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Garça

Garça is a town located in the west-central part of the state of São Paulo, Brazil. The population is 44,409 (2020 est.) in an area of 556 km2.

Established on October 4, 1924, it was one of the cities that had been part of the coffee circle, in the beginning of the 20th century. Garça is known for its coffee plantations, the iron line city and by the Cerejeiras Festival ("cherry tree festival") that takes place every year. The average altitude is 663 m above sea level.

Climate
The climate is subtropical with temperatures ranging from 17.8 °C to 28.5 °C. The precipitation is 1.274,4 mm/a. The rainy season occurs in the summer (December until March), with the temperature hovering between 25 and 30 °C. Low temperatures occur in the months of April and July.

Topography
Garça is situated in a landscape of rolling hills, where many small streams are formed, converging all to the formation of the rivers Rio do Peixe, Tibiriça and Feio.

Soil types

 * Podzol, Marília Variation

Vegetation
The region is characterized by lush vegetation, predominantly grassy, while the native vegetation was primarily tropical forest.

Media
In telecommunications, the city was served by Companhia Telefônica Brasileira until 1973, when it began to be served by Telecomunicações de São Paulo. In July 1998, this company was acquired by Telefónica, which adopted the Vivo brand in 2012.

The company is currently an operator of cell phones, fixed lines, internet (fiber optics/4G) and television (satellite and cable).

Religion
Christianity is present in the city as follows:

Catholic Church
The Catholic church in the municipality is part of the Roman Catholic Diocese of Marília.

Protestant Church
The most diverse evangelical beliefs are present in the city, mainly Pentecostal, including the Assemblies of God in Brazil (the largest evangelical church in the country), Christian Congregation in Brazil, among others. These denominations are growing more and more throughout Brazil.

Famous Garcenses

 * Roberto Carlos, football player.
 * Valdir Peres, football player.

title: Garça


text:
Anton Yelchin

Anton Viktorovich Yelchin (Антон Викторович Ельчин; March 11, 1989 – June 19, 2016) was an American actor. Born in the Soviet Union to a Russian Jewish family, he emigrated to the United States with his parents at the age of six months. He began his career as a child actor, appearing as the lead of the mystery drama film Hearts in Atlantis (2001) and a series regular on the Showtime comedy-drama Huff (2004–2006). Yelchin landed higher-profile film roles in 2009, portraying Pavel Chekov in the Star Trek reboot and Kyle Reese in Terminator Salvation. He reprised his role as Chekov in the sequels Star Trek Into Darkness (2013) and Star Trek Beyond (2016).

Yelchin frequently worked on independent and lower-profile films, headlining the romantic drama Like Crazy (2011), the 2011 remake of Fright Night, the supernatural thriller Odd Thomas (2013), the romance 5 to 7 (2014), the horror comedy Burying the Ex (2014), the neo-noir The Driftless Area (2015), and the horror thriller Green Room (2015). As a voice actor, he voiced Clumsy Smurf in the live-action Smurfs films (2011–2013) and lead role James "Jim" Lake Jr. on the Netflix animated series Trollhunters: Tales of Arcadia (2016–2018). He maintained an active career until his accidental death in 2016 when he was fatally injured by his SUV.

Early life and education
Yelchin was born on March 11, 1989, in Leningrad, Russian SFSR, Soviet Union. His parents, Irina Korina and Viktor Yelchin, were pair figure skaters who were stars of the Leningrad Ice Ballet for 15 years. His family is Jewish, and were subjected to religious and political oppression in the Soviet Union. Yelchin said that his grandparents "suffered in ways [he] can't even begin to understand under Stalin". Nationally, Yelchin's parents were the third-ranked pair team; they thus qualified for the 1972 Winter Olympics, but were not permitted to participate by the Soviet authorities. Yelchin said the reason was unclear: "I don't exactly know what that was – because they were Jewish or because the KGB didn't want them to travel."

Yelchin's family left for the United States in September 1989, when Anton was six months old, and were thereafter granted refugee status from the Department of State. His mother worked as a figure skating choreographer and his father as a figure skating coach, having been Sasha Cohen's first trainer. Yelchin's uncle is the children's author and painter Eugene Yelchin. In an article published in the Los Angeles Times in December 1989, Yelchin's mother stated, "A woman came up, saw Anton, and said, 'He's beautiful. He will be actor.'" Yelchin stated that he "wasn't very good" at figure skating, his parents' profession.

Yelchin grew up in the San Fernando Valley. He attended the Sherman Oaks Center for Enriched Studies in Tarzana, California and enrolled at the University of Southern California in the fall of 2007 to study film.

Yelchin was born with cystic fibrosis, though the details of his medical condition were revealed posthumously in 2017 by a foundation established in his name, the Anton Yelchin Foundation.

Career
After his film debut in A Man Is Mostly Water, Yelchin's early roles in both film and television include Delivering Milo, Along Came a Spider, Taken, and House of D. Yelchin played Bobby Garfield in Hearts in Atlantis (2001), for which he received a Young Artist Award for Best Performance in a Feature Film: Leading Young Actor in 2002. On Showtime's television series Huff, Yelchin played Byrd Huffstodt, the 14-year-old son of the eponymous character (Hank Azaria). In 2004, he guest-starred in the Season Four episode of Curb Your Enthusiasm as Stewart, Cheryl David's cousin and a self-described magician who knows a card trick. In 2006, he guest-starred in the Law & Order: Criminal Intent episode "Tru Love", as a boy who falls in love with his teacher. He also appeared in the Criminal Minds episode "Sex, Birth & Death" as Nathan Harris, a boy who has murderous urges toward prostitutes and approaches Dr. Spencer Reid to help him before he actually does kill.

In Alpha Dog, Yelchin played Zack Mazursky, a character based on real-life murder victim Nicholas Markowitz. USA Today's review described Yelchin's performance as "heartbreakingly endearing". After the film's premiere, Markowitz's mother praised his portrayal of her son. Yelchin subsequently headlined Fierce People, which received a limited release on September 7, 2007. In 2008, he played the title role in Charlie Bartlett, a film about a wealthy teenager in a public high school. He also appeared alongside the Russian duo t.A.T.u. in the film You and I (which was filmed in Moscow during the summer of 2007) and costarred in Middle of Nowhere. Yelchin played supporting roles in two blockbuster films released in May 2009: Star Trek, in which he played teenage navigator Pavel Chekov, and Terminator Salvation, in which he played a young Kyle Reese.

In 2011, Yelchin played Charley Brewster in Craig Gillespie's remake film Fright Night, starred in the romantic drama Like Crazy, and voiced Clumsy Smurf in the film adaptation of The Smurfs, as well as its 2013 sequel. He replaced Russell Tovey for the voice role of Albino Pirate in the American version of the animated film The Pirates! In an Adventure with Scientists! (also known as The Pirates! Band of Misfits) (2012). Yelchin voiced Shun in Studio Ghibli's From Up on Poppy Hill.

Yelchin again played the role of Chekov in the 2013 film Star Trek Into Darkness. He also played the lead in the thriller Odd Thomas (2013) as well as the horror comedy Burying the Ex and the romantic film 5 to 7 (both in 2014). In 2015, Yelchin starred in the independent horror film Green Room, which premiered at the Cannes Film Festival that year and received a limited theatrical release in May 2016, and the neo-noir film The Driftless Area.

Shortly before his death, Yelchin reprised his role as Chekov in Star Trek Beyond, which was released on July 22, 2016. He also completed filming several independent films that were released posthumously. Yelchin also recorded the voice role of Jim Lake Jr. on Guillermo del Toro's Trollhunters: Tales of Arcadia.

Personal life
Yelchin enjoyed playing guitar, which he said gave him fulfillment, and was a fan of acoustic blues music. He once played for a punk band called The Hammerheads.

He was also interested in photography. In January 2018, an exhibit of Yelchin's photography entitled Anton Yelchin: Provocative Beauty was displayed at New York City's De Buck Gallery. Yelchin's photography has since been critically acclaimed by various magazines around the world as exhibits continue.

Yelchin briefly dated his co-star Kristen Stewart when they were filming Fierce People; after his death, she described him as her "first heartbreak".

Death
After Yelchin failed to arrive at a rehearsal on June 18, 2016, he was found by friends at around 1:10 a.m. on June 19, 2016, pinned between his Jeep Grand Cherokee and a brick pillar gate post outside his house in Studio City, Los Angeles, dead from a freak accident. As Yelchin got out of his car and went to check his locked gate for mail, the vehicle apparently rolled back down his driveway, which was on a steep incline, and trapped him against the pillar and a security fence. Yelchin was pronounced dead at age 27 at the scene; the Los Angeles County Coroner's office identified the cause of death as "blunt traumatic asphyxia" and stated that there were "no obvious suspicious circumstances involved".

Tributes
Following Yelchin's death, the producers of Star Trek stated that the role of Chekov would not be recast and that the character would be written out of any subsequent Star Trek films. Star Trek Beyond was dedicated to Yelchin and Leonard Nimoy, who also died between the release of Star Trek Into Darkness and Star Trek Beyond. Smurfs: The Lost Village was dedicated to Yelchin, as he had provided the voice of Clumsy Smurf in the live-action Smurfs films. Additionally, We Don't Belong Here, Rememory, Porto, Newness, Thoroughbreds, and the first two episodes of Trollhunters are dedicated to him, with the entirety of Trollhunters being dedicated to him upon its conclusion in May 2018. Yelchin was also featured in the "In Memoriam" section during the 89th Academy Awards. Following the aftermath of Yelchin's death, actors and other celebrities posted their condolences via social media.

In October 2017, a bronze statue of Yelchin was erected at his grave in the Hollywood Forever Cemetery. Celebrities present at the unveiling ceremony included Jennifer Lawrence, Zoe Saldana, Simon Pegg, J. J. Abrams, Emile Hirsch, Demi Moore, Jon Voight, Drake Doremus, and Jeremy Saulnier. Saldana spoke at the ceremony, paying tribute to Yelchin: "It is a bittersweet moment, because we're here for Anton, and he's not here with us. But, it alleviates my heart knowing that we'll keep him alive. We're going to keep remembering him in the hope that by practicing all the things he believed in and remembering all the love that he gave us, and all the joy he gave us, we're able to just keep him here with us."

Yelchin was memorialized in the online video game Star Trek Online. He received a memorial plaque alongside several other late Star Trek actors, including Nimoy, James Doohan, and Star Trek creator Gene Roddenberry. A Starfleet vessel named "Yelchin" is mentioned twice in Star Trek: Discovery episode "Unification III" (S03E07) and again in the season four finale "Coming Home" (S04E13).

On January 28, 2019, Viktor and Irina Yelchin premiered a documentary about their son—Love, Antosha—at the 2019 Sundance Film Festival.

In the final episode of Star Trek: Picard, a transmission can be heard from an Anton Chekov. Canonically, Anton Chekov is the son of Pavel Chekov, and was voiced by Walter Koenig, the first actor who played Pavel Chekov in Star Trek: The Original Series.

Lawsuit and recalls

Fiat Chrysler Automobiles (FCA), the manufacturer of the Grand Cherokee, was aware of 2014 and 2015 models having a high rate of rollaway incidents due to a gearshift design that could make it difficult for the driver to determine whether the vehicle was in park or still in gear. FCA had already recalled all 2014–15 Grand Cherokees for this concern in April 2016, but the software patch to repair the vehicles did not reach dealers until the week of Yelchin's death. Following his death, FCA accelerated the recall campaign and took steps to get the affected Jeeps repaired more quickly than originally planned.

On August 1, 2016, Yelchin's parents announced through their attorney that they were planning to file a wrongful death lawsuit against Fiat Chrysler. The dealership from which Yelchin purchased the vehicle stated that he was responsible for his own death, because he had allegedly "misused" and "modified" the vehicle. The dealer also asked to be removed from the lawsuit. On March 22, 2018, it was announced that Yelchin's family and Fiat Chrysler had confidentially settled out of court.

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

title: Anton Yelchin


text:
Rosa rubiginosa

Rosa rubiginosa (sweet briar, sweetbriar rose, sweet brier or eglantine; syn. R. eglanteria) is a species of rose native to Europe and western Asia.

Description
It is a dense deciduous shrub 2–3 meters high and across, with the stems bearing numerously hooked prickles. The foliage has a strong apple-like fragrance. The leaves are pinnately compound, 5–9 cm long, with 5–9 rounded to oval leaflets with a serrated margin, and numerous glandular hairs. The flowers are 1.8–3 cm in diameter, the five petals being pink with a white base, and the numerous stamens yellow; the flowers are produced in clusters of 2–7 together, from late spring to mid-summer. The fruit is a globose to oblong red hip 1–2 cm in diameter.

Etymology
Its name eglantine is from Middle English eglentyn, from Old French aiglantin (adj.), from aiglent 'sweetbrier', from Vulgar Latin *aculentus (with the ending of spinulentus 'thorny, prickly'), from Latin aculeus 'prickle', from acus 'needle'. Sweet refers to the sweet, apple fragrance of the leaves, while briar ~ brier refers to it being a thorny bush.

Distribution and habitat
Rosa rubiginosa is native to most of Europe with the exception of the extreme north (above 61°N), where it inhabits pastures and thorny bushes from the montane to the subalpine floor, with a sunny, continental climate. It is somewhat rare, with isolated specimens near roads and pastures frequented by cattle. Its presence is doubtful in western Asia. In Southern Europe it lives in higher altitudes, usually 1000 to 1700 m. In Portugal it is classified as Critically Endangered and is restricted to the Serra da Estrela range.

Cultivation and uses
In addition to its pink flowers, it is valued for its scent and the hips that form after the flowers and persist well into the winter. Graham Thomas recommends that it should be planted on the south or west side of the garden so that the fragrance will be brought into the garden on warm, moist winds. A specimen without any scent, and blush to white flowers may be the closely related fieldbriar, Rosa agrestis.

The tea made from the hips of this rose is very popular in Europe and elsewhere, where it is considered a healthy way for people to get their daily dose of vitamin C and other nutrients. A cup of rosehip tea will provide the minimum daily adult requirement of vitamin C. During World War II the British relied on rose hips and hops as the sources for their vitamins A and C. It was a common British wartime expression to say that: "We are getting by on our hips and hops."

In Tunisia, natural flower water is produced from its flowers.

In Chile and Argentina, where it is known in Spanish as "Rosa Mosqueta", it is cultivated to produce marmalades and cosmetic products, and has escaped into the wild in and near the Andes.

Invasive species

 * It has become an invasive species in most of Argentine Patagonia, particularly where the steppe meets the forest. Cattle spread the seed efficiently through their feces. Poor knowledge of how detrimental it is to the local economy and native species have lead Rosa rubiginosa to become the threat that it is today. It is estimated that it causes several millions of dollars worth of damage each year.
 * Rosa rubiginosa is an invasive species in southeast Australia.
 * It is classified as a restricted plant in New Zealand and is banned from sale, propagation and distribution in the Auckland, Canterbury, and Southland regions. The New Zealand Department of Conservation classifies R. rubiginosa as an "environmental weed". The plant is present in extensive areas of pasture and tussock grasslands in the Otago and Canterbury regions, where the seeds are spread by cattle, possums and birds that eat the hips. Growth from seed is aided by the reduction in competing pasture by rabbits.
 * It is listed as a Category 1 Declared Weed in South Africa. These plants may no longer be planted or propagated, and all trade in their seeds, cuttings or other propagative material is prohibited.

title: Rosa rubiginosa


text: Category:German basketball players

title: Category:German basketball players


text:
Heneage Finch, 3rd Earl of Winchilsea

Heneage Finch, 3rd Earl of Winchilsea (c. 1628 – 28 September 1689) was an English peer and diplomat who served as the English ambassador to the Ottoman Empire from 1660 to 1669.

Early life
Finch was the only surviving son of Thomas Finch, 2nd Earl of Winchilsea and the former Cecille Wentworth of Gosfield Hall, Essex.

His paternal grandparents were Sir Moyle Finch, 1st Baronet and Elizabeth Finch, suo jure 1st Countess of Winchilsea. His father inherited his grandfather's baronetcy from his uncle, Sir Theophilus Finch, 2nd Baronet, who died without issue in 1619. His maternal grandparents were John Wentworth, High Sheriff of Essex and Cecily Unton. His first cousin was Heneage Finch, 1st Earl of Nottingham.

He was educated at Queens' College, Cambridge.

Career
On his return from Ottoman territory in June 1668, King Charles II remarked to Finch, "My Lord, you have not only built a town, but peopled it too". Winchilsea, in an obvious reference to Charles' own brood of natural children, replied that after all, he was the King's representative.

Lord Finch was appointed by his friend George Monck, 1st Duke of Albemarle a Governor of Dover Castle, and Lord Warden of the Cinque Ports in July 1660. He was also Lord Lieutenant of Kent and afterwards ambassador to the Ottoman Empire, and served in this capacity between 1668 and 1672.

Samuel Pepys first referred to him as the Lord Winchilsea.

King Charles II had landed at Kent on his way to London to secure the throne on 25 May 1660. The King arrived in Dover with 20 ships and frigates, the Lord General and his lifeguard were accompanied by the Earl of Winchelsea to the cheer of the crowding locals gathered upon the beach to witness a salute fired from the guns of Dover Castle. The King created him Baron FitzHerbert, of Eastwell in the County of Kent, on 26 June 1660.

Personal life
Finch was married four times and was the father of at least sixteen children. His first marriage was on 21 May 1645 to the Hon. Diana Willoughby, the eldest daughter of Francis Willoughby, 5th Baron Willoughby of Parham and Elizabeth Cecil (a younger daughter and co-heiress of Edward Cecil, 1st Viscount Wimbledon). She died and was buried at Eastwell on 27 March 1648.

His second marriage was in c. 1649 to Lady Mary Seymour (1637–1673), the second daughter of William Seymour, 2nd Duke of Somerset and Lady Frances Devereux eldest daughter of Robert Devereux, 2nd Earl of Essex). Before her death in 1673, their children included:

 * William Finch, styled Viscount Maidstone (c. 1651–1672), who died at sea aboard the Royal Charles during the Battle of Solebay; he married Elizabeth Wyndham, a daughter of Thomas Wyndham, of Felbrigg Hall.
 * Lady Frances Finch (d. 1712), who married Thomas Thynne, 1st Viscount Weymouth.
 * Heneage Finch, 5th Earl of Winchilsea (1657–1726), who married Anne Kingsmill, the daughter of Sir William Kingsmill.
 * Hon. Thomas Finch (b. 1658), who was born before the family went to the Ottoman Empire.
 * Elizabeth

His third marriage was to Catherine Norcliffe on 10 April 1673. The daughter of Sir Thomas Norcliffe and Hon. Dorothy Fairfax (fifth daughter of Thomas Fairfax, 1st Viscount Fairfax), she was twice a widow from her marriages to Christopher Lister, of Thornton, York, and Sir John Wentworth, of Elmshall, York. She died in c. 1678.

His final marriage was on 29 October 1681 to Elizabeth Ayres, only daughter and heiress of John Ayres of London. Before his death in 1689, they were the parents of:

 * John Finch, 6th Earl of Winchilsea, who died unmarried and without issue.

Lord Winchilsea died on 28 September 1689. He was succeeded in his titles by his grandson Charles, as his eldest son William predeceased him.

Descendants
Through his daughter Frances, he was a grandfather of Henry Thynne (1675–1708), and Frances Thynne (who married Sir Robert Worsley, 4th Baronet).

title: Heneage Finch, 3rd Earl of Winchilsea


text: Category:German cyclists

title: Category:German cyclists


text:
Planet CCRMA

Planet CCRMA (pronounced karma) is a collection of Red Hat packages (RPMs ) to help set up and optimize a Red Hat-based workstation for audio work.

Overview
The entire environment, called Planet CCRMA, was developed and tested at Stanford University and made available to the public free-of-charge from a central repository — Planet CCRMA at Home The Planet CCRMA repositories are maintained at CCRMA by Fernando Lopez-Lezcano.

Installing the packages, transforms a Linux workstation or server into a low-latency system for sound and video production and distribution. The ALSA sound card drivers and other applications are provided without installation hassles, and the low-latency is achieved by having applied the real-time preemption patch to the Linux kernel.

Supported Linux distributions

 * Red Hat Linux 7.2, 7.3, 8.0, 9
 * Fedora Linux 1, Core 2, Core 3, Core 4, Core 5, Core 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 24, 28, 29 and 30
 * CentOS 5

title: Planet CCRMA


text:
Bobo Olson

Carl "Bobo" Olson (July 11, 1928 – January 16, 2002) was an American boxer. He was the World Middleweight champion between October 1953 and December 1955, the longest reign of any champion in that division during the 1950s. His nickname was based on his younger sister's mispronunciation of "brother".

Early years
Olson was born in Honolulu, Territory of Hawaii to a Portuguese mother and a Swedish father, hence his other nickname "The Hawaiian Swede". Like many boxers, Olson decided to take up the sport after getting into fights on the streets. Olson received training from boxers who were stationed in Hawaii during World War II, and it was during this period that he picked up his two trademark tattoos.

Using a fake identity card Olson obtained a boxing license at the age of 16. His earliest fights were in his native Kalihi, Hawaii. He had won his first three contests, two by knockout, before his true age was discovered. During 1945, Olson ran off to San Francisco to continue his boxing career. By the time he was 18, he had amassed a record of 13 successive wins (10 by KO). Even at this stage his power and huge reserves of stamina were clear, as was his rather average skill.

Professional career
The first real test of Olson's career came on March 20, 1950, Olson's record at this point was 40 wins and 2 losses, against the Australian Dave Sands. Olson lost to a close points decision in Sydney. Seven months after this Olson had his first fight against Sugar Ray Robinson, for the lowly regarded Pennsylvania State World Middleweight Title. Olson, who was widely seen as a slow starter, failed to get into the fight, even though Robinson was not having one of his best fights. Olson managed to hold on for 11 rounds before being knocked out. Despite his great record it was clear that Olson was still too inexperienced to be fighting at that level.

A year after his loss to Robinson, Olson managed to get a rematch against Dave Sands. This fight was the first to be televised coast-to-coast in America. However, Sands once again proved too much for Olson, he again won by unanimous decision.

On March 13, 1952, Olson fought Robinson again, this time for the world middleweight title. Robinson, who had lost and regained the title against Randy Turpin in his previous two fights, was looking for an easy fight. However, Olson had improved significantly from their first encounter. Through ten rounds the fight was neck-and-neck, and only a dominant finish by Robinson over the last five rounds won him the decision. The Los Angeles Times wrote that Robinson won the first six rounds easily, slowly stacking up points, but that Olson reduced the points margin in the seventh through tenth. Robinson won the fifteenth convincingly with hard rights and lefts. This would be the only time that Olson lasted the duration against Robinson.

Robinson retired for the first time in December 1952, vacating his middleweight crown. The top four contenders fought a tournament for the title. Olson defeated Paddy Young for the American title to gain the right to fight for the vacant world title, Turpin won the other eliminator against Charley Humez.

The title fight against Turpin took place on October 21, 1953, at Madison Square Garden. Turpin dominated the first four rounds, he almost scored a knockdown in the first round, before Olson got a grip on the fight. As the fight progressed Olson took the initiative, he scored knockdowns in the 10th and 11th rounds on the way to a unanimous decision. Following his success Olson was voted Ring magazine's fighter of the year for 1953.

Olson won all seven of his fights in 1954 including defenses of his title against such big names as Kid Gavilan, Rocky Castellani, and Pierre Langlois.

In 1955 Olson, who was finding it increasingly difficult to make weight, stepped up to light heavyweight. His first major fight in this category was against former champion Joey Maxim. Olson won the fight easily on points after scoring knockdowns in both the 2nd and 9th rounds. On June 22 Olson challenged 41-year-old Archie Moore for the light heavyweight title, a fight that many believed Olson would easily win. However, Moore was too strong for Olson and won by knockout after only a minute had elapsed of the third round. After this fight Olson began his decline.

Following two walkover wins, Olson put his middleweight title on the line against Robinson, who was once again number 1 contender following his brief retirement, on December 9, 1955. It was Olson's fourth and final defense of his title, but ended as a stunning comeback for Robinson. Olson, who entered the fight as a 3–1 favorite, was knocked out in the second round. The rematch, fought five months later at Wrigley Field, on May 18, 1956, ended similarly with Olson going down in the fourth. Robinson ended the bout with a hard left hook to the body and a right to the jaw. Olson had made the mistake of dropping his right hand after Robinson's hard left, dropping his only defense in an instant. After this second defeat Olson announced his retirement.

Late career
After a year out of the game Olson returned as a heavyweight to fight Maxim again, a fight he won on points. Olson took another year out following a knockout defeat against Pat McMurtry. Whilst initially coming back as a journeyman, despite being only 30, Olson managed to reestablish himself as a contender. On November 27, 1964, he fought José Torres with the winner going on to fight the champion, Willie Pastrano. Olson was knocked out after 2 minutes of the first round. This defeat effectively ended his career, he would only fight again four more times, with his final fight being a defeat to Gene Fullmer's younger brother, Don.

Life after boxing
Olson retired with a record of 97 wins (47 by KO), 16 losses, and 2 draws from his 115 professional fights. He went on to work with disaffected youngsters before working as a PR officer for the Elevator Operating Engineers Local Union in San Francisco. In 1987 he was a Union Elevator Operator in Lancaster, California, working on new construction at the Antelope Valley Medical Center.

In the 1990s he lived in Northern California for a time. In his later years Olson suffered from Alzheimer's disease. To add quality of life to his later years he and much of his close family returned to Honolulu. He died on January 16, 2002, in Honolulu at Queens Medical Center at the age of 73.

He was inducted into the World Boxing Hall of Fame in 1958, and the International Boxing Hall of Fame in 2000.

title: Bobo Olson


text:
Harold Gilleshammer

Harold Gilleshammer (born April 8, 1942) is a Canadian judge and former politician in Manitoba, Canada. He was a member of the Manitoba legislature from 1988 to 2003, and a Cabinet Minister in the government of Progressive Conservative Premier Gary Filmon from 1990 to 1999.

The son of Olaf Gilleshammer, he was born in Winnipeg, Manitoba. He obtained a Bachelor of Arts in History, Political Science and English from the University of Manitoba and a Bachelor of Education from Brandon University. He subsequently worked as a teacher.

Gilleshammer was first elected to the Manitoba legislature in the provincial election of 1988, in the rural riding of Minnedosa in the province's southwest. The seat has normally been safe for the Conservatives, although a rise in Liberal Party support in 1988 meant that Liberal candidate Terry Drebit was able to pose a credible challenge. Gilleshammer won the election, however, by 1,173 votes. The Progressive Conservatives formed a minority government after the election, although Gilleshammer was not initially appointed to cabinet.

Provincial support for the Liberal Party declined in 1990, and Gilleshammer defeated Drebit by over 2000 votes in that year's provincial election, in a rematch between the two candidates. Shortly after the election, Gilleshammer was named Minister of Family Services. On September 10, 1993, he was promoted to Minister of Culture, Heritage and Citizenship, with responsibility for Multiculturalism, the Liquor Control Act and A.E. McKenzie Co. Ltd. Gilleshammer was easily re-elected in the 1995 general election, finishing over 2400 votes ahead of his nearest opponent.

Following a cabinet shuffle on January 6, 1997, Gilleshammer was named Minister of Labour, with responsibility for the Civil Service Act, the Civil Service Superannuation Act, the Civil Service Supplementary Severance Benefit Act, the Public Servants Insurance Act, and the Workers Compensation Act. Shortly after Gilleshammer's appointment, the Manitoba Human Rights Commission ruled that the province who be required to provide health, dental and vision benefits to the partners of gay government workers.

Following a further cabinet shuffle on February 5, 1999, he was appointed to the high-ranking position of Minister of Finance, with responsibility for the Crown Corporations Public Review and Accountability Act. His pre-election budget offered increased spending in various fields, to be paid for by withdrawals on a government contingency fund (his critics referred to his as concealing a provincial deficit).

The Progressive Conservatives were defeated in the provincial election of 1999, although Gilleshammer was personally re-elected in Minnedosa, defeating New Democratic Party candidate Harvey Paterson by 903 votes. Following the election, he was named as the party's Deputy Leader. Gilleshammer retired from the legislature in 2003. In 2007, Gilleshammer was appointed as a Citizenship Judge by the Canadian Minister of Citizenship and Immigration Diane Finley.

title: Harold Gilleshammer


text:
File:James Taylor - In the Pocket.jpg

Summary
Cover of the James Taylor album In the Pocket (James Taylor album).

title: File:James Taylor - In the Pocket.jpg


text:
Talk:List of stewards of the Chiltern Hundreds

1958 to 1970
Please note that while I can vouch for the exact dates in 1944-1958 and from 1970, I can't be entirely sure about those in between. In particular Peter Smithers' date may have been a few days different, and William Roots date is a complete estimate - but the real date is certainly betweeen 25th and 31st October 1967. Dbiv 20:22, 2 Oct 2004 (UTC)

 * The earlier dates aren't quite correct. Southby resigned in 1947, not 1946, and Williamson in 1948, not 1947. Gzornenplatz 20:47, Oct 2, 2004 (UTC)

 * It was late, the PRO was chucking out, and the file always used the regnal year rather than calendar year. PS: the Civil Service had printed up a stack of Edward VIII appointment notes and decided to use them rather than go to the expense of printing up George VI ones. They were still using the Edward VIII ones in July 1947.Dbiv 23:12, 2 Oct 2004 (UTC)

I've now checked the 1958-70 dates with the London Gazette and corrected those which were inaccurate. Dates of appointments from 1902-44 will appear soon. Dbiv 11:42, 19 Oct 2004 (UTC)

Missing Name?
I'm in the process of compiling information on Samuel Danks Waddy. One source says that he "accepted the Chiltern Hundreds" in December 1879. He does not, however, appear on this list. Is this list incomplete, or is my source incorrect? Thanks, JeremyA 02:00, 21 Jun 2005 (UTC)

 * The list is incomplete - it doesn't include names before 1893 (when appointments appear in the London Gazette). David | Talk 08:14, 21 Jun 2005 (UTC)

Reasons for taking up Stewardship
Perhaps the reasons for taking the title could be included on this list: several of those I checked did so for "honourable reasons" (taking up posts elsewhere etc): while no mention is made in the relevant articles of taking the post in other cases.

Jackiespeel 21:59, 11 September 2006 (UTC)

Thomas Kennedy
Is referred to on the list, but the link goes to a disambiguation page - can someone decide who is involved?

Jackiespeel 17:01, 12 September 2006 (UTC)

John Stonehouse
According to your entry on John Stonehouse, he applied for the stewardship of the Chiltern Hundreds but did not sign the papers, making him ineligible for this list. —Preceding unsigned comment added by 85.210.0.72 (talk • contribs)

 * That refers to when Stonehouse was first arrested in Australia in early 1975. He didn't apply for the Chiltern Hundreds then; he did in August 1976, after he had been repatriated, tried, convicted and sent to jail. Fys. “Ta fys aym”. 18:03, 5 November 2006 (UTC)

David Davis
He is currently down as 12th June (Thursday), but in fact "Mr Davis is expected to take the Chiltern Hundreds on Friday or Monday". Open4D (talk) 12:50, 13 June 2008 (UTC)

 * Needs to wait until there is an formal announcement before it is included here, and be properly sourced. 136.8.150.6 (talk) 14:03, 13 June 2008 (UTC)

Page layout
Anybody know why the reflist & SeeAlso jump above the list of stewards? Bazj (talk) 13:03, 18 June 2008 (UTC) i've tried removing the other elements, and that's not the problem. i think it's something to do with the headings that are used in the table. ninety:one 17:07, 18 June 2008 (UTC) The table was closed with two brackets instead of a bar and bracket. Many, many thanks to TenPoundHammer for taking the time and finding the solution.Bazj (talk) 20:35, 18 June 2008 (UTC)
 * i tried that... or so i thought. thanks TPH! ninety:one 20:36, 18 June 2008 (UTC)

Vacancies
Agree that the post must have been vacant after David Davis' resignation, so he could fight the by-election he caused. But doesn't this apply to some earlier ones as well? At the very least, William McCrea in 1985. Ceemage (talk) 12:12, 22 June 2009 (UTC)talk 12:07, 22 June 2009 (UTC)

Contents Index
There does not seem to be a Contents Index. Is this unique to me/my preferences or this wikipage? Þjóðólfr (talk) 19:32, 13 January 2010 (UTC)
 * What do you mean by a contents index? Ironholds (talk) 19:46, 13 January 2010 (UTC)

 * The article's table of contents has been suppressed using the  magic word. (Oddly, the wikicode is located in the section #1850 - 1900 rather than near the beginning of the article.) The table of contents for the List of Stewards of the Manor of Northstead article is similarly disabled. But in both cases, I don't know why   has been added. — Richardguk (talk) 20:35, 13 January 2010 (UTC)
 * It was added back when the article wasn't cut into sections; unless anyone dissents, feel free to remove it. Ironholds (talk) 22:09, 13 January 2010 (UTC)
 * Thanks for the info. I have removed . Þjóðólfr (talk) 08:42, 17 January 2010 (UTC)

Becoming a peer
There are several who are listed as taking the Chiltern Hundreds on inheriting a peerage or accepting a new creation. Surely they did not need to take the Hundreds as they automatically lost their seats in the Commons by becoming members of the Lords.Captdoc (talk) 14:38, 3 June 2010 (UTC)
 * There is no automatic disqualification in statute that I can find. As section 3 of the House of Lords Act 1999 removes the disqualification on membership of the HOC for hereditary peers that have been kicked out, it can be assumed that a) such a disqualification exists for all other peers and b) that that disqualification is unwritten. Similarly, because special provision is made by section 8 of the House of Lords Precedence Act 1539 for the Great Officers of State who are not Lords to sit on the "Judges' Woolsack" (ie in the middle of the benches) in the House of Lords, it can be assumed that members of the HOC are otherwise disqualified from sitting in the lords. It's something of a grey area and just another part of our constitution that would not do badly from codification. ninety:one  17:09, 3 June 2010 (UTC)

 * Under the Recess Elections Act 1975 (and probably for some time earlier under legislation consolidated by that act), the Speaker must cause a by-election to take place if any two MPs certify during a Commons recess that someone has ceased to be an MP. But section 1(2) provides that a certificate cannot be issued where someone vacates a seat by becoming Steward of the Chiltern Hundreds or the Manor of Northstead. So perhaps these appointments (if created before the members actually became peers) were a device to prevent early by-elections.
 * Alternatively, perhaps these were titles that did not confer membership of the House of Lords, such as with some Irish peerages and courtesy titles.
 * — Richardguk (talk) 18:03, 3 June 2010 (UTC)

Update needed
This list is largely based on Appointments to the Chiltern Hundreds and Manor of Northstead Stewardships since 1850, published by the House of Commons Department of Information Services.

A revised version of that list was published in January 2010, which contains a significant number of new entries, and apparently some revisions. For example, I have just added a missing entry to the Northstead list.

I suggested that this list be fully checked against the new version of the Department of Information Services list. -- Brown HairedGirl (talk) • (contribs) 13:57, 15 August 2010 (UTC)

Richard Bagwell
The History of Parliament states that the Member for Cashel was appointed to the Chiltern Hundreds on 9 November 1801, but he is not given in this list. Opera hat (talk) 18:42, 13 October 2012 (UTC)

Patrick Mercer
Mercer has been added as taking up the office on 29 April 2014, but there is no citation. This has not been announced on the Treasury website, which is where it usually appears. It would seem that Mercer has not yet (as of 30 April) been appointed. Anyone have the reference to suggest otherwise? --Frinton100 (talk) 23:41, 30 April 2014 (UTC)
 * Well, this press release from HM Treasury was available by 21:00 yesterday. It's dated 30 April, but nowhere does it state that the appointment was made on 30 April, or any other date. BBC Radio 4's Today programme was reporting it on 29 April, and BBC TV News were reporting it on 28 April. The official date should be given in the London Gazette, but notices can take some days to appear in there. Here's a search query. -- Red rose64 (talk) 08:35, 1 May 2014 (UTC)

 * The PR is dated 30th April, which will probably be the date he was formally appointed. His personal announcement was made on the 29th, with rumours of it on the BBC on the 28th. Typically, appointments are made at least a day after a resignation is announced, and given that his statement came at about 19.00 on Tuesday, it would seem unlikely he'd be appointed to the Chiltern Hundreds the same day. I have therefore amended the date on his appointment to the 30th with a link to the PR. Frinton100 (talk) 13:10, 1 May 2014 (UTC)
 * Here's the notice from the London Gazette. It's dated 29 April, and uses the text "has this day appointed". -- Red rose64 (talk) 16:25, 5 May 2014 (UTC)

Mark Reckless
The article says:
 * The current office holder is Mark Reckless, who was elected as Conservative MP for Rochester and Strood and asked for appointment as Steward in order to force a by-election at which he stood as candidate of the UK Independence Party.

Surely this can't be correct though, because Reckless stood in the by-election and took his seat back in the Commons (albeit only for a few months till he lost it again in the general election). The whole point of the Steward of the Chiltern Hundreds role is that you are not permitted to be an MP whilst holding it, so he must have resigned as steward before the by-election? Thanks — Amakuru (talk) 15:34, 16 September 2015 (UTC)

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1751 to 1849 split off to List of Stewards of the Chiltern Hundreds 1751-1849 to work around a Wikipedia technical limitation
This page uses a lot of templates. Wikipedia limits the total "expanded size" of a page to 2MB. For details about this limitation, see the explanatory text at the top of Category:Pages where template include size is exceeded.

I added the "?" parameter to the Data missing template, which helped some, pushing the "point of failure" past 1850, which made for a much cleaner split. It also makes the tables easier to read, especially on narrow-screen devices.

I moved the "Up to 1799" and "1800-1849" tables to a new page, List of Stewards of the Chiltern Hundreds 1751-1849.

Ideally, Wikipedia software would not have such limitations and such a split would not be needed. But it does, so something had to be done and a split was the most straightforward solution. davidwr/ (talk)/(contribs)  17:11, 17 February 2020 (UTC)

Dual appointments
The Dual appointments section needs (i) referencing and (ii) clarifying.

Regarding the former, this is to prevent claims of WP:NOR.

As regards the latter, it should be emphasised that these were not simultaneous appointments - a person can't be steward of the Chiltern Hundreds and also steward of the Manor of Northstead at the same time - there would be no point. Other than Charles Beresford, who seems to have been steward of the Chiltern Hundreds twice (1889 and 1900) and subsequently steward of the Manor of Northstead twice (1903 and 1916), are there no people who accepted one of the two offices, and some time later, accepted the same office again? -- Red rose64 🌹 (talk) 23:25, 14 June 2023 (UTC)


text:
Talk:Longboat

I have never heard of the longboats before. Do you mean the knarrs or do you mean the smaller ships that were used for the Russian rivers (but they did have sails)?--Wiglaf 20:22, 2 Oct 2004 (UTC)

 * I don't think this article should deal with Viking ships/boats at all. For me, a longboat is a boat carried aboard a ship as an auxilliary vessel. Vikings did use small longships on rivers, but not longboats.--Stephan Schulz 23:50, 2 September 2005 (UTC)

The link to the Tristan da Cunha longboat seems to be dead. Is there an alternative? -- Resuna (talk) 09:14, 13 June 2013 (UTC)

title: Talk:Longboat


text:
Anaplastic large-cell lymphoma

Anaplastic large-cell lymphoma (ALCL) refers to a group of non-Hodgkin lymphomas in which aberrant T cells proliferate uncontrollably. Considered as a single entity, ALCL is the most common type of peripheral lymphoma and represents ~10% of all peripheral lymphomas in children. The incidence of ALCL is estimated to be 0.25 cases per 100,000 people in the United States of America. There are four distinct types of anaplastic large-cell lymphomas that on microscopic examination share certain key histopathological features and tumor marker proteins. However, the four types have very different clinical presentations, gene abnormalities, prognoses, and/or treatments.

ALCL is defined based on microscopic histopathological examination of involved tissues which shows the presence of at least some ALCL-defining pleomorphic cells. These "hallmark" cells have abnormal kidney-shaped or horseshoe-shaped nuclei, prominent Golgi, and express the CD30 tumor marker protein on their surface membranes. In 2016, the World Health Organization (WHO) separated ALCL into four types: ALK-positive ALCL (also termed ALK+ ALCL), ALK-negative ALCL (ALK− ALCL), primary cutaneous ALCL (pcALCL), and breast implant-associated ALCL (BIA-ALCL). WHO defined BIA-ALCL as an ALCL type provisionally, i.e. subject to redefinition if future studies should support such a change.

ALK-positive and ALK-negative ALCL are aggressive systemic lymphomas. They are differentiated based on their expression of an abnormal ALK protein made by a somatic recombination in the ALK gene. ALK, i.e. anaplastic lymphoma kinase, is a protein product of the ALK gene located on chromosome 2. In ALK-positive ALCL, a portion of the ALK gene has merged with another site on the same or different chromosome to form a chimeric gene consisting of part of the new site and part of the ALK gene coding for ALK's activity. This chimeric gene overproduces a fusion protein with excessive ALK activity. ALK is a tyrosine kinase that activities PI3K/AKT/mTOR, Ras-activated ERKs, Janus kinase-activated STAT proteins, and other cell signaling pathways as well as the expression of various genes by epigenetic mechanisms. Activations of these signaling pathways and genes may stimulate cell growth, proliferation, survival, and/or other behaviors that promote malignancy. ALK-negative ALCL, while not involving ALK translocations, has, in a variable percentage of cases, various translocations, rearrangements, and mutations that may contribute to its development.

pcALCL and BIA-ALCL are far less aggressive lymphomas that tend to be localized to one or a very few sites. pcALCL presents as a single or, less commonly, multifocal skin papules or tumors that typically are limited to the dermis without infiltrating to the subcutaneous tissues or spreading to other sites. Its neoplastic cells may contain some gene translocations including, in very rare cases, ones with the ALK gene that are similar to those in ALK-positive ALCL. BIA-ALCL is caused by and develops around a breast implant. It typically presents many years after the surgical implantation as a deformation, textural change, and/or pain emanating in the area around implanted breast. In most cases, the disease is localized to the involved breast. BPI-ALCL is associated with occasional mutations in one or two genes but has not been reported to be associated with products of gene translocations or rearrangements.

Signs and symptoms
ALK-positive ALCL occurs mostly but not exclusively in children and young adults and is slightly more common in males. Most individuals present with stage III or IV (i.e. advanced) disease. They evidence systemic symptoms including B symptoms such as fever, night sweats, and weight loss in 75% of cases; lymph node enlargement (90%) including those in the mediastinum (36%); and lymphomatous lesions in the skin (26%), bone (14%), soft tissues (15%), lung (12%), and/or liver (8%). Tumor cells are found in the bone marrow in up to 40% of the cases when immunohistochemical analysis is performed. Involvement of the central nervous system or a leukemia-like circulation of malignant cells in the blood occurs only very rarely. Most patients, including up to 90% of young children and adolescents, have circulating autoantibodies directed against the ALK fusion protein expressed by their tumor cells.

Diagnosis
ALK-positive ALCL is diagnosed by histological and immunological examinations of involved tissues, typically lymph nodes. These tissues have lymphoma-like infiltrates that have variable numbers of ALCL "hallmark" cells, i.e. cells with kidney- or horseshoe-shaped nuclei that strongly express CD30 as detected by immunohistochemistry and an ALK fusion protein as detected by fluorescence in situ hybridization. These cells are scattered throughout the infiltrates. WHO classifies these infiltrates into 5 patterns: a common pattern consisting of large variably shaped cells with large nuclei that typically contain multiple nucleoli (60–70% of cases); a small-cell pattern consisting of small to medium-sized neoplastic cells with clear cytoplasm and "hallmark" cells that are concentrated around small blood vessels (5–10% of cases); a lymphohistiocytic pattern consisting of small neoplastic cells along with abundant histiocytes (10% of cases); a Hodgkin's-like pattern in which the architecture resembles the nodular sclerosis pattern of Hodgkin lymphoma (3% of cases); and a composite pattern consisting of two or more of the just described patterns (15% of cases). Detection of circulating autoantibody against ALK supports the diagnosis. Individuals with low levels of these autoantibodies are at an increase risk of relapsing after treatment.

Gene and molecular abnormalities
In 80–85% of cases, the ALK detected in ALK-positive ALCL is a NPM1-ALK fusion protein. It is made by a fusion of NPM1 gene, which makes nucleophosmin 1, located on the long or "q" arm of chromosome 5 at position 35 (notated as 5q35) with the ALK gene located on the short or "p" arm of chromosome 2 at position 23 (notated as 2p23) to form a chimeric gene notated as (2;5)(p23;q35). In 13% of cases ALK fuses with the TPM3 gene or in <1% of cases for each of the following genes: TFG, ATIC, CLTC, TPM4, MSN, RNF213 (also termed ALO17), MYH9, or TRAF1. All of these fusion proteins are considered to act like NPMI-ALK in possessing high ALK activity that promotes the development and progression ALK-positive ALCL by activating the cell signaling pathways cited in the Introduction. 15% Of individuals with ALK-positive ALCL also have point mutations in the NOTCH1 gene. While most of these abnormalities are thought to be detrimental not all are. For example, DUSP22 gene rearrangements are associated with favorable outcomes in ALK-positive (as well as ALK-negative) ALCL.

Treatment and prognosis
A recommended induction therapy for ALK-positive ALCL in individuals with lesions containing more than 10 percent CD30-positive cells consists of brentuximab vedotin (a drug consisting of an anti-CD30 antibody attached to a cell-killing agent, monomethyl auristatin E); two chemotherapy drugs, cyclophosphamide and the anthracycline doxorubicin; and the corticosteroid, prednisone. This regimen gave a progression-free survival rate of 48.2 months in one study and overall survival rates of 70–90% at five years in other studies. For >60 year old and medically unfit individuals of any age, the standard CHOP regimen (cyclophosphamide, doxorubicin, prednisone, and the chemotherapeutic agent vincristine) is used. For younger, medically fit individuals, the chemotherapeutic agent etoposide is added to the CHOP regimen (CHOP plus etoposide is termed the "CHOEP" regimen). For patients with lesions that contain <10% CD30-positive neoplastic cells, brentuximab vedotin, which targets these cells, is not used. Rather, patients are treated with an anthracycline-based chemotherapy regimen. Patients >60 years or less medically fit are given cyclophosphamide, doxorubicin, vincristine, and prednisone while patients ≤60 years old are given CHOP plus etoposide or one of various other intensive chemotherapy regiments. The intensive chemotherapy regimens give 5 year overall survival rates of 70–93%. The role of radiation therapy for ALK-positive ALCL is unclear but has been used for patients who cannot tolerate or do not achieve complete responses to the drug regimens and to patients with organ-threatening or life-threatening tumorous infiltrates. The role of autologous or less preferably allogenic hematopoietic stem cell transplantation (transplantation using the individuals own bone marrow, i.e. autologous, or a donor's, i.e. allogenic) after achieving a complete remission following induction therapy is also unclear. Individuals with relapsed or refractory disease are treated with brentuximab vedotin if they did not receive the drug previously or had not received it in the previous 6 months. A small study reported overall response rates, complete response rates, and disease-free survival rates at 24 months of 63%, 45%, and 54%, respectively, using this regimen. Those who attain a complete response on this drug and can tolerate it are than treated with bone marrow transplantation. Finally, patients who fail or relapse on these treatments are given salvage therapy regimens that have been used for relapsed or refractory aggressive B cell malignancies such as GDP (i.e. gemcitabine, dexamethasone, and cisplatin), DHAP, and ICE.

Drugs that inhibit ALK activity such as crizotinib and alectinib have been successful in establishing complete and partial remissions in a limited number of patients with advanced, refractory ALK-positive ALCL. These and other drugs are undergoing clinical trials to determine there safety and effectiveness in treating ALK-positive ALCL. (Also see clinical trials that use ALK inhibitors in ALK-positive ALCL and clinical trials that use ALK inhibitors in ALK-positive cancers.)

Signs and symptoms
Unlike ALK-positive ALCL, ALK-negative ALCL tends to occur in older adults (median age at diagnosis: 55–60 years) and presents primarily with lymph node involvement; only 20% of patients with ALK-ALCL present with extra-nodal disease in sites such as the skin, bone, and soft tissues. Nonetheless, most individuals (~67%) present with advanced stage grade III or IV disease in which neoplastic infiltrates occur in multiple lymph node locations and/or extra-nodal sites. ALK autoantibodies are not found in this type of ALCL. The prognosis of ALK-negative ALCL is often quoted as being worse than that for ALK-positive ALCL but this may reflect the older age and advanced stage at which ALK-negative disease presents: studies comparing age- and grade-matched ALK-positive to ALK-negative ALCL patients show little differences in prognoses.

Diagnosis
The histology of ALK-negative ALCL, similar to ALK-positive ALCL, consist of "hallmark" cells that strongly express CD30. Unlike ALK-positive ALCL, however, ALK-negative ALC does not fall into different morphological patterns. The histological of this disease may overlap with and be difficult to distinguish from other CD30-positive T-cell lymphomas or the nodular sclerosis form of Hodgkin lymphoma. Cases in which ALK-negative ALCL is not distinguishable from the latter lymphomas are best diagnosed as peripheral T-cell lymphoma not otherwise specified (PTL, NOS). The histology of ALK-negative ALCL may also overlap with tumors of non–T-cell lineage such as various carcinomas. The differential diagnoses of ambiguous cases may be helped by examining the tumor cells for the expression of certain marker proteins. For example, expression of CD56, MUC1 (also termed EMA for epithelial membrane antigen), and clusterin and strong uniform expression of CD30 support the diagnosis of ALK-negative ALCL over PTL, NOS, while variable CD30 expression and extensive expression of T-cell receptor proteins favor PTCL-NOS over ALK-negative ALCL. Detection of certain gene abnormalities (see next section) may also help distinguishing these diseases.

Gene and molecular abnormalities
ALK-negative ALCL tumor cells show products made by chimeric genes: DUSP22-IRF4 (many of which are fused at particular site and termed DUSP22-FRA7H) in 30% of the cases; TP63-TBL1XR1 in 8% of cases; and NFKB2-ROS1, NCOR2-ROS1, NFKB2-TYK2, or PABPC4-TYK2 in rare cases. They also show mutations in the JAK1 and/or STAT3 genes in 18% of cases; the MSC gene in 15% of cases, and the NOTCH1 gene in 15% of cases. About 24% of cases have a truncated ERBB4 gene. DUSP22 gene rearrangements have been associated with favorable outcomes in ALK-negative ALCL while TP63 gene arrangements are often associated with a poorer prognosis in various cancers. ALK-negative ALCL cells overexpress overactive STAT3 in 47% of cases and JAK1 in many cases. Many of these gene abnormalities appear to contribute to the development of ALK-negative ALCL.

Treatment and prognosis
The various treatments of ALK-negative ALCL generally follow those used for ALK-positive ALCL. However ALK-negative individuals more often present at an advanced stage of disease that requires intensive therapy. The aggressive treatments outline in the section on ALK-positive ALCL are used with the exception that patients with more favorable clinical and tumor tissue indicators as defined by having an International Prognostic Index score above 2 (particularly those who are under the age of 66) who obtain a complete remission after initial therapy are recommended for follow-up bone marrow transplantation. The International T-Cell Project reported on the treatment of 220 patients with ALK-negative ALCL; 15 received only supportive care, 168 were treated with anthracycline-containing chemotherapeutic regimens, 31 with anthracycline plus etoposide–containing chemotherapeutic regimens, 6 with other regimens; 16 with high-dose chemotherapy plus autologous stem cell bone marrow transplantation, and 4 with radiotherapy alone. Of the 205 patients that had more that supportive therapy, the overall and complete response rates were 77% and 63%, respectively. After a median follow-up of 52 months, the median progression free and overall survival times were 41 months and 55 months, respectively; 3- and 5-year progression-free rates were 52% and 43%, respectively; and 3- and 5-year overall survival rates were 60% and 49%, respectively. Chemotherapy treatments containing both anthracycline and etoposide were associated with superior overall survival rates (3- and 5-years of 76% and 69%, respectively) compared to chemotherapy treatment regiments containing an anthracycline but not etoposide (3- and 5-year overall survival rates of 56% and 44%, respectively). Progression-free survival rates with the latter two types of chemotherapy treatment regimens were not appreciably different.

Signs and symptoms
pcALCL is the second most common lymphoma in the category of Cutaneous T cell lymphoma cutaneous T cell lymphomas that includes lymphomatoid papulosis, various borderline CD30-positive cutaneous T cell lymphomas, and mycosis fungoides. The median age at diagnosis for pcALC is 61 years. The disease has a male predominance and appears to be more common in Caucasian populations. Individuals with pcALCL typically present with reddish masses that initially appear in the skin or, much less frequently, the lymph nodes or various organs. These masses are nodules or tumors that are often ulcerated, greater than 2 cm in diameter, and localized to a single site. In 20% of cases, however, they occur in multiple sites. In about 10% cases followed for many years, pcALCL presenting as skin lesions progresses to extracutaneous sites, mainly to regional draining lymph nodes. Over these same long periods, however, the disease's lesions partially regress in about 50% of cases but then relapse in about 40% of cases.

Diagnosis
pcALCL lesions exhibit large malignant T-cells or null cells (i.e. cells lacking many T-cell receptor proteins) with "Hallmark" cell features of anaplasia, pleomorphism, and kidney- and horse shaped-nuclei. These lesions are often limited to the dermis but can extend into the surrounding subcutaneous tissue and/or epidermis. Rarely, the lesions, termed pyrogenic variants, are rich in polymorphonuclear neutrophils. The neoplastic cells strongly express CD30 (100% of cases), CD2 (78%), CD4 (54–90% of cases), cytotoxicity marker proteins, and various other marker proteins that help distinguish it from other ALCL, cutaneous T-cell lymphomas, and cancers. While these cells typically are ALK-negative, they do express ALK-containing fusion proteins in rare cases. The latter cases have a relatively benign course compared to ALK-positive ALCL and are treated as variants of pcALCL rather than ALK-positive ALCL.

Gene and molecular abnormalities
Similar to ALK-negative ALCL, pcALCL have chromosomal rearrangements in their DUSP22 (20–30% of cases) and TP63 (5% of cases) genes and a mutation in the MSC (i.e. musculin) gene (6% of cases). Between 1993 and 2019, the Dutch registry had 6 (i.e. 2%) of 319 pcALCL cases that expressed ALK. Three of these cases were due to the NPM1-ALK chimeric gene that predominates in ALK-positive ALCL while the remaining three were due to TRAF1-ALK, ATIC -ALK, or TPM3-ALK chimeric genes. All 6 patients shared exactly the same breakpoint site in the ALK at exon 20 on the ALK gene.

Treatment and prognosis
Most pcALCL individuals present with isolated lesions that are effectively managed with radical surgical excision and/or radiation therapies; this approach is regarded as front-line therapy for localized disease. However, individuals with extensive disease and/or multiple tissue involvement respond poorly to front line treatment. These as well as individuals who relapse after front-line therapy need further treatment. In one study of 65 patients with pcALCL, 95% treated with surgical excision achieved complete remission but 41% of them relapsed within 22 months while 64% of patients treated with surgery plus radiotherapy developed recurrent disease within 55 months. In another study of 135 patients with this disease, 39% had relapses limited to the skin, 15% developed extracutaneous disease, and 9% ultimately died from pcALCL. Individuals with refractory, recurrent, and/or extensive disease have been treated more aggressively. In various studies, 10 of 13 such patients responded within 4 weeks to treatment with the chemotherapeutic agent, methotrexate; 10 of 16 patients obtained complete remissions of their skin lesions when treated with the anti-CD30 monoclonal antibody, brentuximab verdotin, and 48 of 53 patients treated with the aggressive chemotherapeutic CHOP regimen had complete responses. However, most of these patients developed recurrent disease within four months. As currently recommended, brentuximab vedotin is use initially to treat widespread systemic disease; a single chemotherapeutic drug rather than aggressive combination chemotherapy with CHOP or similar regimens is used to treat patients not responding to brentuximab verdotin; aggressive chemotherapy regimens are used to treat widespread nodal and/of visceral disease and disease which failed on other regiments; and, although there is little data supporting this, employ allogeneic bone marrow transplantation for patients with multiple relapses that have progressed on systemic therapy. Recurrences, regardless of treatment type, are common. pcALCL has an estimated five-year failure-free survival rate of 55 percent. Nonetheless, the disease has a 10-year overall survival rate of 90%. Typically leg involvement portends a worse prognosis: it has a five-year disease-specific survival rate of 76 percent compared with 96 percent for disease in other locations. Involvement of local nodes alone in patients with skin lesions does not seem to portend an adverse prognosis.

Signs and symptoms
BIA-ALCL is a complication of silicon-filled and saline-filled breast implants which develops 9 years to 10 years (median times) after surgical implantation. First described in 1997, it is estimated that the prevalence of BIA-ACLC in individuals with implants that have a textured surface is 1 in 30,000 while the risk of it is 70-fold lower in individuals who have a smooth surface implant or have no implant at all (i.e. in patients that have another type of ALCL). These relations strongly suggest that BIA-ACLC develops primarily if not exclusively in patients with textured implants. In all cases, however, many researchers suspect that BIA-ALCL is an under-recognized, misdiagnosed, and under-reported complication of breast implants. Two-thirds of individuals with BIA-ALCL present with swelling, discomfort, and/or (rarely) pain in the affected breast. This is due to the development of a tumor mass and/or swelling caused by an effusion (i.e. fluid) that accumulates between the breast implant surface and the fibrous capsule that has grown around it. The effusion fluid typically contains white blood cells, tumor cells, and high levels of protein. Besides or in addition to breast swelling, patients present with a breast mass in 30% present of cases, enlarged lymph nodes in the armpit or around the chest clavicle bones in 20% of cases, and/or in a small percentage of cases lesions in more distant tissues. Rarely, patients have presented with skin rash or itching on or around the involved breast. Using the Ann Arbor staging system, 83% of patients present with stage 1 localized disease while the remaining 10, 0, and 7% of patients present with what is normally regarded as more aggressive stage II, III, or IV diseases, respectively. Thus, about 17% of individuals present with a more aggressive disease that has spread from its original breast implant site to nearby lymph nodes, to areas outside of the capsule, or to more distal tissues.

Diagnosis
In most individuals with BIA-ALCL, the affected breast has a thickened capsule around the implant and effusion fluid between the capsule and implant. Neoplastic cells are located in and typically limited to the capsule and effusion. Histological examination of the capsules shows large anaplastic cells but cells with all the features of ALCL "hallmark" are often difficult to detect. In addition to these neoplastic cells, the capsule lesions contain, sometimes in a large excess that makes diagnosis difficult, a variety of non-malignant cells such as small lymphocytes, histiocytes, and granulocytes (the granulocytes are mostly eosinophils). The histology of palpable masses exhibit a different pathological picture: the tumor masses have multinodular areas that consist of necrosis or fibrous tissue interspaced with areas that consist of large neoplastic cells that have abundant cytoplasm and abnormally shaped nuclei within a fibrotic and chronic inflammatory cell background. Again, typical ALCL-defining "hallmark" cells may be difficult to find in these masses. The effusions show abundant, uniform-appearing, non-cohesive large cells with irregularly-shaped nuclei, prominent nucleoli and abundant cytoplasm. The histology and pathological features of diseased lymph nodes and tissues outside of the breast implant are indistinguishable from those seen in ALK-negative ALCL. The neoplastic cells in the capsules, effusions, and tissues strongly and uniformly express CD30, CD4 (75–84% of cases), EMA (48–90%), CD43 (86–95%), CD45 (44–74%), and in a far fewer percentage of cases various other marker proteins. These cells do not express ALK and often lack the characteristic surface marker proteins of T-cells. Identification of the status of these markers helps diagnose the disease.

Gene and molecular abnormalities
No chromosome translocations, chimeric genes, or fusion proteins have been described in BIA-ALCL although the neoplastic cells in the disease have been described to have gene copy number variations involving gains in gene copies on the p arm of chromosome 19 and losses of gene copies in the p arms of chromosome 10 and 1. The neoplastic cells in BIA-ALCL show mutations of the STAT3 gene in 64% of cases and reports of mutations in JAK1, JAK3, DNMT3A, and TP53 genes. The development of BIA-ALCL, it has often been suggested, may be at least in part a T-cell-induced, inflammation-driven cancer response to the implant.

Treatment and prognosis
The treatment regimens for BIA-ALCL recommended by 1) a multidisciplinary expert review panel, 2) the National Comprehensive Cancer Network, and 3) the French National Cancer Institute (Agence Nationale de Sécurité du Médicament [ANSM]) are very similar, commonly used, and summarized here. BIA-ALCL staging is done to identify patients with BIA-ALCL confined to the implant, capsule, and effusion from more disseminated disease. The staging preferably employs the TMN system designed to stage solid tumors. This is based on historical data suggesting that BIA-ALCL progresses locally like solid tumors rather than liquid tumors such as other lymphomas. BIA-ALCL patients have surgical removal of the implant, capsule, and associated masses. Patients with localized disease (e.g. TMN stage 1A to 2A) that is completely excised by removal of the implant, the entire capsule, and any masses (must leave negative resection margins) receive no further therapy. About 85% of all BIA-ALCL patients should qualify to receive this treatment regimen. Patients with unresectable chest wall invasion, regional lymph node involvement (i.e. TMN Stage 2B to 4), or residual disease after surgery receive an aggressive adjuvant chemotherapy regimen such as EPOCH, CHOP, or CHOP plus etoposide. Alternatively, the immunotherapeutic drug, brentuximab vedotin, may be used as initial therapy alone or in combination with a chemotherapy regimen to treat disseminated disease. While larger studies are needed, case reports suggest that brentuximab vedotin may be effective frontline monotherapy, either after surgical excision or as primary treatment for unresectable BIA-ALCL. Radiation therapy has been used in cases that have unresectable chest wall invasion (NMN stage IIE). Although the number of cases evaluated is low, 93% of patients without a mass and 72% with a mass achieved complete remission; median survival for disease having a discrete breast mass was 12 years but was beyond 12 years and not reached over the study period for patients not having a discrete breast mass.

title: Anaplastic large-cell lymphoma


text:
Sōsai

The Japanese word Sosai (Japanese:総裁, "Sōsai") means roughly "president" or "director-general". It is used in several ways:

Political

 * Sosai, or president of the government, was only once the title of the imperial prime minister: from 1 January 1868 (before there was no cabinet, only chief advisers: Kampaku to the nominally reigning emperor and both Rōjū and Tairō to the de facto ruling shōgun) until 11 June 1868: Prince Arisugawa Taruhito (1835–1895); next the prime ministerial office is styled U Daijin "Ministers to the Right", in 1871 shortened to Daijin.
 * Sosai also was the title of Admiral Takeaki Enomoto (1836–1908), the elected president (27 January 1869 – 27 June 1869) of the short-lived rebellious Ezo Republic on the present Hokkaidō Island, vanquished by Imperial troops.
 * Sosai, or President of Liberal Democratic Party, is the office of the head of the LDP.

Others
This office also exist in various sports, in particular budō, business and charitable organizations. The term is also used to translate the head of various foreign organizations.

The most famous of such people is Sōsai Ōyama Masutatsu, who earned this appellation by creating a karate style called Kyokushinkai and spreading karate in the western world.

Mas Oyama is an exceptional icon to be called "Sosai" because of his contributions especially in the world of Martial Arts and in the overall history of Japan.

title: Sōsai


text:
Talk:Declarative programming language

His O
IMO SQL isn't a programming language, rather a query language.

Makefiles
Is a Makefile declarative programming?

 * No. Unless you use non-standard features, it's hardly "programming", to begin with.  (And if you do use those features, it's imperative programming.)  --Piet Delport 11:22, 2 January 2006 (UTC)

 * Yes. It allows one to make a computer perform some actions to achieve desired effects. It is a bit like SQL, classified here as programming language but from a different side. In SQL there are implicit loops, wound around fetched data, and in make there are implicit conditionals threaded between targets. In fact I am not really sure if a real, Turing complete, programming lnaguage with both loops and conditional statemets can be a declarative one. --steelman 22:24, 1 August 2006 (UTC)

Wrong sentence
It is wrong: "Sometimes, functional programming languages are called declarative programming languages". Eduard Proydakov.
 * Well, technically speaking, I'm sure this is true. People do, after all, often make mistakes. Whether or not this is noteworthy or sufficiently common is dubious. Functional programming language certainly *aren't* declarative programming languages, however. Barring a good citation to justify the need for stating this, it should be excised. --63.166.226.83 (talk) 22:29, 20 May 2008 (UTC)

More precise clarification of "Declarative" required
In support of the previous discussion topic, there are a number of other definitions of what precisely constitutes "Declarative" that need to be considered.

See for instance Functional Programming is not [declarative]:

A pertinent quote from the preface to the first edition of SICP, which clearly defines the differing philosophies:

''Underlying our approach to this subject is our conviction that "computer science" is not a science and that its significance has little to do with computers. The computer revolution is a revolution in the way we think and in the way we express what we think. The essence of this change is the emergence of what might best be called procedural epistemology--the study of the structure of knowledge from an imperative point of view, as opposed to the more declarative point of view taken by classical mathematical subjects. Mathematics provides a framework for dealing precisely with notions of "what is". Computation provides a framework for dealing precisely with notions of "how to".

And in section 1.1.7 (2nd ed.):

''The contrast between function and procedure is a reflection of the general distinction between describing properties of things and describing how to do things, or, as it is some times referred to, the distinction between declarative knowledge and imperative knowledge. In mathematics we are usually concerned with declarative (what is) descriptions, whereas in computer science we are usually concerned with imperative (how to) descriptions.''

I would hesitate to make the artificial division between Computer Science and Mathematics, though. Mathematics definitely has both the declarative - functions, and the imperative - formulas that define how to calculate functions (there may be recursive implications to formulas, which can themselves be defined in terms of functions, but this seems to be a dangerous route to go down and may lead into Gödel's incompleteness theorem territory).

Perhaps, it could be said that the current perception of the difference between Computer Science and Mathematics varies in the emphasis placed upon how important declarative versus imperative modes of conceptualizing are. posted by TheUser on June 1 2005 -- please sign your posts by typing ~

 * That discussion on LtU is interesting, but I take the discussion there with a grain of salt. (Actually, I take any discussion not by Ehud or Anton or a few others with a grain of salt, but there's no need to play favorites here.)  The best point made in the discussion is that strictly declarative programs don't express algorithms.  This is and is not true.  What about:

fib = 1 : 1 : zipWith (+) fib (tail fib)
 * A little shaky. I mean, there's only one sensible way to compute that, and Haskell does it.  But what then:

fac n = product [1..n]
 * That's about as declarative as I can make the definition of the factorial of n: the product of the digits from 1 to n. There are a number of ways product could work, I don't care how it does it.  I also don't care about how [1..n] is constructed. In fact, Haskell won't construct a list (from the bottom or the top) and then go up (or down) it, but instead go from 1 up to n, multiplying on the way.

 * As for my rewrite, I cleared up the text a lot, adding examples of purely declarative languages and the question as to whether or not they're programming languages. I don't think this page is a good place to play out that debate, and it's enough to leave it as a question.  I also cleaned up the list of decl. PLs.  Might be nice to link to the Rogue-like game in Prolog.

 * What the page does need now, though, are more examples of declarative programming in action. It's the sort of thing you only know when you see it, and the more examples the better. --Mgreenbe 11:41, 6 December 2005 (UTC)

Merge proposal
I'm proposing this page be merged with declarative programming since there doesn't seem to be a lot of reason to support both pages. Neither one deals with much entirely distinct from the other.

What might be more interesting is a List Of Declarative Programming Languages page, however!

Since a declarative programming language is part of the bigger idea of declarative programming, I guess it should be merged into that page, but I'm not going to assume that logic is necessarily in accordance with Wikipedia policy. —Preceding unsigned comment added by 63.166.226.83 (talk) 22:34, 20 May 2008 (UTC)

 * Strongly object - 144.131.104.81 (talk) 11:12, 24 September 2008 (UTC)
 * Support. Can't see what could be hurt, and both pages need help badly.  List of declarative programming languages sounds like (a) a quagmire, as it invites c2 style discussion, and (b) better as a category.  But — be bold!  Does 144.131.104.81 want to elaborate their problem (or perhaps log in, since an IP address with no contributions and an empty talk page isn't exactly compelling)? --mgreenbe (talk) 15:22, 25 September 2008 (UTC)
 * N.B. Category:Declarative programming languages already exists. --mgreenbe (talk) 00:47, 28 September 2008 (UTC)

 * Done. Both pages needed serious help, so I merged them. Tejoka (talk) 06:52, 5 October 2008 (UTC)

title: Talk:Declarative programming language


text: Category:South African golfers

title: Category:South African golfers