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Prunus salicina

Prunus salicina (syn. Prunus triflora or Prunus thibetica), commonly called the Japanese plum or Chinese plum, is a small deciduous tree native to China, Taiwan and Southeast Asia. It is an introduced species in Korea, Japan, Israel, the United States, and Australia.

Prunus salicina should not be confused with Prunus mume, a related species also commonly called Chinese plum or Japanese plum. Prunus japonica is also another tree that is a separate species despite having a Latin name similar to Prunus salicina's common name.

Names
Some names for this plant, in addition to Japanese or Chinese plum, are Willow-leaf cherry, Asian Plum, in English, Ameixa or Ameixa-japonesa in Portuguese, 李 lǐ in Mandarin and Japanskt plommon in Swedish.

The generic name, Prunus, comes from the Greek Prunum, meaning plum. The specific epithet, salicina, is derived from the Latin word for willow.

Description
Prunus salicina grows up to 9-12 m tall, and its branches are purplish brown to reddish brown and its lateral shoots are yellowish red.

The leaves are 6–12 cm long and 2.5–5 cm broad, with scalloped margins, which when young is often mixed with simple gland-tipped teeth. The leaves' shape tend to be oblong, though it sometimes varies slightly more obovate (broader above the middle), narrowly elliptic, or in rare cases being slightly ovate (broader half below the middle). The base of the leaf is wedge-shaped, and its apex ranges from acute (pointed) to caudate (having a slender short tail). The upper side of the leaf is dark green and lustrous, and have 6 or 7 secondary veins on either side of midvein, not extending to leaf margin.

The winter buds of the Prunus salicina are purplish red, and are occasionally hairy at scale margins, though this is rare. The flowers are produced in early spring, around April, each about 2 cm in diameter with five white petals, and come in groups of 3. The pedicel is 1–1.5 cm, and its sepals are oblong-ovate and about 5mm, hairless on the outside, with loosely serrated margins. The sepal's apex is acute to obtuse. The petals of the flower are white, oblong-obovate, with a wedge-shaped base and a jagged margin near the apex. The ovary is hairless and the stigma disc-shaped.

The fruit is a drupe, 4–7 cm in diameter with yellow-pink flesh. The skin can be yellow, red, or sometimes green or purple, and has a powdery coating. The shape of the drupe is spherical, egg-shaped, or conical, and it is 3.5–5 cm in diameter, though it can reach 7 cm in diameter in horticultural forms. They fruit from July to August. When fully ripe it can be eaten raw. In comparison to the Prunus domestica, the Prunus salicina, fruit has a higher flavor and aroma, better texture, more color, bigger size, and good nutritional values.

The pit of the Prunus salicina is ovoid (egg-shaped) to oblong, and wrinkled.

Growth pattern
The Japanese plum, like other Prunus fruit tree species, is mostly self-incompatible and requires cross pollination to ensure fruit set because this genus is unable to bear fruit parthenocarpically. Several cultivars or varieties have however been identified with self-compatibility.

Distribution and habitat
Prunus salicina is native to China, Taiwan, Myanmar, Laos and Vietnam. In China, it grows in sparse forests, forest margins, thickets, along trails in mountains and stream sides in valleys, at elevations of 200–2600 meters. It grows best in temperate warmer regions, as it requires moderate temperatures and is usually early flowering.

The domestication center of origin of Prunus salicina is southwestern China, from the Yangtze River Basin. Wild populations of this species are reported as thriving in the provinces of Shaanxi and Gansu. It is recorded as an introduced species in both Australia and Japan.

Ecology
Prunus salicina is strongly dependent on endomycorrhizal relationships, similar to other species of plum. Ectomycorrhizal relationships with the fungus Hebeloma hiemale was shown to increase net growth in Prunus cerasifera  x salicina, compared to chemical fertilizer, compost and a control.

The effects of the Prunus salicina in improving soil in karst areas in China, have been mixed. A study conducted in Guiyang Karst Park, Guizhou, China, concluded that Prunus salicina, in combination with the moss species, Homomallium plagiangium, Cyrto-hypnum pygmaeuman and Brachythecium perminusculum, and the herbs Veronica arvensis and Youngia japonica, were suitable pioneer plant species to cultivate for use in restoration of regions of karstic soil erosion. Planted on cropland suffering from rocky desertification, in the city of Hechi, Prunus salicina increased the carbon-to-nitrogen ratio, and the soil quality at the 10–20 cm soil layer, though in general, it had limited influence on soil improvement because of its fast growing and high output, increasing the absorption of nutrients from the soil.

Cultivation
The main producing country of Japanese plums is China, followed by the United States of America, Mexico, Italy, Spain, Pakistan, Korea, Australia, Chile, France, South Africa and Argentina. The most famous variety of this fruit in Vietnam is the Tam Hoa plum grown in Bắc Hà town, in Lào Cai Province.

Japanese cultivars were introduced into the United States in the latter half of the 19th century, where subsequent breeding produced many more cultivars, generally with larger fruit. Plant breeder Luther Burbank developed a number of cultivars by hybridizing Prunus salicina with Prunus simonii and other native North American diploid plums such as Prunus americana, Prunus hortulana or Prunus munsoniana. In the late 19th and early 20th centuries, from these hybridizations Burbank selected cultivars such as ‘Beauty’, ‘Eldorado’, ‘Formosa’, ‘Gaviota’, ‘Santa Rosa’, ‘Shiro’, and ‘Wickson’, some of which are still widely grown. One of the famous cultivars, “Santa Rosa”, named after the city in California.

Most of the fresh plums sold in North American supermarkets are Prunus salicina cultivars or hybrids. They are grown on a large scale in a number of other countries, for example, they dominate the stone fruit industry in Western Australia. In France in 2020, Japanese plums production volumes are now higher than that of European plums.

There is an important work of breeding and selection of new Japanese plum cultivars and varieties around the world from different breeding programs. As a result, the Community Plant Variety Office of the European Union (CPVO) registered 155 new Japanese plum cultivars from 1995 to 2021. The table below presents a short list of varieties.

Threats
In open field cultivation this species is vulnerable to several vector or pollen-borne viral diseases affecting Prunus including Plum pox virus and Prunus necrotic ringspot virus. Japanese plums are also well-known for their susceptibility to European stone fruit yellows phytoplasma, with strong symptoms including yellowing, leaf roll, premature fruit drop and dieback. Additional threats to this species remain unknown, and while there are several known threats to the forests of China, including logging, deforestation and air and water pollution it is unknown whether these have a direct effect on Prunus salicina. As of 2023, its threat status on the IUCN Red List is Least Concern, and this species' population is stable. The IUCN Red List recommends "the incorporation of population management and monitoring in protected areas where this species is known to occur" and "additional ex situ collection, ensuring the full range of genetic diversity found in the wild is represented in genebanks."

Culinary
Since Prunus salicina Linn. fruit has a short-shelf life (3–4 days) under room temperature as well as cold storage (1–2 weeks), it is often prepared into jams, jellies, wine, and other beverages. Black pepper, coriander, cumin, clove, black cardamom, saffron, nutmeg, cinnamon, poppy seed, ginger, woodfordia, asparagus, withania, adhatoda, and rosemary have been reported to be used in preparing aromatized plum wine. The Santa Rosa plum cultivar produces the best quality wine, in comparison Methley, and Green Gage.

In China, candied fruits are also sold preserved, flavoured with sugar, salt, and liquorice. A study on foraging in the Gongba Valley (Zhouqu county in Gansu, China) identified Prunus salicina as one of the most commonly eaten wild fruits. Liquor made from Prunus salicina fruit is mixed with Prunus mume liquor, and oolong tea liquor to make a Japanese-style plum liquor, wumeijiu (smoked plum liquor), in Taiwan.

In Japan, while it is less commonly eaten than closely related Prunus mume, it is pickled and colored in a similar manner. Especially in Eastern Japan, many summer festivals sell pickled fruits covered in mizuame candy called anzuame (apricot candy, as apricots were traditionally used for the recipe).

In both countries, it is also used half ripe as a flavouring in a liqueur called sumomo shu (すもも酒) in Japanese.

For other uses of this and similar species see plum.

Medicinal
The fruits are also used in Traditional Chinese medicine, to enhance immunity against infectious agents and to treat cancers. Japanese plums cv. Crimson Globe may be taken as a source of antioxidants with a potential to counteract oxidation. Prunus salicina fruit may contain immunostimulatory (stimulating the immune system by inducing activation or increasing activity) components that potentially may be useful in human and veterinary medicine. Compared to other fruits, Japanese plums, include a reasonable source of fiber and proper source of bioactive compounds (such as vitamin C and phenolic composition). Their phenolic composition positively correlates to their antioxidant properties. A study evaluating ethanol extracts from 400 herbs found that the Japanese plum was the most effective Glucosyltransferase (GTF) inhibitor and showed the highest antibacterial activity. There has been research into whether the fruit of the Japanese plum has cancer-protective effects because of its antioxidant properties, but as of 2023, it is unclear what role antioxidants in general, play in cancer protection and treatment.

Toxicity
As with other stone fruits, the pit and leaves are poisonous to humans, as they contain amydalin, which breaks down to hydrogen cyanide. While poisoning from unintentional ingestion of a few pits is unlikely, it recommended to avoid ingestion, and to never consume crushed up pits.

title: Prunus salicina


text:
Ottawa Fury SC

Ottawa Fury Soccer Club was a Canadian soccer team based in Ottawa, Ontario. The team played in the USL Premier Development League (PDL) from 2005 to 2013. The organization joined the North American Soccer League (NASL) as Ottawa Fury FC beginning in the 2014 season. The team's home stadium was the Algonquin College soccer complex; its colours were white, red and blue.

The Fury operated a women's soccer team, Ottawa Fury Women, in the USL W-League, a team in the USL's Super-20 League, a league for players 17 to 20 years of age run under the United Soccer Leagues umbrella, as well as multiple youth teams.

History
Ottawa Fury entered the PDL in 2005, joining fellow Canadian teams Thunder Bay Chill and Abbotsford Rangers in the American-based competition. Under the leadership of head coach Colin McCurdy – a Northern Irish legend from his time at Belfast club Linfield – the Fury began brightly, beating Westchester Flames 3–0 in their opening fixture, and winning two of their next four, including a 5–3 victory at home over the Albany Admirals which featured a hat trick from Kevin Omokhua. Unfortunately, Ottawa could never quite string a run of results together; throughout the season, win would follow loss would follow win, although their points tally did keep them high in the standings all year long. A staggering 10–2 annihilation of Brooklyn Knights (which saw Francis Mavula net four goals) and an impressive 6–3 victory on the road over the Westchester Flames were the highlights of the rest of the regular season. A 4–3 defeat to Cape Cod Crusaders on the final day of the season left the Fury third in the Northeast behind Cape Cod, just out of the playoffs. Kevin Omokhua and Francis Mavula were a threatening strike force, netting 21 times between them, while Desmond Tachie contributed 7 goals and 7 assists.

Ottawa moved to the New England Division in 2006, and started the new season in decent form, with a win and two ties in their first three games. However, the Fury stuttered through June, losing 2–1 to Albany Admirals, and being beaten three times in thirteen days by the Cape Cod Crusaders. The 4–4 tie with Rhode Island Stingrays at the beginning of June, in which they threw away a 2-goal lead in the last 15 minutes, may have signalled a downturn in Fury's form, but to their credit they rallied towards the season's end. Ottawa won six of their last eight games, including a 3–0 revenge win over Rhode Island, but their late charge towards the playoffs was in vain; they finished the regular season second in the division, a full 20 points behind Cape Cod Crusaders, and failed to secure the post-season wild-card slot. Kevin Omokhua was again Ottawa's outstanding player in front of goal, with 11 for the season.

Head coach McCurdy left at the end of 2006, and he was replaced by Chris Roth; unfortunately, his first season at the helm was a difficult one, as Fury suffered their worst run of results in the franchise's history. Despite an opening tie with Cape Cod Crusaders and a 3–2 win over PDL new boys Long Island Rough Riders in their first two games, Fury suffered an immediate down-turn in form. Fury won just one game in June – 4–0 over Vermont Voltage – and quickly fell out of contention for playoff consideration. Five straight games without a win in July, and eight in total, sent the Fury to the bottom of the Northeast Division table, and only a 4–0 final day win over bottom side Rhode Island Stingrays kept the Canadians from finishing last in the division. Will Beaugé was Fury's top scorer, with six goals, while English midfielder Yan Klukowski contributed 4 assists.

Head coach Roth was replaced by Stephen O'Kane in the off-season, and seemed to have a positive effect on the squad. Ottawa bounded back spectacularly in 2008, enjoying what turned out to be the most successful – but ultimately frustrating – year in franchise history. Despite a rocky start in which they lost their opening two games, Fury responded with four wins in their next five games, including a 5–2 blowout over Vermont Voltage, a 4–1 rollover of Rhode Island Stingrays, and a comprehensive 3–0 win over Long Island Rough Riders. Ottawa's scintillating form continued throughout July, when they enjoyed a 9-game unbeaten run stretching back to the aforementioned Long Island game. Fury were powerhouses in front of goal – they crushed the Rhode Island Stingrays 5–0, and followed this up with a 7–0 annihilation of New Hampshire Phantoms, which saw seven different Fury players find the net. They entered their last game knowing that a win over Vermont would most likely give them the New England Division title over Cape Cod Crusaders; shockingly, they fell to a 3–0 defeat, and then were nudged out of the playoffs by Newark Ironbound Express, who finished second in the Northeast, and finished equal on points, but took the final playoff spot on head-to-head results. Will Beaugé and Florian Decamps were Fury's top scorers, with seven goals each, while Da Costa and Andrew Rigby both contributed four assists.

Assistant Coach Klaus Linnenbruegger stepped up to take over the helm of the Ottawa Fury PDL. Linnenbruegger, who played professionally with Bielefeld in Germany, successfully coached Fury Youth teams over the previous seven seasons and is a past head coach of the Ottawa Wizards. The long-time Fury coach replaced Steve Payne who left the club by mutual consent.

NASL in 2014
On June 20, 2011, the North American Soccer League (NASL) announced that Ottawa had been awarded an expansion team. The new team will be owned by the Ottawa Sports and Entertainment Group and play home games at Frank Clair Stadium at Lansdowne Park. On February 26, 2013, it was announced that the new team would be named Ottawa Fury FC and carry on the Ottawa Fury legacy.

Honours

 * USL PDL Northeast Division Champions (4): 2009, 2010, 2012, 2013

Head coaches

 * Colin McCurdy (2005–2006)
 * 🇨🇦 Chris Roth (2007)
 * 🇨🇦 Stephen O'Kane (2008–2009)
 * 🇨🇦 Carl Valentine (2010)
 * 🏴 Steve Payne (2011)
 * 🇩🇪 Klaus Linnenbruegger (2011)
 * 🇨🇦 Stephen O'Kane (2012–2013)

Stadia

 * Keith Harris Stadium; Ottawa, Ontario (2005–2007)
 * Soccer Complex at Algonquin College; Ottawa, Ontario (2008–2013)

Average attendance
Attendance stats are calculated by averaging each team's self-reported home attendances from the historical match archive.

 * 2005: 322
 * 2006: 259
 * 2007: 260
 * 2008: 330
 * 2009: 383
 * 2010: 379
 * 2011: 220
 * 2012: 188
 * 2013: 256

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

title: Ottawa Fury SC


text: Talk:Potassium pentanoate

title: Talk:Potassium pentanoate


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Obligatory Baháʼí prayers

Obligatory Baháʼí prayers are prayers which are to be said daily by Baháʼís according to a fixed form decreed by Baháʼu'lláh. Prayers in the Baháʼí Faith are reverent words which are addressed to God, and refers to two distinct concepts: obligatory prayer and devotional prayer (general prayer). The act of prayer is one of the most important Baháʼí laws for individual discipline. Along with fasting, obligatory prayer is one of the greatest obligations of a Baháʼí, and the purpose of the obligatory prayer is to foster the development of humility and devotion. The obligation of daily obligatory prayer was prescribed by Baháʼu'lláh, the founder of the Baháʼí Faith, in his book of laws, the Kitáb-i-Aqdas.

It is forbidden to perform the obligatory prayers in congregation, so the daily obligatory prayers are offered individually, though it is not required that they be said in private.

History
In the Bayán the Báb prescribed an obligatory prayer of the nineteen  rak'ah (prostrations). He never wrote the text of this prayer, making the implementation of this law dependent on the coming of the Promised One. The Báb explained that the prayer symbolizes a spiritual journey from the realm of the body to the realm of the heart, which can be described as an arc of ascent, mirroring the arc of descent from God to creation.

In the Kitáb-i-Aqdas, Baháʼu'lláh confirmed the law of daily obligatory prayer and wrote that the specific obligatory prayer was recorded in a separate tablet or writing. Baháʼu'lláh wrote the text mentioned, but never released it in order to avoid provoking conflict with Muslims. Instead, sometime before the writing of the supplement to the Kitáb-i-Aqdas, the Questions and Answers, Baháʼu'lláh wrote a set of three obligatory prayers which are the ones used by Baháʼís today. The original obligatory prayer involved nine rak'ah and was to be said in the morning, noon and in the afternoon, probably three cycles at a time. After Baháʼu'lláh's death a strongbox holding the text of the original obligatory prayer was stolen by Mírzá Muhammad ʻAlí.

Significance
The obligatory prayer is a primary religious obligation starting at the age of fifteen and it is the most important kind of prayer. The purpose of the obligatory prayer is to foster the development of humility and devotion. The Baháʼí writings strongly warn against neglecting the prayers or minimizing their importance. The obligatory prayers are a personal spiritual obligation, and failure to observe the law is seen to have only a spiritual penalty.

Current prayers

Unlike general prayers in the Baháʼí Faith, there are specific regulations concerning the obligatory prayers; however, obligatory prayer is a personal spiritual obligation and thus no Baháʼí administrative sanction can be obtained if a Baháʼí fails to say their prayer daily.

Baháʼu'lláh wrote three obligatory prayers — the short, the medium and the long — and Baháʼís are free to choose to say one of the three each day. The short and the medium prayer have to be said at specific times; the short has to be said once between noon and sunset and the medium has to be said three times daily: once between dawn and noon, once between noon and sunset and once between sunset and two hours after sunset. The long prayer can be said at any time in the day. The medium and long prayers also include movements and gestures during the prayers, which are themselves obligatory except when a person is physically incapable of performing them. Shoghi Effendi has written that the motions and gestures are symbolic and are used to help maintain concentration during the prayers. Furthermore, the obligatory prayer is to be preceded by ablutions, the cleaning of the hands and face, and one has to face the Qiblih, which is the Shrine of Baháʼu'lláh.

Short prayer
The short prayer is a brief affirmation of the power of God and the servitude of the worshipper. The prayer should be said while standing in an attitude of humility before God, and it should be said between noon and sunset. The text of the prayer is:

 * "I bear witness, O my God, that Thou hast created me to know Thee and to worship Thee. I testify, at this moment, to my powerlessness and to Thy might, to my poverty and to Thy wealth. There is none other God but Thee, the Help in Peril, the Self-Subsisting."

Medium prayer
The medium obligatory prayer must be said three times during the day: once between sunrise and noon, once between noon and sunset, and once after sunset till two hours after sunset. It includes a series of positions and movements from one position to the next, along with specific supplications. The prayer stresses the power and loftiness of God, and the grace that is shown through his revelation. The text of the medium obligatory prayer can be found in Baháʼu'lláh's Prayers and Meditations.

Long prayer
The long obligatory prayer can be said anytime during the day. It includes a series of positions and movements from one position to the next, along with specific supplications. The prayer also includes parts where says the Greatest Name of God in the form of "Allah-u-Abha" at several points. About this prayer, Baháʼu'lláh has stated: "...the long Obligatory Prayer should be said at those times when one feeleth himself in a prayerful mood. In truth, it hath been revealed in such wise that if it be recited to a rock, that rock would stir and speak forth; and if it be recited to a mountain, that mountain would move and flow. Well is it with the one who reciteth it and fulfilleth God's precepts. Whichever prayer is read will suffice." The text of the long obligatory prayer can be found in Baháʼu'lláh's Prayers and Meditations. This prayer is known in Arabic as salat and as namaz in Persian, and is similar to the Islamic salat.

Laws
There are a number of laws and practices associated with the obligatory prayers concerning how to say the obligatory prayer, when Baháʼís are exempt from saying the obligatory prayers, and what to do if one misses saying an obligatory prayer.

Practices
There are certain practices that must be associated with the saying of the obligatory prayers. They include performing ablution, which consist of washing the hands and face, before the obligatory prayer. In the case that water is unavailable, or its use harmful to the face or hands, the verse "In the Name of God, the Most Pure, the Most Pure" should be repeated five times. The prayer should be said while the reader is facing the Qiblih which is the Shrine of Baháʼu'lláh. It is also preferable for the reader to be standing while saying the obligatory prayers in an attitude of humble reverence. Baháʼí's are also obliged to repeat the Greatest Name (Alláh-u-Abhá) 95 times a day while sitting. Ablutions are also prescribed for this, but it is not necessary to do them again if the repetitions are done right after the daily obligatory prayer.

Exemptions
Exemptions from saying the obligatory prayer include:
 * Children under the age of 15.
 * Those that are of ill-health.
 * Those that are older than 70.
 * Women who are menstruating are exempt from saying their obligatory prayer. They should instead perform their ablutions and repeat the verse "Glorified be God, the Lord of Splendour and Beauty" ninety-five times.

Missed prayers
In the case of a missed prayer due to insecurity such as during travel, each missed prayer can be compensated for by the repetition of certain verses and movements. The person should perform a single prostration (laying the forehead on any clean surface) in the place of each unsaid obligatory prayer and the prostrations should be performed while saying the verse "Glorified be God, the Lord of Might and Majesty, of Grace and Bounty." The prostrations should then be followed by saying the verse "Glorified be God, the Lord of the kingdoms of earth and heaven" eighteen times while the person is sitting cross-legged.

Obligatory prayer for the departed
Baháʼu'lláh wrote also a specific prayer for the dead, known as the Obligatory prayer for the departed, which is an unrelated practice, despite the similarity in terminology. This prayer is to be said before the interment of a Baháʼí who has reached the age of fifteen. It is a congregational prayer: the words are read aloud by a single person while others who are present stand in silence.

title: Obligatory Baháʼí prayers


text:
Hung Shing Temple

Hung Shing Temples or Tai Wong Temples are temples dedicated to Hung Shing Tai Wong. Hung Shing temples have been widely built in southern China, especially Guangdong province and in Hong Kong.

Existing temples
There are several Hung Shing Temples in Hong Kong, including 6 on Lantau Island and one only in urban Kowloon. The table provides a partial list of these temples. Hung Shing Festivals are celebrated on the 13th day of the 2nd month in Chinese calendar at the Hung Shing Temples in Ap Lei Chau, Tai Kok Tsui, Cheung Chau, Sha Lo Wan and Kau Sai Chau.

Note 1: A territory-wide grade reassessment of historic buildings is ongoing. The grades listed in the table are based on these updates  (8 June 2023). The temples with a "Not listed" status in the table below are not graded and do not appear in the list of historic buildings considered for grading. Note 2: While most probably incomplete, this list is tentatively exhaustive.

Former temples
Several temples have been ruined and have disappeared, including:
 * Temple at Mui Wo. Built in the Ming dynasty, repaired in 1843. Completely disappeared.
 * Temple at Pui O. Built in the Ming dynasty. Ruined as in 1979.
 * Temple in Tung Chung, inside Tung Chung Fort. Ruined as in 1979.

title: Hung Shing Temple


text:
Talk:Niccolò de' Conti

Untitled
I noticed a spelling mistake in the article entitled "Niccolò Da Conti". Should be "occurred" not "occured". This is in the summary section at the beginning of the article. However, there is no Edit button here. How do I correct the mistake?

 * For the opening section, which has no [Edit] link to it, click on the "Edit this page" at the top of the page. RickK 06:27, Jun 6, 2005 (UTC)

So did he die a muslim or christian?

Dating problems
Quoth the article:

 * Around 1440 Da Conti sailed back to India ... from where he travelled overland via Mt. Sinai to Cairo ... Niccolò Da Conti returned to Venice in 1444...

But also:

 *  Poggio's recording of Niccolò's account, made in 1439...

How can these dates be reconciled? --Jfruh 15:48, 6 Jun 2005 (UTC)

Date Questions Indeed?
I too have a problem with some of the dates and source materials in this interesting article. Having just read 1421 by Gavin Menzies I wanted to know more about Da Conti - I think more expertise is required here but it's a good start just the dates seem a bit screwy just when did Poggio and Da Conti sit down and was it in Venice, etc? --Robdav69 22:00 24 July 2006 (GMT)

Niccolò de' Conti or Niccolò Conti?
Niccolò da Conti— the da/dei is never capitalised— signifies "Niccolò from Conti", as Leonardo da Vinci was from Vinci. The name Niccolò de' Conti signifies "Niccolò of the Conti family", or "Niccolò of the lineage of the [unspecified] counts". The question remains whether he is simply Niccolò Conti. --Wetman (talk) 22:08, 4 December 2007 (UTC)

Fair use rationale for Image:EugeneIV.jpg
Image:EugeneIV.jpg is being used on this article. I notice the image page specifies that the image is being used under fair use but there is no explanation or rationale as to why its use in this Wikipedia article constitutes fair use. In addition to the boilerplate fair use template, you must also write out on the image description page a specific explanation or rationale for why using this image in each article is consistent with fair use.

Please go to the image description page and edit it to include a fair use rationale. Using one of the templates at Fair use rationale guideline is an easy way to insure that your image is in compliance with Wikipedia policy, but remember that you must complete the template. Do not simply insert a blank template on an image page.

If there is other fair use media, consider checking that you have specified the fair use rationale on the other images used on this page. Note that any fair use images lacking such an explanation can be deleted one week after being tagged, as described on criteria for speedy deletion. If you have any questions please ask them at the Media copyright questions page. Thank you.

BetacommandBot (talk) 21:01, 13 February 2008 (UTC)

Fair use rationale for Image:EugeneIV.jpg
Image:EugeneIV.jpg is being used on this article. I notice the image page specifies that the image is being used under fair use but there is no explanation or rationale as to why its use in this Wikipedia article constitutes fair use. In addition to the boilerplate fair use template, you must also write out on the image description page a specific explanation or rationale for why using this image in each article is consistent with fair use.

Please go to the image description page and edit it to include a fair use rationale. Using one of the templates at Fair use rationale guideline is an easy way to ensure that your image is in compliance with Wikipedia policy, but remember that you must complete the template. Do not simply insert a blank template on an image page.

If there is other fair use media, consider checking that you have specified the fair use rationale on the other images used on this page. Note that any fair use images lacking such an explanation can be deleted one week after being tagged, as described on criteria for speedy deletion. If you have any questions please ask them at the Media copyright questions page. Thank you.

BetacommandBot (talk) 13:27, 25 February 2008 (UTC)

Dates of birth and death
The 11th edition of the Encyclopaedia Britannica didn't know when he was born or died. No source is cited for these dates in our article, so how do we know them? Andrew Dalby 20:29, 15 July 2017 (UTC)
 * OK, I found a source and cited it. Andrew Dalby 20:41, 15 July 2017 (UTC)

= = Conflict in what translation say on size of ships = = = The Hakluyt Society translation of Niccolo de' Conti account on the ship size is different by 100% from the size given in the source used by Needham. Hakluyt Society translation by J. Winters Jones clearly list 2000 butts, not 2000 tons. Since the article was using the J. Winter Jones' translation, I changed the word tons to butts, which is what the reference used. A butt is half a ton. Needham's reference of 2000 tons was based on on an old Tudor English translation, and reflects the archaic spelling. Since the J. Winter Jones translation was based directly on the Italian, and uses the unusual "butts", I think is is more likely to be accurate. But in any case,the difference in the translations must be noted. Attached in the reference was a link to a scanned copy of the Hakluyt Society's book, so anyone can open up the link and verify for themselves.

If we want the passage to say 2000 tons, then a different reference should be used for the quote, but it still needs to be pointed out that some translations have the ship dimensions as half that size. It would be interesting to see what the original Italian has. Perhaps different manuscripts have different units listed, or some obscure unit whose value wasn't clearly know, which count account for the differences in translation.

The other think about the passage was the rather misleading comment about these ships being 4 times the size Western galleons. While that is true for most galleons, it is not true for Manila galleons were also 2000 tons. And the large carracks could be 1000 tons, which could be the same size as the Junks Conti mentions. Conti was a Venetian, and when he says bigger than our ships, it is not clear whether he means bigger than Venetian ships, or European ships in general. Venetians at the time were mostly using galleys, which were probably smaller than the largest round ships and carracks that the were available in the West at the time. It is possible that Marco Polo and Niccolo de' Conti were thinking about just Venetian ships.

The passage also does not clearly identify these ships as Chinese. It comes after the discussion of navigation methods by Indian sailors, but the ship construction matches what we know of Chinese ships. Perhaps, because these ships sailed in Indian waters, Conti regarded them as Indian ships. Or there were some Indians or local Chinese constructing ships along Chinese designs.

— Preceding unsigned comment added by 198.111.162.10 (talk) 21:59, 2 March 2019 (UTC)

Source cited uses "butts" an old unit, not tons as originally said in the article. Changes should be let stand
Qiushufang keeps undoing the change, but they should stand. The source reference in the Conti quote about the size of the ships says 2000 butts, not 2000 tons as the article listed. There are other translations that do give 2000 tons, namely the reference used by Needham, but that is not what the Wikipedia article was quoting. I have added links that show the value of the butt. I have tried to talk to Qiushufang, but he has not responded to any of my comments.

Since Wikipedia is often the main source that people use for a topic, it is important to let the reader know that there are major differences in the size given in different translations. I see no reason when why the comments should not stand. I am OK with using the original language of 2000 tons, and just making a comment that other translations have 2000 butts, which is only equivalent to 1000 tons. But I don't agree with just undoing the changes without discussion. — Preceding unsigned comment added by 198.111.162.10 (talk) 01:43, 7 March 2019 (UTC)

title: Talk:Niccolò de' Conti


text: Category:Fictional clones

title: Category:Fictional clones


text:
Gitelman syndrome

Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. It is the most frequent hereditary salt-losing tubulopathy. Gitelman syndrome is caused by disease-causing variants on both alleles of the SLC12A3 gene. The SLC12A3 gene encodes the thiazide-sensitive sodium-chloride cotransporter (also known as NCC, NCCT, or TSC), which can be found in the distal convoluted tubule of the kidney.

Disease-causing variants in SLC12A3 lead to a loss of NCC function, i.e., reduced transport of sodium and chloride via NCC. The effect is an electrolyte imbalance similar to that seen with thiazide diuretic therapy (which causes pharmacological inhibition of NCC activity).

Gitelman syndrome was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified.

Signs and symptoms
Affected individuals may not have symptoms in some cases. Symptomatic individuals present with symptoms almost identical to those of patients who are on thiazide diuretics, given that the affected transporter is the target of thiazides.

Clinical signs of Gitelman syndrome include a high blood pH in combination with low levels of chloride, potassium, and magnesium in the blood and decreased calcium excretion in the urine. In contrast to people with Gordon's syndrome, those affected by Gitelman syndrome generally have low or normal blood pressure. Individuals affected by Gitelman syndrome often complain of severe muscle cramps or weakness, numbness, thirst, waking up at night to urinate, salt cravings, abnormal sensations, chondrocalcinosis, or weakness expressed as extreme fatigue or irritability. Though cravings for salt are most common and severe, cravings for sour foods (e.g. vinegar, lemons, and sour figs) have been noted in some persons affected. More severe symptoms such as seizures, tetany, and paralysis have been reported. Abnormal heart rhythms and a prolonged QT interval can be detected on electrocardiogram and cases of sudden cardiac death have been reported due to low potassium levels. Quality of life is decreased in Gitelman syndrome

Phenotypic variations observed among patients probably result from differences in their genetic background and may depend on which particular amino acid in the NCCT protein has been mutated. A study by Riviera-Munoz et al. identified a subset of individuals with Gitelman syndrome with a severe phenotypic expression. The clinical manifestations observed in this group were neuromuscular manifestations, growth retardation, and ventricular arrhythmias. The patients were mostly male and were found to have at least one allele of a splice defect on the SLC12A3 gene.

Cause

Gitelman syndrome is caused by disease-causing variants on both alleles of the SLC12A3 gene, which encodes NCC, the sodium-chloride cotransporter. The sodium-chloride cotransporter is a protein made up of 1021 amino acids and 12 transmembrane domains. A large number of disease-causing variants throughout the SLC12A3 gene have been reported, including missense, nonsense, frame-shift, splice-site and intronic variants. In 2012, more than 180 mutations of this transporter protein had already been described.

The sodium-chloride cotransporter is a protein located in the cell membrane. It participates in the control of ion homeostasis at the distal convoluted tubule of the nephron. Thus, loss of NCC function reduces sodium and chloride reabsorption in the distal convoluted tubule. This can lead to a lower blood pressure in these patients.

Loss of NCC function has several other effects. Loss of SLC12A3 has been shown to lead to a shorter distal convoluted tubule, at least in mice. Therefore, other functions of the distal convoluted tubule might be perturbed as well. This is one of the possible reasons that magnesium reabsorption is reduced in patients, often leading to a low level of magnesium in the blood.

Secondly, processes in the distal convoluted tubule itself are altered as well. For instance, transcellular calcium reabsorption is increased. This has been suggested to be the result of a putative basolateral Na+/Ca2+ exchanger and apical calcium channel. Furthermore, continued action of the basolateral Na+/K+-ATPase might create an electrical gradient favourable for the reabsorption of divalent cations by secondary active transport. This is another mechanism that might be responsible for decreased magnesium reabsorption.

Another effect of the inactivated sodium-chloride cotransporter is the subsequent activation of the renin-angiotensin aldosterone system (RAAS). RAAS activation is a byproduct of the failure of the distal convoluted tubule in reabsorbing electrolytes, specifically sodium and chloride leading to cellular dehydration. RAAS attempts to compensate for this dehydration resulting in low serum blood potassium.

Some patients have symptoms that fit with a diagnosis of Gitelman syndrome, while a genetic defect in the SLC12A3 gene cannot be found. In these cases, a different genetic defect can sometimes be identified, although some cases remain idiopathic.

Diagnosis
Diagnosis of Gitelman syndrome can be confirmed after eliminating other common pathological sources of hypokalemia and metabolic alkalosis. A complete metabolic panel (CMP) or basic metabolic panel (BMP) can be used to evaluate serum electrolyte levels. Electrolyte measurement and aldosterone levels can be done via urine. The pathognomonic clinical markers include low serum levels of potassium, sodium, chloride, and magnesium in the blood as a result of urinary excretion. Urinary fractional excretion potassium is high or inappropriately normal in the context of hypokalaemia, and high levels of urinary sodium and chloride are observed. Other clinical indicators include elevated serum renin and aldosterone in the bloodstream, and metabolic alkalosis. The symptomatic features of this syndrome are highly variable ranging from asymptomatic to mild manifestations (weakness, cramps) to severe symptoms (tetany, paralysis, rhabdomyolysis). Symptom severity is multi-factorial, with phenotypic expression varying amongst individuals within the same family. Genetic testing is another measure of identifying the underlying mutations which cause the pathologic symptoms of the disease. This mode of testing is available at select laboratories.

When only one pathogenic variant is found with regular diagnostics, screening of SLC12A3 introns can be considered.

Work-up to exclude the differential diagnosis of the electrolyte abnormalities is key.

Differential diagnosis
Many diseases (both genetic and non-genetic) can give symptoms which are very similar to Gitelman syndrome. The following are some examples, as well as examples of how they can differ from classic Gitelman syndrome.
 * In Gitelman syndrome hypocalciuria is present, and a urine calcium:creatinine ratio may help distinguish it from Bartter syndrome as the two disorders can be clinically indistinguishable. Secondly, hypomagnesemia is present in most patients with Gitelman syndrome, while it is present in only some patients with Bartter syndrome. Lastly, in Bartter syndrome maximal urine concentrating ability is lost.
 * Laxative abuse can mimic the serum electrolyte abnormalities, but fractional excretion of potassium will be low
 * Diuretic abuse could be suspected if urinary chloride excretion varies by time of day but may require a diuretic assay to detect
 * Surreptitious vomiting can cause metabolic alkalosis and hypokalaemia, but urinary chloride levels will be low
 * Medication history; Proton-pump inhibitors can cause an isolated hypomagnesaemia phenotype, and aminoglycosides such as gentamicin can cause a transient metabolic alkalosis with hypokalaemia and hypomagnesaemia that resolves 2–6 weeks after drug termination.
 * Primary aldosteronism will cause metabolic alkalosis and hypokalaemia, but hypertension will be present and serum renin will be low
 * EAST syndrome, though neurological features will predominate
 * Renal cysts and diabetes syndrome can cause hypomagnesaemia and hypocalcuria, but is distinguished by early onset chronic kidney disease and an autosomal dominant inheritance pattern of renal cysts and/or diabetes
 * A small percentage of Gitelman syndrome cases can be attributed to disease-causing variants in the CLCNKB gene. Disease-causing variants in this gene are responsible for Bartter syndrome type 3, which can present with electrolyte abnormalities that are clinically indistinguishable to Gitelman syndrome. When mutations are not found within the SLC12A3 gene, genetic screening of this gene is recommended to rule out involvement of CLCNKB gene.
 * Variants in the mitochondrial transfer RNAs encoding the tRNA for isoleucine (MT-TI) and the tRNA for phenylalanine (MT-TF) in the mitochondrial DNA can also cause a Gitelman-like syndrome. These homoplasmic mitochondrial DNA mutations are maternally inherited.

Treatment
To treat the symptoms related to the electrolyte abnormalities, supplementation is often needed. Dietary modification of a high salt diet incorporated with potassium and magnesium supplementation to normalize blood levels is the mainstay of treatment. Large doses of potassium and magnesium are often necessary to adequately replace the electrolytes lost in the urine. Diarrhea is a common side effect of oral magnesium which can make replacement by mouth difficult but dividing the dose to 3-4 times a day is better tolerated. Severe deficits of potassium and magnesium require intravenous replacement. Aldosterone antagonists (such as spironolactone or eplerenone) or epithelial sodium channel blockers such as amiloride have also been suggested as possible treatments, because they decrease urinary wasting of potassium. However, a consensus expert statement from 2017 warns that such drugs should only be used with caution in Gitelman syndrome because of the possible side effects (e.g., aggravated sodium depletion).

Most asymptomatic individuals with Gitelman syndrome can be monitored without medical treatment.

In patients with early onset of the disease such as infants and children, indomethacin is the drug of choice utilized to treat growth disturbances. Indomethacin in a study by Blanchard et al. 2015 was shown to increase serum potassium levels, and decrease renin concentration. Adverse effects of indomethacin include a decrease in the glomerular filtration rate, and gastrointestinal disturbances. Therefore, these drugs should also be used only with caution in Gitelman syndrome.

Cardiac evaluation is promoted in the prevention of dysrhythmias and monitoring of QT interval activity. Medications that extend or prolong the QT interval (macrolides, antihistamines, beta-2 agonists) should be avoided in these patients to prevent cardiac death.

Epidemiology
Estimates of the prevalence of Gitelman syndrome range from 1 in 80,000 to 1 in 500 people, depending on the population. The ratio of men to women affected is 1:1. This disease is encountered typically after the 1st decade of life, i.e., during adolescence or adulthood. However, it can occur in the neonatal period. Heterozygous carriers of the SLC12A3 gene mutations are 1% of the population. A person with Gitelman syndrome has a low probability of passing the disease to their offspring. This chance is roughly 1 in 400, unless they are both carriers of the disease.

History
The condition is named for Hillel Jonathan Gitelman (1932– January 12, 2015), an American nephrologist working at University of North Carolina School of Medicine. He first described the condition in 1966, after observing a pair of sisters with the disorder. Gitelman and his colleagues later identified and isolated the gene responsible (SLC12A3) by molecular cloning.

title: Gitelman syndrome


text:
Amelia Best

Amelia Martha (Millie) Best MBE (29 April 1900 – 14 November 1979) was one of the first two women elected to the Tasmanian House of Assembly.

Best was born in Lower Barrington, Tasmania, Australia. She ran an arts and crafts business in Launceston and was involved in the Voluntary Aid Detachment (VAD) Canteen Services during World War II.

She was elected to the House of Assembly representing the Liberal Party in the seat of Wilmot in 1955. She lost her seat in 1956, was re-elected in 1958 and lost her seat again in 1959.

title: Amelia Best


text: User talk:84.9.86.151

title: User talk:84.9.86.151