult to reconcile with this model, given the rarity of the disease. In chimeric knockout mice, PIG-A– cells also constitute a minor, static fraction of the marrow or circulating hematopoietic compartments, and PIG-A– and normal cells behave similarly in paired tissue culture assays (12–14). In most laboratories, PNH patient bone marrow or blood, while often globally deficient in hematopoietic progenitor numbers, has not shown unanticipated outgrowth of either the PIG-A– or normal phenotype cells in colony-forming or long-term culture assays that would indicate a functional difference (15–18). Only one group has reported a major difference between PIG-A– cells and controls in susceptibility to apoptosis, but this finding has not been reproduced in other laboratories (ref. 19 and our unpublished data). Furthermore, there is no known molecular mechanism for GPI-anchored proteins to influence programmed cell death.
Models for clonal expansion in PNH. (a) In the first model, the PIG-A mutation sufficiently affects cellular function to cause an intrinsic growth advantage. (b) Extrinsic factors are invoked for other models; immune effects are illustrated, but differential responses to hematopoietic growth factors, inhibitory cytokines, or stromal cells are also possible. (c) GPI-anchor deficiency might produce a global deficit in immune recognition, as for example through absence of a costimulatory molecule on the target, providing a general selective advantage to the mutated cells. (d) Alternatively, a GPI-anchor protein might be antigenic, by resemblance to an exogenous antigen or after antigenic spread. (e) Finally, altered protein processing due to the absence of anchor structures might change the nature and quantity of peptides derived from normally GPI-anchored proteins, as well as their MHC presentation. As illustrated, cell surface proteins are normally recycled to the membrane or degraded by lysosomes for class II presentation; in PNH, anchorless proteins likely are processed by the proteasome for class I presentation. Differences in immune response to normal and PNH cells should follow.
A second class of models to explain the etiology of PNH holds that the PIG-A defect must be combined with some extrinsic factor to promote clonal expansion (Figure 2b). The frequent association of PNH with AA first suggested that the hypocellular failed marrow might be such a permissive environment (20, 21). However, while PNH clones are present in a very large proportion of AA patients (about 20% in our recent report; ref. 22), PNH does not occur after chemotherapy or radiation-induced aplasia, following stem cell transplant, or in constitutional Fanconi's anemia (22). The presence of PNH does appear to correlate with immunologically mediated marrow failure, and is a positive predictor of response to immunosuppressive therapy in AA and myelodysplasia. In addition, PNH is strongly associated with the MHC haplotype HLA-DR2 (our unpublished data). This MHC association might indicate that an interaction between certain GPI-anchored proteins and the immune system is crucial for PNH pathogenesis. For example (see Figure 2e), the absence of these proteins in certain genetic backgrounds might allow PNH cells to escape immune surveillance. Indeed, a number of mammalian GPI-anchored proteins serve immune functions or act as ligands for T-cell receptors. Work with one inhibitory T-cell clone derived from an AA patient showed that antibodies to the GPI-anchored CD59 protein, which may interact with the T-cell surface protein CD2, appear to block killing of lymphoblastoid cell targets (23). In PNH, loss of CD59 could result in less efficient killing of GPI-deficient hematopoietic target cells by putative autoimmune T-cell clones. Similar mechanisms could also affect natural killer–mediated cell killing; for example, we described a GPI-anchor protein–deficient Ramos cell line that was extremely resistant to natural killer cell lysis, but the PIG-A gene in these cells was normal (24). Recently, an interesting mechanism was described for proinflammatory cytokine production after heat shock protein stimulation through CD14 (25), suggesting that lack of certain GPI-anchored proteins may locally lead to impaired intra- and extracellular signaling. Nevertheless, extensive efforts (many of them unreported) by several laboratories to determine a difference between normal and PIG-A– target cells in a wide variety of immunologic assays have been unsuccessful (26). In our unpublished studies, for example, using paired normal and PIG-A– cell lines and primary clinical samples as targets, we have been unable to document differences in susceptibility to autologous and allogeneic T-cell cytotoxicity or ability to activate T cells, or in their proliferation after challenge with cytokines or Fas agonists.
In this issue of the JCI, Chen and colleagues identify a major difference in in vitro proliferation between PIG-A– and PIG-A+ CD34 cells taken from the marrow of PNH patients (27). Remarkably, this difference appears to represent deficiency among the "normal" cells in these individuals, rather than an advantage for the PIG-A mutant cells. When a few hundred CD34 cells, sorted by the presence or absence of CD59 to identify normal and PNH populations, were cultured in the presence of growth factors, the cells with the PNH phenotype behaved normally, producing several hundred thousand progeny, while CD34 cells of normal phenotype from PNH patients showed little growth. This spectacular difference stands in contrast to most previous studies of whole marrow and CD34 cells using standard colony and long-term marrow cultures — in which bone marrow cells derived from PNH patients give rise to progeny of both normal and mutant phenotypes. No methodologic explanation for this discrepancy is evident. However, a similar result has been observed in immunodeficient mice that were infused with bone marrow from PNH patients; in this experiment, the abnormal clone engrafted but little or no normal human hematopoiesis could be detected (28).
The suggestion that loss of PIG-A expression restores normal proliferation to otherwise poorly growing or short-lived hematopoietic cells clearly requires further support. Nevertheless, this possibility could help explain the presence of multiple PIG-A– clones in PHN individuals, and it appears to be compatible with both the "extrinsic" and "intrinsic" models of PNH shown in Figure 2. Unfortunately, however, it sheds little light on the stability of PIG-A+ and PIG-A– cell populations in these subjects. The most direct inference from the current work is that the PNH cells have survived some in vivo injury sustained by the normal progenitors, consistent with the hypothesis of immune escape. That this insult might indeed be immunologic is suggested by the expression of Fas on the normal but not on the GPI-anchor protein–deficient cells and concomitant sensitivity to Fas ligand–mediated apoptosis. Although the authors suggest that this finding supports a resistance to programmed cell death among PNH cells, the result cannot be generalized to other apoptosis inducers. There is no obvious mechanism for altered CD95 expression secondary to GPI-anchored protein deficiency, and again such differences have not been revealed in other immunologic assays. The ability to demonstrate functional differences in inhibition (Fas agonist) and stimulation (Fas antagonist in the absence of an obvious source of Fas ligand) in poorly growing cells is admirable.
Nevertheless, the character of the interaction between a PIG-A– clone and either the normal hematopoietic environment or the failed marrow milieu — and indeed of the cause-and-effect sequence of PNH and AA — remains frustratingly unsettled. Several relationships can be hypothesized and tested (Figure 2, b–e). In the first, a general deficit in effector recognition of a defective cellular target — due, for example, to decreased binding of costimulatory molecules secondary to the GPI-anchor protein deficiency — would explain the emergence of normally quiescent but now resistant PNH clones under conditions of autoimmune attack (Figure 2b). The data of Chen and colleagues (27) are consistent with this view, but in the context of many contradictory experiments, the effect would necessarily be subtle and manifest only under special in vivo circumstances. In addition, such a dependence of PNH cell viability on immune status is hard to reconcile with the stability of PNH clones over time and despite changes in blood counts and treatment regimens. In the second and third models, in contrast, the mutated cell has a more primary role in the development of bone marrow failure. GPI-anchored proteins might serve as antigens, either due to molecular mimicry with exogenous peptides (perhaps derived from a viral protein; Figure 2d) or subsequently as part of a process of antigenic spread. In the third model, the PNH clone itself would induce autoimmunity. As illustrated in Figure 2e, for example, a global alteration in protein trafficking due to absence of GPI anchors is invoked. As a result, GPI-anchorless proteins in the PIG-A– cell are processed by proteasomes and their peptides are displayed by class I MHC molecules, in contrast to the normal pathway of membrane-bound protein degradation via the lysosome and class II molecules. This model would provide for both GPI-anchored protein antigenicity (increased or novel peptide presentation by class I MHC) and escape (decreased class II display). Under normal circumstances, the PNH clone would be suppressed. In other, "tolerant" individuals, clonal expansion might occur unimpeded, leading to predominantly hemolytic PNH. In the setting of an aberrant or exaggerated immune response, normal hematopoiesis would suffer, leading to AA. There may be major, unanticipated consequences of failed GPI-anchor synthesis beyond deficient expression of certain membrane proteins.
In PNH, models and experiments will need to account for a number of remaining puzzling questions that are both clinically relevant and of general biologic importance. Biochemically, little is understood of the presumed special function of the GPI anchor in the mammalian cell — in altering the mobility of membrane proteins, in internal signal transduction, in collaboration with other proteins in rafts, in cell-cell protein transfer, and even in shedding from the cell surface, since there is sufficient inactive phospholipase C in plasma to release all GPI-anchored proteins from circulating cells. Other questions relate to the dynamics of hematopoietic cells in PNH: Why is there such a tiny proportion of PIG-A– progeny in normal individuals? Why do PIG-A– clones persist for years, even decades, supplying the entire blood production of a patient? And why do clones appear to become extinguished in rare individuals? Clinically, we need to account not only for the close relationship of a clonal, somatically acquired genetic disorder and immunologically mediated bone marrow failure, but also for evidence of generalized marrow depression in all forms of PNH, the multiplicity of clones in disease, and the inexorable progression to refractory fatal thrombosis or AA in many patients. Continued examination of this rare disease should yield further insights into human hematopoietic cell biology, biochemistry, and immunology.
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Version 1 (September 1, 2000): No description


Everton manager Roberto Martinez felt mental fatigue played a part in a disjointed performance against Fulham which was turned around late on to win 4-1.
Having gone ahead through Leon Osman's 18th-minute goal, the Toffees failed to press home their advantage and Dimitar Berbatov equalised from the penalty spot midway through the second half.
However, just when it seemed the visitors were threatening a winner Seamus Coleman, Gareth Barry and Kevin Mirallas all scored in the last 17 minutes to make the scoreline look somewhat harsh on the Cottagers.
Martinez felt his side suffered after a significant victory at Old Trafford and a well-deserved draw at Arsenal last weekend.
"It wasn't one of our best days. I was a bit fearful before the game as mentally we were going to be fatigued after the two away games which were very demanding," said the Spaniard.
"Physically we were fine but mentally the way we moved the ball it wasn't as sharp as usual, we couldn't see our normal patterns going forward.
"The first half we controlled the game and had we scored the second goal (earlier) it would've changed the game.
"Second half you have to give great credit to Fulham. They were well organised, pressing us high up, stopping us from playing.
"Once you get that equaliser I have seen many times before the home team collapse and you start panicking and you lose the game.
"What we did really well was the mindset changed. We didn't have anything to lose, we just wanted to win the game and we were brave, adventurous and creative in the final third.
"I don't think it was a 4-1 performance but we deserved the three points."
The only downside was a hamstring tear to youngster Gerard Deulofeu which is likely to rule him out for several weeks.
"Gerard is the big negative. He is a sprinter and those players are exposed to those injuries and he has pulled his hamstring," said Martinez.
"We don't know how big the tear is going to be but we expect Gerard to be out for some time.
"It is unfortunate because I thought he was ready to play a big role in the side but we are going to have to be patient and wait for him to come back in the final third of the season as strong as he can be."
Fulham boss Rene Meulensteen was in full agreement with Martinez about the scoreline flattering the hosts.
"I do think it didn't reflect the actual game," said the Dutchman.
"I thought we came back really strongly in the second half, changed a few things, put them under pressure, and that resulted in a few early chances.
"We got the equaliser and then conceded too soon after. That took the wind out of our sails.
"The 3-1 settled the game from that corner. We spoke about it, to concede another for 4-1, it didn't reflect the game."


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FA WSL
FA WSL opening date announced in the middle of Champions League qualifiers
Arsenal will have to hit the ground running when the season 2021/22 starts with the FA WSL season opener planned in a congested period amidst crucial Champions League ties.
HIGH WYCOMBE, ENGLAND – MARCH 14: Louise Quinn and Katie McCabe of Arsenal women celebrate with the trophy after the WSL Continental Cup Final between Arsenal Women and Manchester City Ladies at Adams Park on March 14, 2018 in High Wycombe, England. (Photo by Catherine Ivill/Getty Images)
The FA have announced the season opener will take place on Friday 3 September.
This will make it a tough week for Arsenal with Champions League Qualifying Round 2 set for the 31 Aug/1 Sep and the second leg on 08/09 Sep.
You do wonder if Arsenal will try to get the opener moved to Saturday or Sunday.
Let's remind ourselves who we can meet in the Qualifying Round 2 as we will not be seeded due to our low 27.700 UEFA coefficient.
Arsenal can get Lyon, Wolfsburg, Slavia Prague and Rosengard. We cannot be drawn against Manchester City, as per the rules. It is quite clear that those qualifying round games could define Arsenal's season, as early elimination from the Champions League would have certainly a knock-on effect on the remainder of the season.
Of course, we have to get through the Qualifying Round 1, first, and Arsenal will be seeded for that round.
There are some potential banana slips with Bordeaux, Hoffenheim, Levante and Rosenborg tough opponents to have to overcome in a one-legged tie.
It is also important to remember that all our Olympic players will not be available for nearly all of preseason. That means no Kim Little, Leah Williamson, Lotte Wubben-Moy, Mana Iwabuchi, or Vivianne Miedema.
Potential new signings, like Nikita Parris, will also miss most of pre-season if signed. That would mean at least seven players missing from a current squad of 21 players.
The logistics of doing a full pre-season without about a third of the squad is not great and an early exit from the Olympics would actually help the club in getting players back as early as possible.
Hopefully, we will see a new manager announced soon and at least three more signings to beef up the squad, as Arsenal will end up playing in five competitions next season: UEFA WCL, FA WSL, FA Cup 20/21, FA CUP 21/22 and FA WSL Conti Cup.
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Following the Arsenal Ladies since 2004/05. Arsenal LFC season ticket holder since they appeared in 2006/07. Likely to be found watching women's football every week-end all over England... and the world. I am also a silver member

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So many people are intimidated by making bone broth, which is sad because it's incredibly beneficial for our immunity, gut lining, and bones and muscles. I believe that it's better to strip a recipe down of its more time-consuming steps rather than complicate it and turn people off from making it in the first place. Yes, you can add onions, carrots, celery, and seasonings to your bone broth. You can keep a close eye on it and skim it every few hours. You can be particular about using bones all from the same animal. But this is my bare bones recipe (see what I did there?) that still does exactly what you need it to do. Once you have the broth down, you can add all the good stuff later. Cue the Sweet & Spicy Breakfast Broth! Forget Folgers. This is the best part of waking up.
See Stacey's complete Bone Broth post on her blog!


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Samsung's The Frame 4K UHD TV offers not just a cinematic UHD movie experience, but also an art mode that lets you select works from Samsung's Gallery Collection or display your own. You can even customize the matting and frame, with walnut, oak, and white interchangeable options sold separately to match the decor of any room. This 55″ wall-mount model (UN55LS003AF) hangs flush with no gap between it and the wall. And the picture quality? 4K/UHD delivers impressive detail while HDR shows extreme contrasts in light. Meanwhile, Active Crystal Color produces a wider color gamut, making images look more lifelike. Plus, this Smart TV lets you access connected devices from your remote or smartphone.


text:
Why do Catholic priests wear pink during Lent?
Why do priests wear pink in Lent?
What color does the priest wear during Lent?
Why is pink on the 4th Sunday of Lent?
What Sunday does the priest wear pink?
Why do priests wear rose vestments?
What are the Sundays of Lent called?
Why did the priest wear purple?
What color do Catholic priests wear on Ash Wednesday?
Do Catholic priests wear black vestments?
What is another name for fourth Sunday of Lent?
Why is Gaudete Sunday so important?
What is the Third Sunday of Easter called?
How many Sundays are there in Lent?
What means Lent?
Pink: A special color worn only twice during the liturgical year. It represents a time of joy amid a period of penance and prayer.
Advent and Lent are periods of preparation and repentance and are represented by the colour purple.
It's optional, but I've always liked it — when the Church's sacred ministers wear "pink" on Laetare Sunday — Roman Catholicism's Fourth Sunday of Lent. The day's theme comes from the entrance antiphon reflecting on Isaiah 66:10-11: "Rejoice, Jerusalem, and all who love her.
Now that I've established the difference between pink and rose, the next questions are why that color and why do we wear it on the Third Sunday of Advent? (Priests also wear rose-colored vestments on the Fourth Sunday of Lent) The Third Sunday of Advent is known as "Gaudete Sunday" or "Rejoice Sunday." We are reminded …
THIS IS UNIQUE: You asked: What did Jesus do when he fasted for 40 days?
Rose. Rose vestments are only worn twice in the liturgical year, during the third sunday of Advent, and the fourth sunday of Lent. These colors are worn on these days to show the joy and love in Christ. They are to remind Catholics of the joy in the times of penance and worship.
Eastern Orthodoxy and Byzantine Rite
The 40 days of Great Lent includes Sundays, and begins on Clean Monday and are immediately followed by what are considered distinct periods of fasting, Lazarus Saturday and Palm Sunday, which in turn are followed straightway by Holy Week.
Why do Catholic priests wear purple? Purple: Worn during the Advent and Lent seasons, purple reflects sorrow and suffering. Sorrow as the faithful await the arrival of the Savior and suffering to mark Jesus Christ's 40 days in the desert (Lent).
Most of this time of preparation is symbolized by the color Violet, though the season is bracketed by the mourning Black of Ash Wednesday and Good Friday.
Priests may wear rose vestments, symbolizing joy, on Gaudete Sunday during Advent and Laetare Sunday during Lent. They may wear black vestments, representing mourning, on All Souls Day.
Laetare Sunday (/liːˈtɛːri/ or /lʌɪˈtɑːri/) is the fourth Sunday in the season of Lent, in the Western Christian liturgical calendar. Traditionally, this Sunday has been a day of celebration, within the austere period of Lent.
THIS IS UNIQUE: What does the Bible say about making peace with others?
Gaudete Sunday is a counterpart to Laetare Sunday, and provides a similar break about midway through a season which is otherwise of a penitential character, and signifies the nearness of the Lord's coming.
Because this Gospel reading is the parable of the Good Shepherd, the Fourth Sunday of Easter is now also known as Good Shepherd Sunday (a name formerly given to the Third Sunday of Easter to which the reading was originally assigned).
It is the holy season of Lent, with the objective to be consciously sacrificing as a representation of the 40 days Jesus spent fasting and praying in the desert after his baptism. There are 46 days between Ash Wednesday and Easter Sunday, with six Sundays total.
Lent is a period of 40 days during which Christians remember the events leading up to and including the death of Jesus Christ, whose life and teachings are the foundation of Christianity. The 40-day period is called Lent after an old English word meaning 'lengthen'.


text:
Watch: Drive hits rules official riding across the fairway in a cart
By EXTRA SPIN STAFF
A rules official looks for a golf ball in his cart.
Perhaps "Fore" would have helped in this situation?
At the European Tour's Hero Indian Open, David Horsey bombed a drive down the middle of the fairway. Away from all the hazards, right? Wrong! A rogue rules official was just trotting down the fairway in his golf cart, minding his own business without a care in the world. Except he was in the landing zone for the players actually playing in the event on the hole he's driving down.
The ball lands to the left of the cart and hits the rules official on the bounce. Luckily, the ball stayed in the fairway, and Horsey made his par.
You don't see this every day… pic.twitter.com/sNprvC53ZE
— The European Tour (@EuropeanTour) March 12, 2017
From the Black Swan to the weatherman, ranking the 11 best golf moments in 'Curb Your Enthusiasm'
#AskAlan mailbag: Will we actually see stroke penalties for pace of play in 2020?
What it's like completing Phil Mickelson's 6-day coffee and water fast (with Lefty as my coach)
Jack Nicklaus' 80th birthday call with reporters was a reminder of a bygone era
Pete Dye was an ageless wonder, and there will never be another course designer like him


text:
Black Panther: Wakanda Forever è un film del 2022 diretto e co-scritto da Ryan Coogler.

Basato sul personaggio di Pantera Nera della Marvel Comics, è il trentesimo film del Marvel Cinematic Universe e l'ultimo della cosiddetta "Fase Quattro", nonché sequel della pellicola del 2018 Black Panther, e ha come protagonisti Letitia Wright, Lupita Nyong'o, Danai Gurira, Winston Duke, Dominique Thorne, Florence Kasumba, Michaela Coel, Tenoch Huerta, Martin Freeman e Angela Bassett. Nel film, il Wakanda deve combattere per proteggere la propria nazione dopo la morte di re T'Challa.

Il film è stato candidato a diversi premi cinematografici, tra i quali cinque Oscar 2023, vincendo l'Oscar ai migliori costumi.

Trama
T'Challa, re del Wakanda, è morto per una grave malattia che sua sorella Shuri ha provato a curare ricreando sinteticamente "l'erba a forma di cuore", che era stata distrutta da Erik Killmonger, ma senza successo.

Un anno dopo, il Wakanda subisce pressioni da parte di altre nazioni per condividere il proprio vibranio, con alcuni stati che hanno provato a rubarlo con la forza. Ramonda, la regina madre, implora Shuri di continuare la sua ricerca sull'erba a forma di cuore, sperando di creare così una nuova Pantera Nera che possa difendere il Wakanda, ma lei rifiuta perché crede che la Pantera Nera sia ormai una figura relegata al passato. La caccia al vibranio ha portato la CIA a utilizzare una nuova macchina di rilevamento del vibranio, per trovare quello che pensano sia un deposito sottomarino di vibranio. L'intera squadra di ricerca viene attaccata e uccisa da Namor e dalla sua gente dalla pelle blu che respira acqua, ma la CIA crede che il responsabile dell'attacco sia proprio il Wakanda. Namor va da Ramonda e Shuri, aggirando facilmente l'avanzata sicurezza del Wakanda, chiedendo loro di trovare e consegnargli lo scienziato creatore della macchina di rilevamento del vibranio, altrimenti attaccherà il Wakanda.

Shuri e Okoye, con l'aiuto del loro amico agente della CIA Everett Ross, si recano a Boston per incontrare lo scienziato responsabile: una studentessa del MIT di nome Riri Williams. Il gruppo viene inseguito dall'FBI e poi dai guerrieri di Namor, che sconfiggono Okoye e portano Shuri e Riri sott'acqua per incontrare Namor. Ramonda priva Okoye del suo dovere di Dora Milaje e cerca Nakia, trasferitasi ad Haiti, per chiederle aiuto a trovare Shuri e Riri. Shuri incontra Namor, che le mostra il suo regno sottomarino di Talokan, che ha protetto per secoli ed è ricco di vibranio. Astioso verso il mondo in superficie che lo ha respinto, Namor aspira a un'alleanza con il Wakanda contro il resto del mondo, ma promette di distruggere prima lo stesso Wakanda se rifiutano di allearsi. Nakia aiuta Shuri e Riri a fuggire, e Namor si vendica con un attacco contro la capitale del Wakanda, durante il quale Ramonda muore annegata salvando Riri. Namor promette di tornare dopo una settimana con tutto il suo esercito; nel frattempo Ross viene arrestato dalla sua ex-moglie Valentina Allegra de Fontaine, neo-direttrice della CIA, per aver passato informazioni riservate ai Wakandiani. Shuri, usando un residuo dell'erba che ha dato alla gente di Namor le loro abilità subacquee, riesce a ricostruire sinteticamente l'erba a forma di cuore. Shuri ingerisce l'erba per diventare la nuova Black Panther e, dopo aver incontrato Killmonger nel Piano Ancestrale, viene accettata dalle altre tribù.

Nonostante il suggerimento di M'Baku di trattare per ottenere la pace, Shuri è determinata a vendicarsi per la morte della madre e ordina un immediato contrattacco contro Namor. I wakandiani usano la nave Sea Leopard per tendere una trappola, attirando Namor e i suoi guerrieri in superficie, e ne consegue una battaglia. Shuri separa Namor dal resto del suo popolo, con l'intenzione di prosciugarlo e indebolirlo. I due si schiantano su una spiaggia deserta e ne segue uno scontro in cui Shuri viene pugnalata gravemente; usando il motore del Royal Talon Fighter, Shuri dà fuoco a Namor e riesce a soggiogarlo, decidendo però di risparmiargli la vita e offrirgli un'alleanza per tenere al sicuro il suo popolo, ricordando la misericordia mostrata da suo fratello T'Challa. Namor accetta, rendendosi conto che il loro desiderio di vendetta non dovrebbe influenzare i loro popoli e la battaglia finisce. La cugina di Namor, Namora, è sconvolta dal fatto che Namor abbia ceduto a Shuri, ma lui la rassicura dicendo che l'empatia di Shuri per la loro gente può tornare utile e che il Wakanda ha bisogno di loro perché non ha altri alleati. Ormai al sicuro, Riri torna a Boston, lasciando nel Wakanda la sua armatura di Ironheart, mentre Okoye fa evadere Ross durante il suo trasferimento dalla prigione federale. Shuri fa visita a Nakia ad Haiti dove brucia la sua veste cerimoniale funebre come voleva sua madre.

Nella scena durante i titoli di coda, Shuri viene a sapere che Nakia e T'Challa hanno avuto un figlio che Nakia ha allevato in segreto, Toussaint, ma in realtà il suo vero nome wakandiano è proprio T'Challa.

Personaggi
 Shuri / Black Panther, interpretata da Letitia Wright: la principessa del Wakanda che progetta nuove tecnologie per la nazione. Dopo la morte nell'agosto 2020 di Chadwick Boseman, che ha recitato nel primo film come T'Challa / Black Panther, a Shuri è stato assegnato un ruolo più importante in questo film, diventando la nuova Black Panther.
 Nakia, interpretata da Lupita Nyong'o: una spia sotto copertura per il Wakanda, proveniente dalla tribù del fiume.
 Okoye, interpretata da Danai Gurira: il capitano delle Dora Milaje, le forze speciali del Wakanda.
 M'Baku, interpretato da Winston Duke: un potente guerriero che è il capo della tribù di montagna del Wakanda, i Jabari.
 Riri Williams / Ironheart, interpretata da Dominique Thorne: un geniale inventore che ha creato un'armatura che rivaleggia con quella costruita da Tony Stark / Iron Man.
 Ayo, interpretata da Florence Kasumba: un membro e la seconda in comando delle Dora Milaje.
 Aneka, interpretata da Michaela Coel: una guerriera wakandiana.
 K'uk'ulkan / Namor, interpretato da Tenoch Huerta: il re di una razza di abitanti di Talokan. Huerta ha imparato una lingua Maya per il ruolo.
 Everett Ross, interpretato da Martin Freeman: un agente della CIA.
 Ramonda, interpretata da Angela Bassett: la regina madre del Wakanda che è in lutto per la morte di suo figlio T'Challa.

Inoltre Isaach De Bankolé, Danny Sapani e Dorothy Steel riprendono i loro ruoli dal primo film, con quest'ultima alla sua ultima apparizione sullo schermo dopo la sua morte nell'ottobre 2021. Mabel Cadena interpreta Namora, cugina di Namor, e Alex Livinalli appare come Attuma, mentre María Mercedes Coroy interpreta la madre di Namor. Lake Bell interpreta la dottoressa Graham, Julia Louis-Dreyfus riprende con un cameo il ruolo della Contessa Valentina Allegra de Fontaine, Michael B. Jordan appare come Erik "Killmonger" Stevens, riprendendo il ruolo dal primo film, e Trevor Noah torna a dare la voce a Griot, intelligenza artificiale creata da Shuri. Fanno parte del cast anche Kamaru Usman e Richard Schiff. Chadwick Boseman appare alla fine della pellicola tramite filmati d'archivio presi dai precedenti film MCU.

Produzione

Sviluppo
La realizzazione della pellicola è stata annunciata nell'ottobre 2018, quando Ryan Coogler ha firmato un accordo come regista del sequel di Black Panther, e il mese successivo è stato confermato il ritorno di Letitia Wright nel ruolo di Shuri. Nel luglio 2019 anche Danai Gurira ha dichiarato che avrebbe ripreso il ruolo di Okoye, e nello stesso mese, al San Diego Comic-Con, Kevin Feige ha confermato che il sequel era in sviluppo. Il mese seguente anche Martin Freeman ha confermato il suo ritorno come Everett Ross, e sempre ad agosto, al D23 Expo, è stato dato al film il titolo provvisorio di Black Panther II, mentre alla fine del 2019 la costumista di Black Panther Ruth E. Carter ha dichiarato che avrebbe lavorato anche al sequel.

Pre-produzione
Nel novembre 2020 sono stati annunciati nel cast Lupita Nyong'o, Winston Duke e Angela Bassett, che riprendono i loro precedenti ruoli di Nakia, M'Baku e Ramonda, mentre nel maggio 2021 è stato rivelato che il titolo ufficiale del film sarebbe stato Black Panther: Wakanda Forever.

Riprese
Le riprese principali sono iniziate il 29 giugno 2021 ad Atlanta e sono terminate il 24 marzo 2022 a Porto Rico. Nel luglio 2021 Michaela Coel è entrata a far parte del cast in un ruolo non definito, mentre il mese successivo Dominique Thorne è stata annunciata nel ruolo di Riri Williams / Ironheart. Il budget del film è stato di 250 milioni di dollari.

Post-produzione
Autumn Durald è il direttore della fotografia. Nel giugno 2022 Tenoch Huerta ha confermato che sarebbe apparso nel film, e il mese successivo, al San Diego Comic-Con, è stato annunciato che avrebbe interpretato K'uk'ulkan / Namor. Sempre al Comic-Con sono stati rivelati i ruoli di Coel, Mabel Cadena e Alex Livinalli, rispettivamente come Aneka, Namora e Attuma, ed è stato anche confermato il ritorno di Florence Kasumba nel ruolo di Ayo.

Colonna sonora

Le musiche del film sono state composte da Ludwig Göransson, già compositore della colonna sonora del film del 2018. Il 28 ottobre 2022 è stato pubblicato il primo estratto dalla colonna sonora, Lift Me Up, interpretato dalla cantante Rihanna e scritto da Göransson, Ryan Coogler, Muni Long e Tems. L'album, Black Panther: Wakanda Forever - Music from and Inspired By, è stato pubblicato da Hollywood Records, Roc Nation e Def Jam Recordings il 4 novembre 2022.

Promozione
Il primo teaser trailer è stato distribuito online il 24 luglio 2022, mentre il trailer e il poster ufficiale sono stati pubblicati il 3 ottobre successivo.

Il 4 novembre 2022, sulla piattaforma Disney+, sono stati pubblicati tre episodi di Marvel Studios: Legends, dedicati rispettivamente a T'Challa, Shuri e alle Dora Milaje.

Distribuzione

Data di uscita
Inizialmente previsto prima il 6 maggio 2022 e poi l'8 luglio, il film è uscito nelle sale cinematografiche italiane il 9 novembre 2022, mentre in quelle statunitensi l'11 novembre.

Edizione italiana
La direzione del doppiaggio e i dialoghi italiani sono stati curati da Marco Guadagno e Philippe Morville.

Edizioni home video
Il film è disponibile sulla piattaforma Disney+ dal 1º febbraio 2023, e in DVD, Blu-ray e 4K Ultra HD dal 7 febbraio.

Accoglienza

Incassi
Al 16 marzo 2023 Black Panther: Wakanda Forever ha incassato  in Nord America e  nel resto del mondo, per un incasso complessivo di , a fronte di un budget di produzione di $250 milioni.

Globalmente il film ha esordito con 331,7 milioni di dollari nei primi cinque giorni; inoltre è il sesto maggior incasso mondiale del 2022 e il terzo maggior incasso nel Nord America del 2022.

Nord America
Il film ha incassato $28 milioni nelle anteprime del giovedì, mentre nel primo giorno di programmazione ha incassato $84,3 milioni in 4,396 schermi. Nel week-end d'esordio ha ottenuto il primo posto incassando $181,3 milioni, per un totale di $220,7 milioni nella prima settimana. Ha mantenuto il primo posto anche nel secondo week-end incassando $66,5 milioni, nel terzo week-end incassando $45,6 milioni, nel quarto week-end incassando $17,5 milioni, e nel quinto week-end incassando $11,1 milioni, per poi scendere al secondo posto nel sesto week-end incassando $5,4 milioni.

Internazionale
Nel resto del mondo, il film ha incassato $10,1 milioni nel giorno di apertura, mentre nei primi cinque giorni ha incassato complessivamente $150,3 milioni, con il Regno Unito che è stato il mercato più redditizio con un incasso di $15 milioni, seguito dalla Francia con $13,7 milioni e dal Messico con $12,8 milioni. In Italia ha incassato 717 mila euro nel primo giorno e €4,1 milioni nei primi cinque giorni, per poi incassare in totale €8,5 milioni.

Critica
Il film è stato accolto positivamente dalla critica. Sull'aggregatore di recensioni Rotten Tomatoes ha una percentuale di gradimento dell'84%, con un voto medio di 7,2 su 10 basato su 429 recensioni; il consenso critico del sito recita: "Un toccante tributo che fa proseguire in modo soddisfacente il franchise, Black Panther: Wakanda Forever è un trionfo ambizioso ed emotivamente gratificante per il MCU". Su Metacritic ha un punteggio di 67 su 100 basato su 62 recensioni.

Riconoscimenti
 2023 – Premio Oscar
 Migliori costumi a Ruth E. Carter
 Candidatura alla miglior attrice non protagonista ad Angela Bassett
 Candidatura al miglior trucco e acconciatura a Camille Friend e Joel Harlow
 Candidatura alla migliore canzone a Lift Me Up
 Candidatura ai migliori effetti speciali a Geoffrey Baumann, Craig Hammack, R. Christopher White e Dan Sudick
 2023 – Golden Globe
 Migliore attrice non protagonista ad Angela Bassett
 Candidatura alla migliore canzone originale a Lift Me Up
 2023 – Premio BAFTA
 Candidatura alla migliore attrice non protagonista ad Angela Bassett
 2023 – Critics' Choice Awards
 Miglior attrice non protagonista ad Angela Bassett
 Migliori costumi a Ruth E. Carter
 Candidatura alla migliore canzone originale a Lift Me Up
 Candidatura alla migliore scenografia a Hannah Beachler
 Candidatura ai migliori effetti speciali
 2023 – Screen Actors Guild Award
 Candidatura alla miglior attrice non protagonista ad Angela Bassett
 Candidatura alle migliori controfigure cinematografiche

Altri media
Nell'autunno 2023 uscirà la serie televisiva Ironheart come sequel del film, con Dominique Thorne che tornerà nel ruolo della protagonista Riri Williams / Ironheart.

Nel febbraio 2021 è stato rivelato che era in sviluppo con Ryan Coogler una serie televisiva ambientata nel Wakanda, mentre nel maggio successivo Danai Gurira ha firmato un accordo per riprendere il suo ruolo di Okoye.

Note
Annotazioni

Fonti

Altri progetti

Collegamenti esterni

Film diretti da Ryan Coogler
Film del Marvel Cinematic Universe
Film 3-D
Film IMAX
Film d'azione
Film d'avventura

redpajama_set_name: RedPajamaWikipedia


text:
using System;
using Brickweave.Cqrs.SqlServer.Entities;
using Brickweave.Cqrs.SqlServer.Services;
using Brickweave.Cqrs.Services;
using Brickweave.Serialization;
using Microsoft.EntityFrameworkCore;
using Microsoft.Extensions.DependencyInjection;
using Microsoft.Extensions.DependencyInjection.Extensions;
using Brickweave.Cqrs.DependencyInjection;
using Microsoft.Extensions.Logging;

namespace Brickweave.Cqrs.SqlServer.DependencyInjection
{
    public static class CqrsOptionsBuilderExtensions
    {
        private static bool _longRunningCommandsEnabled;
        private static bool _longRunningCommandCleanupEnabled;

        public static CqrsOptionsBuilder EnableLongRunningCommands<TDbContext>(this CqrsOptionsBuilder builder,
            Func<TDbContext, DbSet<CommandQueueData>> getCommandQueueDbSet, Func<TDbContext, DbSet<CommandStatusData>> getCommandStatusDbSet)
            where TDbContext : DbContext
        {
            if (_longRunningCommandsEnabled)
                throw new InvalidOperationException("Long-running commands are already enabled.");

            _longRunningCommandsEnabled = true;

            builder.Services()
                .AddScoped(s => (ICommandStatusProvider)Activator.CreateInstance(
                    typeof(SqlServerCommandStatusProvider<>).MakeGenericType(typeof(TDbContext)),
                    s.GetService<TDbContext>(),
                    getCommandStatusDbSet,
                    s.GetService<IDocumentSerializer>()))
                .AddScoped((Func<IServiceProvider, ILongRunningCommandProcessor>)(s => new LongRunningCommandProcessor(
                    s.GetService<ICommandQueue>(),
                    s.GetService<IEnqueuedCommandDispatcher>(),
                    s.GetService<ILogger<LongRunningCommandProcessor>>())))
                .AddScoped<IEnqueuedCommandDispatcher, CommandDispatcher>()
                .Replace(new ServiceDescriptor(
                    typeof(ICommandQueue), s => Activator.CreateInstance(typeof(SqlServerCommandQueue<>).MakeGenericType(typeof(TDbContext)),
                        s.GetService<IDbContextFactory<TDbContext>>(),
                        getCommandQueueDbSet,
                        getCommandStatusDbSet,
                        s.GetService<IDocumentSerializer>()), ServiceLifetime.Singleton));

            return builder;
        }

        public static CqrsOptionsBuilder EnableCommandCleanup(this CqrsOptionsBuilder builder, TimeSpan deleteCommandsAfter)
        {
            if (_longRunningCommandCleanupEnabled)
                throw new InvalidOperationException("Long-running command cleanup is already enabled.");

            _longRunningCommandCleanupEnabled = true;

            builder.Services()
                .AddSingleton((Func<IServiceProvider, ILongRunningCommandCostodian>)(s => new LongRunningCommandCostodian(
                    s.GetService<ICommandQueue>(),
                    deleteCommandsAfter,
                    s.GetService<ILogger<LongRunningCommandCostodian>>())));

            return builder;
        }
    }
}

redpajama_set_name: RedPajamaGithub


BETHEL — A village police officer in Western Alaska was selected to receive the Shirley Demientieff Award for her efforts in improving the lives of Alaska Native women and children.
Gov. Bill Walker is scheduled to present the award Thursday to Mountain Village Officer Anna Bill at the Alaska Federation of Natives Convention in Anchorage, KYUK-AM reported.
Bill had gone back to work only a couple days before Walker called her, telling her she was the recipient. Bill had resigned from the job while on medical leave for an on-the-job injury caused by an assault.
"I think I resigned out of anger and frustration," Bill said. "I was going through a phase where my PTSD had gotten the better of me, and I was so mad at everybody in the world."
Bill was previously the village's only law enforcement officer. She stayed on call around the clock and volunteered her extra hours knowing that the city lacked the funding to pay for all her work. Before Bill had resigned, she responded to 66 attempted suicide calls in less than a year.
Bill sought counseling during her leave, and she also received encouragement from Mountain Village residents telling her to "don't give up" and to "keep going."
"And so as that came along, it made me think about how much I really miss my job," Bill said.
The night before she was due back to work, a person in the community had died by suicide.
"It took a lot out of me just thinking about, you know, what if he'd had somebody to talk to? Or what if I'd signed on a day before? Or, you know, there's always these 'what ifs'," Bill said.
Bill said she hopes the award will motive government officials to better fund public safety in rural Alaska.


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      assert(children[1].left == 0, 'wrap_column RTL root_child0.left should be 0');
      children[1].left = 30;
      assert(children[2].left == 0, 'wrap_column RTL root_child2.left should be 0');
      children[2].left = 30;
      assert(children[3].left == -30, 'wrap_column RTL root_child3.left should be -30');
      children[3].left = 0;
    }

    setupTestTree(
        e,
        undefined,
        LTRLayoutTree[i],
        genericLayoutTree[i],
        'root',
        null);

    e.YGNodeCalculateLayout('root', e.YGDirectionLTR, genericLayoutTree[i].experiments);
    e.push('');

    assertTestTree(e, LTRLayoutTree[i], 'root', null);
    e.push('');

    e.YGNodeCalculateLayout('root', e.YGDirectionRTL, genericLayoutTree[i].experiments);
    e.push('');

    assertTestTree(e, RTLLayoutTree[i], 'root', null);

    e.emitTestEpilogue(genericLayoutTree[i].experiments);
  }
  e.emitEpilogue();

  e.print();
}

function assertTestTree(e, node, nodeName, parentName) {
  e.AssertEQ(node.left, e.YGNodeLayoutGetLeft(nodeName));
  e.AssertEQ(node.top, e.YGNodeLayoutGetTop(nodeName));
  e.AssertEQ(node.width, e.YGNodeLayoutGetWidth(nodeName));
  e.AssertEQ(node.height, e.YGNodeLayoutGetHeight(nodeName));

  for (var i = 0; i < node.children.length; i++) {
    e.push('');
    var childName = nodeName + '_child' + i;
    assertTestTree(e, node.children[i], childName, nodeName);
  }
}

function checkDefaultValues() {
  // Sanity check of the Yoga default values by test-template.html
  [
    {style:'flex-direction', value:'column'},
    {style:'justify-content', value:'flex-start'},
    {style:'align-content', value:'flex-start'},
    {style:'align-items', value:'stretch'},
    {style:'position', value:'relative'},
    {style:'flex-wrap', value:'nowrap'},
    {style:'overflow', value:'visible'},
    {style:'flex-grow', value:'0'},
    {style:'flex-shrink', value:'0'},
    {style:'left', value:'undefined'},
    {style:'top', value:'undefined'},
    {style:'right', value:'undefined'},
    {style:'bottom', value:'undefined'},
    {style:'display', value:'flex'},
  ].forEach(function(item) {
    assert(isDefaultStyleValue(item.style, item.value),
        item.style + ' should be ' + item.value);
  });
}

function setupTestTree(e, parent, node, genericNode, nodeName, parentName, index) {
  e.emitTestTreePrologue(nodeName);

  for (var style in node.style) {
    // Skip position info for root as it messes up tests
    if (node.declaredStyle[style] === "" &&
        (style == 'position' ||
         style == 'left' ||
         style == 'top' ||
         style == 'right' ||
         style == 'bottom' ||
         style == 'width' ||
         style == 'height')) {
      continue;
  }

    if (!isDefaultStyleValue(style, node.style[style])) {
      switch (style) {
        case 'direction':
          e.YGNodeStyleSetDirection(nodeName, directionValue(e, node.style[style]));
          break;
        case 'flex-direction':
          e.YGNodeStyleSetFlexDirection(nodeName, flexDirectionValue(e, node.style[style]));
          break;
        case 'justify-content':
          e.YGNodeStyleSetJustifyContent(nodeName, justifyValue(e, node.style[style]));
          break;
        case 'align-content':
          e.YGNodeStyleSetAlignContent(nodeName, alignValue(e, node.style[style]));
          break;
        case 'align-items':
          e.YGNodeStyleSetAlignItems(nodeName, alignValue(e, node.style[style]));
          break;
        case 'align-self':
          if (!parent || node.style[style] !== parent.style['align-items']) {
            e.YGNodeStyleSetAlignSelf(nodeName, alignValue(e, node.style[style]));
          }
          break;
        case 'position':
          e.YGNodeStyleSetPositionType(nodeName, positionValue(e, node.style[style]));
          break;
        case 'flex-wrap':
          e.YGNodeStyleSetFlexWrap(nodeName, wrapValue(e, node.style[style]));
          break;
        case 'overflow':
          e.YGNodeStyleSetOverflow(nodeName, overflowValue(e, node.style[style]));
          break;
        case 'flex-grow':
          e.YGNodeStyleSetFlexGrow(nodeName, node.style[style]);
          break;
        case 'flex-shrink':
          e.YGNodeStyleSetFlexShrink(nodeName, node.style[style]);
          break;
        case 'flex-basis':
          e.YGNodeStyleSetFlexBasis(nodeName, pointValue(e, node.style[style]));
          break;
        case 'left':
          if (genericNode.rawStyle.indexOf('start:') >= 0) {
            e.YGNodeStyleSetPosition(nodeName, e.YGEdgeStart, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetPosition(nodeName, e.YGEdgeLeft, pointValue(e, node.style[style]));
          }
          break;
        case 'top':
          e.YGNodeStyleSetPosition(nodeName, e.YGEdgeTop, pointValue(e, node.style[style]));
          break;
        case 'right':
          if (genericNode.rawStyle.indexOf('end:') >= 0) {
            e.YGNodeStyleSetPosition(nodeName, e.YGEdgeEnd, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetPosition(nodeName, e.YGEdgeRight, pointValue(e, node.style[style]));
          }
          break;
        case 'bottom':
          e.YGNodeStyleSetPosition(nodeName, e.YGEdgeBottom, pointValue(e, node.style[style]));
          break;
        case 'margin-left':
          if (genericNode.rawStyle.indexOf('margin-start:') >= 0) {
            e.YGNodeStyleSetMargin(nodeName, e.YGEdgeStart, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetMargin(nodeName, e.YGEdgeLeft, pointValue(e, node.style[style]));
          }
          break;
        case 'margin-top':
          e.YGNodeStyleSetMargin(nodeName, e.YGEdgeTop, pointValue(e, node.style[style]));
          break;
        case 'margin-right':
          if (genericNode.rawStyle.indexOf('margin-end:') >= 0) {
            e.YGNodeStyleSetMargin(nodeName, e.YGEdgeEnd, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetMargin(nodeName, e.YGEdgeRight, pointValue(e, node.style[style]));
          }
          break;
        case 'margin-bottom':
          e.YGNodeStyleSetMargin(nodeName, e.YGEdgeBottom, pointValue(e, node.style[style]));
          break;
        case 'padding-left':
          if (genericNode.rawStyle.indexOf('padding-start:') >= 0) {
            e.YGNodeStyleSetPadding(nodeName, e.YGEdgeStart, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetPadding(nodeName, e.YGEdgeLeft, pointValue(e, node.style[style]));
          }
          break;
        case 'padding-top':
          e.YGNodeStyleSetPadding(nodeName, e.YGEdgeTop, pointValue(e, node.style[style]));
          break;
        case 'padding-right':
          if (genericNode.rawStyle.indexOf('padding-end:') >= 0) {
            e.YGNodeStyleSetPadding(nodeName, e.YGEdgeEnd, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetPadding(nodeName, e.YGEdgeRight, pointValue(e, node.style[style]));
          }
          break;
        case 'padding-bottom':
          e.YGNodeStyleSetPadding(nodeName, e.YGEdgeBottom, pointValue(e, node.style[style]));
          break;
        case 'border-left-width':
          if (genericNode.rawStyle.indexOf('border-start-width:') >= 0) {
            e.YGNodeStyleSetBorder(nodeName, e.YGEdgeStart, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetBorder(nodeName, e.YGEdgeLeft, pointValue(e, node.style[style]));
          }
          break;
        case 'border-top-width':
          e.YGNodeStyleSetBorder(nodeName, e.YGEdgeTop, pointValue(e, node.style[style]));
          break;
        case 'border-right-width':
          if (genericNode.rawStyle.indexOf('border-end-width:') >= 0) {
            e.YGNodeStyleSetBorder(nodeName, e.YGEdgeEnd, pointValue(e, node.style[style]));
          } else {
            e.YGNodeStyleSetBorder(nodeName, e.YGEdgeRight, pointValue(e, node.style[style]));
          }
          break;
        case 'border-bottom-width':
          e.YGNodeStyleSetBorder(nodeName, e.YGEdgeBottom, pointValue(e, node.style[style]));
          break;
        case 'width':
          e.YGNodeStyleSetWidth(nodeName, pointValue(e, node.style[style]));
          break;
        case 'min-width':
          e.YGNodeStyleSetMinWidth(nodeName, pointValue(e, node.style[style]));
          break;
        case 'max-width':
          e.YGNodeStyleSetMaxWidth(nodeName, pointValue(e, node.style[style]));
          break;
        case 'height':
          e.YGNodeStyleSetHeight(nodeName, pointValue(e, node.style[style]));
          break;
        case 'min-height':
          e.YGNodeStyleSetMinHeight(nodeName, pointValue(e, node.style[style]));
          break;
        case 'max-height':
          e.YGNodeStyleSetMaxHeight(nodeName, pointValue(e, node.style[style]));
          break;
        case 'display':
          e.YGNodeStyleSetDisplay(nodeName, displayValue(e, node.style[style]))
          break;
      }
    }
  }

  if (parentName) {
    e.YGNodeInsertChild(parentName, nodeName, index);
  }

  for (var i = 0; i < node.children.length; i++) {
    e.push('');
    var childName = nodeName + '_child' + i;
    setupTestTree(
        e,
        node,
        node.children[i],
        genericNode.children[i],
        childName,
        nodeName,
        i);
  }
}

function overflowValue(e, value) {
  switch (value) {
    case 'visible': return e.YGOverflowVisible;
    case 'hidden': return e.YGOverflowHidden;
  }
}

function wrapValue(e, value) {
  switch (value) {
    case 'wrap': return e.YGWrapWrap;
    case 'wrap-reverse': return e.YGWrapWrapReverse;
    case 'nowrap': return e.YGWrapNoWrap;
  }
}

function flexDirectionValue(e, value) {
  switch (value) {
    case 'row': return e.YGFlexDirectionRow;
    case 'row-reverse': return e.YGFlexDirectionRowReverse;
    case 'column': return e.YGFlexDirectionColumn;
    case 'column-reverse': return e.YGFlexDirectionColumnReverse;
  }
}

function justifyValue(e, value) {
  switch (value) {
    case 'center': return e.YGJustifyCenter;
    case 'space-around': return e.YGJustifySpaceAround;
    case 'space-between': return e.YGJustifySpaceBetween;
    case 'space-evenly': return e.YGJustifySpaceEvenly;
    case 'flex-start': return e.YGJustifyFlexStart;
    case 'flex-end': return e.YGJustifyFlexEnd;
  }
}

function positionValue(e, value) {
  switch (value) {
    case 'absolute': return e.YGPositionTypeAbsolute;
    default: return e.YGPositionTypeRelative
  }
}

function directionValue(e, value) {
  switch (value) {
    case 'ltr': return e.YGDirectionLTR;
    case 'rtl': return e.YGDirectionRTL;
    case 'inherit': return e.YGDirectionInherit;
  }
}

function alignValue(e, value) {
  switch (value) {
    case 'auto': return e.YGAlignAuto;
    case 'center': return e.YGAlignCenter;
    case 'stretch': return e.YGAlignStretch;
    case 'flex-start': return e.YGAlignFlexStart;
    case 'flex-end': return e.YGAlignFlexEnd;
    case 'space-between': return e.YGAlignSpaceBetween;
    case 'space-around': return e.YGAlignSpaceAround;
    case 'baseline': return e.YGAlignBaseline;
  }
}

function pointValue(e, value) {
  switch (value) {
    case 'auto': return e.YGAuto;
    case 'undefined': return e.YGUndefined;
    default: return value;
  }
}

function displayValue(e, value){
  switch(value){
    case 'flex': return e.YGDisplayFlex;
    case 'none': return e.YGDisplayNone;
  }
}

var DEFAULT_STYLES = new Map();

function isDefaultStyleValue(style, value) {
  let defaultStyle = DEFAULT_STYLES.get(style);
  if (defaultStyle == null) {
    switch (style) {
      case 'position':
        defaultStyle = new Set(['relative']);;
        break;

      case 'left':
      case 'top':
      case 'right':
      case 'bottom':
      case 'start':
      case 'end':
        defaultStyle = new Set(['undefined']);
        break;

      case 'min-height':
      case 'min-width':
        defaultStyle = new Set(['0', '0px', 'auto']);
        break;

      default:
        var node = document.getElementById('default');
        defaultStyle = new Set([getComputedStyle(node, null)[style]]);
        break;
    }
    DEFAULT_STYLES.set(style, defaultStyle);
  }
  return DEFAULT_STYLES.get(style).has(value);
}

function getRoundedSize(node) {
  var boundingRect = node.getBoundingClientRect();
  return {
    width: Math.round(boundingRect.right) - Math.round(boundingRect.left),
    height: Math.round(boundingRect.bottom) - Math.round(boundingRect.top)
  };
}

function calculateTree(root, roundToPixelGrid) {
  var rootLayout = [];

  for (var i = 0; i < root.children.length; i++) {
    var child = root.children[i];
    var layout = {
      name: child.id !== '' ? child.id : 'INSERT_NAME_HERE',
      left: child.offsetLeft + child.parentNode.clientLeft,
      top: child.offsetTop + child.parentNode.clientTop,
      width: child.offsetWidth,
      height: child.offsetHeight,
      children: calculateTree(child, roundToPixelGrid),
      style: getYogaStyle(child),
      declaredStyle: child.style,
      rawStyle: child.getAttribute('style'),
      experiments: child.getAttribute('experiments')
          ? child.getAttribute('experiments').split(' ')
          : [],
    };

    var size = getRoundedSize(child);
    layout.width = size.width;
    layout.height = size.height;

    rootLayout.push(layout);
  }

  return rootLayout;
}

function getYogaStyle(node) {
  return [
    'direction',
    'flex-direction',
    'justify-content',
    'align-content',
    'align-items',
    'align-self',
    'position',
    'flex-wrap',
    'overflow',
    'flex-grow',
    'flex-shrink',
    'flex-basis',
    'left',
    'top',
    'right',
    'bottom',
    'margin-left',
    'margin-top',
    'margin-right',
    'margin-bottom',
    'padding-left',
    'padding-top',
    'padding-right',
    'padding-bottom',
    'border-left-width',
    'border-top-width',
    'border-right-width',
    'border-bottom-width',
    'width',
    'min-width',
    'max-width',
    'height',
    'min-height',
    'max-height',
    'display',
  ].reduce(function(map, key) {
    map[key] = node.style[key] || getComputedStyle(node, null).getPropertyValue(key);
    return map;
  }, {});
}

var Emitter = function(lang, indent) {
  this.lang = lang;
  this.indent = indent;
  this.indents = [];
  this.lines = [];
};

Emitter.prototype = Object.create(Object.prototype, {
  constructor:{value:Emitter},

  pushIndent:{value:function() {
    this.indents.push(this.indent);
  }},

  popIndent:{value:function() {
    this.indents.pop();
  }},

  push:{value:function(line) {
    if (line instanceof Array) {
      line.forEach(function(element) {
        this.push(element);
      }, this);
      return;
    } else if (line.length > 0) {
      line = this.indents.join('') + line;
    }
    this.lines.push(line);
  }},

  print:{value:function() {
    console.log(this.lines.join('\n'));
  }},
});


text:
Tag: NCAOC
An Invitation to the Governor's Mansion
July 24, 2013 / Jillian / 0 Comments
This summer, I have been fortunate to be a supervisor for the N.C. State Government Internship Program, run by the Youth Advocacy and Involvement Office of the Department of Administration.
It's a highly selective program – both for students and for government agencies. After an intense, months-long process of putting together internship proposals and interviewing candidates, we were matched with a terrific grad student (pictured with me, above) to help the content effort for our intranet redesign project. It turned out to be a great partnership, and I'm sad our intern's tenure is coming to a close on Friday.
My formal invitation to the reception
The highlight of the internship program is a reception hosted by the governor at the Executive Mansion. This year, interns and supervisors were welcomed with cookies and cold drinks on a blistering hot day, and we were treated to an address by Governor Pat McCrory as he stood on the staircase of his home. He touched on his previous internship experience, the importance of public service, and a brief tour of the mansion.
The governor prepares to address the interns
Our intern definitely deserved such an honor for his hard work and achievements, and I'm sure the other interns are equally as deserving! It was a pleasure to take part in this year's program – and a real treat to have my first visit to the Executive Mansion with the governor himself as the guide.
Check out the Governor's Office's coverage of the event:
Governor's Newsletter
Event Flickr gallery
NCJC Safety Newsletters
Did you know that June is National Safety Month?
A few weeks ago, the N.C. Judicial Center (NCJC) Emergency Planning and Safety committees asked my help to disseminate information to NCJC staff to mark the occasion. I sat down with several managers on the committees to listen to their needs, and these main themes surfaced: fires, high-wind events (tornadoes and hurricanes), and domestic violence and health-related emergencies. We took those themes and sketched out a month-long communications plan:
Include general safety articles in the two June editions of the NCJC Building Bulletin (BB) newsletter
Produce three weekly "special editions" of the BB that would each cover one of these safety themes
There was a treasure trove of information on each of our three themes, but it was not very well-organized. I combed through notes and draft articles provided by committee members, old safety announcements from the BB, the NCJC Emergency Operations Procedures policy, and other HR documents and policies. For each edition, I organized my notes into a series of articles, which I then laid out in our standard HTML newsletter template. I created all the images and graphics, as well. All this, on top of my normal (overloaded) workload! Whew!
Check out the final products:
Fire Safety Newsletter
High Wind Safety Newsletter
Health, Violence, and Other Events Safety Newsletter
Fortunately, though, my hard work paid off as this series of safety-themed newsletters has been exceptionally well-received by committee members, executive managers, and staff. For example, a copy of the High Wind newsletter found its way to the Chief Justice of the N.C. Supreme Court's office, and a request was made to send future editions to members of her staff.
The NCJC Safety Information webpage is accessible by mobile devices during an emergency event.
Also, as part of the publishing process, the committees wanted to include links to the newsletters from our static HTML intranet website (which is behind a firewall and only accessible from computers on the Judicial Branch network). That part was easy. However, they also requested that the newsletters be readily accessible by smartphones during an emergency – which posed a problem, as smartphones cannot access our intranet. So, I quickly created a basic HTML page outside our intranet, which includes links to the safety newsletters, policies, and other information that could be important during an event.
For more details on my newsletter work, check out:
Email Newsletter blog post
March 14, 2013 / Jillian / 0 Comments
The majority of my job responsibilities involve effectively communicating messages to internal, as opposed to external, audiences. When I'm not busy working on the redesign of the Judicial Branch's employee intranet site, I'm usually working on one of the N.C. Administrative Office of the Courts' employee newsletters. Check out examples of my newsletter work.
N.C. JUDICIAL CENTER BUILDING BULLETIN
I am the editor of the award-winning N.C. Judicial Center (NCJC) Building Bulletin, which reports on office news for the 400+ employees on our campus. The Building Bulletin has been my responsibility since June 2012, after a part-time resource dedicated to this newsletter left the organization. The newsletter has traditionally been sent monthly, but under my direction we've started sending updates at least twice each month. My role as editor is to generate content ideas, write and edit articles, take and edit photos, create graphics, and build the newsletter in HTML/CSS. We are currently in the process of implementing the GovDelivery email newsletter delivery service, but at this point everything is still done manually.
I start with a yearly editorial calendar Excel spreadsheet, where I store content ideas for each month's edition. We have a handful of recurring features — for instance, our Meet Your Neighbor staff feature and monthly photography contest — and some seasonal topics that we cover annually. NCJC staff can submit articles or ideas, and I'm also constantly thinking of new content based on what's happening around the office. Our main goal is to share information and get staff involved in the office community.
Once I have an idea of the content, I start building the newsletter as a webpage using an HTML/CSS template. Our former graphic designer created the branded template, and I've built on it over the past several months. I write new articles, edit audience-submitted content, design graphics in Adobe Photoshop CS6, take new or edit existing photos, create any surveys — and then drop them into the HTML code. It's a time-consuming process, but HTML/CSS gives me the freedom to tweak the layout to my exact specifications. One of our internal developers created a program that generates photo gallery webpages from a list of image files, so I will run that program as needed, as well.
Shortly before the publish date, I'll send the finished newsletter file to my team members for review. Then, I'll make any last-minute changes before uploading the newsletter files (the main HTML files as well as any images, PDFs, or photo galleries) to our FTP server. At this point, I check the newsletter URL in Internet Explorer, the official browser that all Judicial Branch employees use, for any strange behaviors. If everything looks good, I'll send the newsletter webpage as an email via Outlook.
Once we get GovDelivery up and running, the production of the newsletter will be a much simpler process. I'll still be tasked with producing the right articles, images, and graphics, but building and sending the newsletter will be a more automated process.
NCJC EMPLOYEE APPRECIATION COMMITTEE
As a member of the N.C. Judicial Center's Employee Appreciation Committee (EAC), I help promote upcoming events and fundraisers — primarily through email newsletters and flyers — to the roughly 400 campus employees on an as-needed basis. The EAC newsletter currently follows the same production process as the NCJC Building Bulletin (outlined above), from which it also borrows its design template. I do create custom header banners for each issue, though.
INSIDE THE CHAMBERS
This newsletter, published weekly whenever the N.C. General Assembly is in session, provides relevant legislative updates to all 7,000+ employees of the N.C. Judicial Branch.
When Inside the Chambers launched during the 2012 legislative short session, our former graphic designer based the HTML template on that of the Building Bulletin, but with a customized header banner. The newsletter started out with weekly commentary, budget news, and the latest legislation updates from our Legal and Legislative Services Division — but, in 2013 it evolved into a dedicated vehicle for disseminating legislation updates.
This newsletter follows the same production process as the Building Bulletin, but it differs from the others in that I am not solely responsible for generating content. In this case, I've worked with our Legal team to define a standard process and schedule for submitting content so I can hit my publishing deadlines.
As you can see, a lot of behind-the-scenes work goes into the creation of these newsletters. These are the three newsletters that I manage, but there are also others that I help edit or oversee each month. In addition to editing and production work, I've also worked with communications and technology staff to create guidelines and define procedures for Judicial Branch staff to follow when setting up additional newsletters. Newsletter work only comprises about 10-15% of my job, but it's a chance to be creative, share interesting stories, and get others involved in company events and culture.
Make sure you check out the rest of my newsletter work.
The N.C. Administrative Office of the Courts' Communications Office is responsible for managing several email newsletters for the NCAOC and the N.C. Judicial Branch. Jillian Kuhn Warren oversees and edits many of these newsletters, spending roughly 15% of her workweek on them. Her three primary newsletters are listed below.
Currently, Jillian creates all content (copy, images, etc.), produces the newsletter as a webpage with HTML and CSS, uploads the newsletters to the web via FTP, and sends the newsletters via Outlook. Read more details in her Email Newsletters blog post. She has done extensive research and presented proposals on various email newsletter delivery services, and the NCAOC is in the process of implementing the GovDelivery system.
Jillian is the editor and primary contributor to this award-winning monthly newsletter for employees of the N.C. Judicial Center.
Before Jillian became editor, the Building Bulletin looked like this: May 2012. Multiple staff members, including one dedicated part-time employee, published one edition each month and often spent a late night at work prior to the publish date. Now, with Jillian as the sole editor, Building Bulletin publishes at least two editions per month and is always ready on time.
N.C. Judicial Center Employee Appreciation Committee
Jillian is the editor of this periodic newsletter to inform N.C. Judicial Center employees of events held by the Employee Appreciation Committee.
Employee Appreciation Week 2013
National Donut Day Fundraiser (and the accompanying event flyer)
Mother's Day Flowers Fundraiser
EAC Events March Madness 2013
Krispy Kreme Fundraiser 2013
Holiday Feast Invitation 2012
Employee Appreciation Week July 2012
N.C. Judicial Center Safety
Jillian is the editor of these special-edition newsletters that recognize National Safety Month and provide relevant emergency information to N.C. Judicial Center staff on behalf of the Emergency Planning and Safety committees. Learn more through her NCJC Safety Newsletters blog post.
Jillian is the production editor of this newsletter that provides weekly legislative updates to all employees of the N.C. Judicial Branch while the N.C. General Assembly is in session.
February 25, 2013 edition
Praise for Jillian's Newsletters
"Thank you for providing our employees so much information and helping to make this a fun place to work." – an executive manager
"BB thanks for the article and thanks for being such a class act." – a manager
"I thought today's BB was quite good — a very nice presentation/blend of news, stuff and fluff." – a coworker
On Friday, September 16, I won the Excellence in Communications Award from the North Carolina Association for Government Information Officers (NCAGIO), during a ceremony at the association's annual seminar in Chapel Hill. My email newsletter, the N.C. Judicial Center Building Bulletin, took home Honorable Mention (third place) in the Publications Category.
The NCJC Building Bulletin is a monthly email newsletter for employees who work in the N.C. Judicial Center. I've been the editor since June.
Check out the October issue of the NCJC Building Bulletin
For the awards, the judges reviewed the following three issues of the Building Bulletin:
I am responsible for all newsletter content. Staff members are encouraged to submit story ideas and drafts, but I also create original articles and images. Then, I put all the content into an HTML template, upload the files to an FTP server, and email the newsletter webpage via Outlook. We're in the process of transitioning to an email newsletter software service that will eliminate all the hand-coding of HTML that I currently do each month.
I put a lot of hard work into the Building Bulletin, and I'm so proud that it was honored by the NCAGIO!
November 6, 2012 / Jillian / 0 Comments
I've been using Adobe Photoshop for about a decade now. I first remember using it in college for my film courses, and I've been using it personally and professionally ever since. However, I've never had any formal Photoshop training.
Currently, I'm halfway through the N.C. Office of State Personnel (OSP) Professional Skills Program's Photoshop 2 course, and I'll have earned my certificate from the program by the end of the week. So far, after the first day of class, I've actually learned a lot! Over the years I've developed my own workarounds and "hacks" to achieve certain effects, but the class has taught me easier and more efficient ways to get the same results. I've already been able to put my new skills into practice in my projects at work.
This is the second course I've taken through OSP. Earlier in the year, I arranged for a group of my coworkers and me to take their Web Writing and Search Engine Optimization course as a precursor to our web redesign content migration efforts. Hopefully I'll have the opportunity to take more courses in the future!
Using Google Calendar to Manage Tasks


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L'Estadi comunal d'Andorre-la-Vieille est un stade à multi-usages basé à Andorre-la-Vieille, en Andorre. Il est principalement utilisé pour les rencontres de football. Le stade possède également une piste d'athlétisme.

L'enceinte a une capacité de 838 places.

Histoire
Il sert de stade d'accueil pour les rencontres du championnat d'Andorre de football de première et de deuxième division, les matchs se partagent entre ce stade et l'Estadi comunal d'Aixovall. Il accueille également les rencontres de Coupe d'Andorre et de la Supercoupe d'Andorre de football.

Jusqu'à l'inauguration de l'Estadi Nacional en 2014, l'Estadi comunal accueillait aussi les rencontres à domicile de l'équipe d'Andorre de football.

Le stade a aussi accueilli les épreuves d'athlétisme des jeux des petits États d'Europe 2005.

Équipement sportif achevé en 1990
Comunal Andorre-la-Vieille
Comunal Andorre-la-Vieille
Comunal Andorre-la-Vieille
Andorre-la-Vieille


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FOX59 TV Schedule
Overnight traffic to be impacted starting Sunday as INDOT works to 'modernize' downtown I-65 bridges
Posted 10:21 AM, September 29, 2016, by Bill Remeika, Updated at 04:24PM, September 29, 2016
INDIANAPOLIS, Ind. — The Indiana Department of Transportation (INDOT) has awarded a $4.6 million contract to Proshot Concrete for maintenance and modernization of the Interstate 65 bridges spanning the north side of downtown Indianapolis from Senate Avenue to Alabama Street.
Work is underway underneath the bridges, including concrete patching, painting steel and wrapping bridge piers with a fiber-reinforced plastic to protect and strengthen the structure.
Construction on the bridge decks above is scheduled to begin Sunday, Oct. 2 and will significantly affect overnight traffic.
During a maximum of 20 overnight closures, crews will seal joints between each bridge span to prevent moisture from penetrating and deteriorating the structures' concrete and steel. Concrete pavement will also be repaired during the overnight closures.
Northbound I-65 closures
On Sunday, Oct. 2 and Monday, Oct. 3, the northbound I-65 Exit 113 ramps to and from Meridian and Pennsylvania streets will close starting at 9 p.m. until 6 a.m.
On Wednesday, Oct. 5 and Thursday, Oct. 6, work on northbound I-65 will close all lanes between 9 p.m. and 6 a.m. Nightly closures on northbound I-65 will resume at 9 p.m. on Sunday, Oct. 9 through 6 a.m. on Friday, Oct. 14. The Exit 113 ramps to and from Meridian and Pennsylvania Streets will remain open while northbound I-65 is closed.
Advanced warning signs are being installed to direct through traffic – including large trucks – to take I-465 around Indianapolis.
During the overnight closures of northbound I-65:
The northbound I-65 Exit 114 ramp to Dr. Martin Luther King, Jr. Street/West Street will close temporarily, and
The Pine Street entrance ramp to northbound I-65 will close temporarily.
Southbound I-65 closures
After northbound work is complete, night crews will move to complete similar work on southbound I-65. Specific dates and closures will be announced as work on northbound I-65 progresses over the next two weeks.
Ramp work will close the southbound I-65 Exit 113 ramps to and from Meridian Street during the weeknights between 9 p.m. and 6 a.m.
Work on southbound I-65 will close all but one lane during the weeknights between 9 p.m. and 6 a.m. The Exit 113 ramps to and from Pennsylvania and Meridian Streets will remain open while lanes are closed on southbound I-65.
During the overnight lane closures, the entrance ramp from Dr. Martin Luther King, Jr. Street/West Street to southbound I-65 will close.
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Chinese Cuisine.
Hong Kong Cafe has quickly won the hearts (and stomachs) of it's customers. Earning the Best of Madison Award (for Oriental Restaurants) after only one year in business, is an accomplishment to be noted. Here you will find authentic Chinese cuisine - not the "American-styled" that you will find in most "Chinese" restaurants. The menu offers a huge selection of traditional Chinese foods and they will gladly create a meal that meets the most discriminating of tastes. The food is healthy, using little oil and lots of vegetables and most dishes contain no MSG. Just one try and this will become your favorite restaurant too.
"...For a traditional Chinese experience, head to Mills Street on a Saturday or Sunday from 11 a.m. to 2:30 p.m. for dim sum. With dim sum, you order little plates of assorted steamed buns and dumplings, meats, seafood and vegetables. All this is kept track of on a tally sheet... Be sure to try the unsalad-like Chinese shrimp salad. It's made with shrimp fried in a light batter and served with pineapple and broccoli in a sweet, velvety mayo-like sauce. Sounds odd, but it is quite popular and delicious. Other popular dim sum items include steamed shrimp dumplings and pan-fried turnip cake. "It's wonderful to win all the awards," Leung says. "It means that all of my family's hard work has been recognized....""
- Madison.com, "HONG KONG CAFE'S CANTONESE SATISFIES MADISONIANS"
Lunch Menu Download
Dinner Menu Download
Monday - Thursday: 11am-9pm
Friday, Saturday: 11am-10pm
Order Online EATSTREET
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Private hire vehicles cannot ply for hire in the street or at taxi ranks.
Journeys must be pre-booked, normally by phone or in person at a cab office. Failure to do so is an offence and invalidates the vehicle's insurance cover. Fares for private hire vehicles are not regulated by the council - the cost of a journey will normally be based on a rate per mile or should be agreed with the company before the journey.
Private hire vehicles licensed by the council must display a yellow plate on the front and the rear and a smaller internal plate. Roof signs are not permitted. Private hire drivers must also wear an ID badge issued by the council which includes his/her photograph.
The main Acts of Parliament covering the licensing of Private Hire Vehicles are contained in Part II of the Local Government (Miscellaneous Provisions) Act 1976.
NB: The vehicle will also be subject to a visual inspection carried out by an authorised licensing officer of the council.
NB: making a false statement at any time to obtain a vehicle licence is a serious offence.
The appropriate fee is paid (fee table below).
Has the vehicle ever been classified as a category write-off?
Vehicles which have been classified as Category A or B will not be considered suitable to be a licensed.
Once the fee has been paid, the vehicle has passed the Council's inspection test and the private hire vehicle insurance has been verified then the vehicle licence and identification plates will be issued to you from the licensing department.
Dependent on the age of the vehicle, interim testing may be required during the period of the licence, as shown below.
The age of the vehicle will be determined on the start date of the licence from the date of first registration as stated on the vehicle registration document.