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Adobe Creative Suite

Adobe Creative Suite (CS) is a discontinued software suite of graphic design, video editing, and web development applications developed by Adobe Systems.

The last of the Creative Suite versions, Adobe Creative Suite 6 (CS6), was launched at a release event on April 23, 2012, and released on May 7, 2012. CS6 was the last of the Adobe design tools to be physically shipped as boxed software as future releases and updates would be delivered via download only.

On May 6, 2013, Adobe announced that CS6 would be the last version of the Creative Suite,  and that future versions of their creative software would only be available via their Adobe Creative Cloud subscription model. Adobe also announced that it would continue to support CS6 and would provide bug fixes and security updates through the next major upgrades of both Mac and Windows operating systems (as of 2013). The Creative Suite packages were pulled from Adobe's online store in 2013, but were still available on their website until January 2017.

Applications

The following table shows the different details of the core applications in the various Adobe Creative Suite editions. Each edition may come with all these apps included or only a subset.

Editions
Adobe sold Creative Suite applications in several different combinations called "editions", these included:
 * Adobe Creative Suite 6 Design Standard is an edition of the Adobe Creative Suite 6 family of products intended for professional print, web, interactive and mobile designers.
 * Adobe Creative Suite 6 Design & Web Premium is an edition of the Adobe Creative Suite 6 family of products intended for professional web designers and developers.
 * Adobe Creative Suite 6 Production Premium is an edition of the Adobe Creative Suite 6 family of products intended for professional rich media and video post-production experts who create projects for film, video, broadcast, web, DVD, Blu-ray Disc, and mobile devices.
 * Adobe Creative Suite 6 Master Collection contains applications from all of the above editions.

Adobe Flash Catalyst, Adobe Contribute, Adobe OnLocation, and Adobe Device Central, previously available in CS5.5, have been dropped from the CS6 line-up. Adobe Prelude and Adobe Encore are not released as standalone products. Adobe Encore is available as part of Adobe Premiere Pro. Adobe InCopy, a word processing application that integrates with Adobe InDesign, is also part of the Creative Suite family, but is not included in any CS6 edition.

In March 2013, it was reported that Adobe would no longer sell boxed copies of the Creative Suite software, instead offering digital downloads and monthly subscriptions.

Creative Suite 1 and 2
The first version of Adobe Creative Suite was released in September 2003 and Creative Suite 2 in April 2005. The first two versions (CS and CS2) were available in two editions.

The Standard Edition included:
 * Adobe Bridge (since CS2)
 * Adobe Illustrator
 * Adobe InCopy
 * Adobe InDesign
 * Adobe Photoshop
 * Adobe Premiere Pro (since CS2)
 * Adobe ImageReady
 * Adobe Version Cue
 * Design guide and training resources
 * Adobe Stock Photos

The Premium Edition also included:
 * Adobe Acrobat Professional (Version 8 in CS2.3)
 * Adobe Dreamweaver (since CS2.3)
 * Adobe GoLive

Creative Suite helped InDesign become the dominant publishing software, replacing QuarkXPress, because customers who purchased the suite for Photoshop and Illustrator received InDesign at no additional cost.

Adobe shut down the "activation" servers for CS2 in December 2012, making it impossible for licensed users to reinstall the software if needed. In response to complaints, Adobe then made available for download a version of CS2 that did not require online activation, and published a serial number to activate it offline. Because there was no mechanism to prevent people who had never purchased a CS2 license from downloading and activating it, it was widely thought that the aging software had become freeware, despite Adobe's later explanation that it was intended only for people who had "legitimately purchased CS2". The later shutdown of the CS3 and CS4 activation servers was handled differently, with registered users given the opportunity to get individual serial numbers for offline activation, rather than a published one.

Creative Suite Production Studio
Adobe Creative Suite Production Studio (previously Adobe Video Collection) was a suite of programs for acquiring, editing, and distributing digital video and audio that was released during the same timeframe as Adobe Creative Suite 2. The suite was available in standard and premium editions.

The Adobe Production Studio Premium edition consisted of:
 * Adobe After Effects Professional
 * Adobe Audition
 * Adobe Bridge
 * Adobe Encore DVD
 * Adobe Premiere Pro
 * Adobe Photoshop
 * Adobe Illustrator
 * Adobe Dynamic Link (Not sold separately)

The Standard edition consisted of:
 * Adobe After Effects Standard
 * Adobe Bridge
 * Adobe Premiere Pro
 * Adobe Photoshop

Since CS3, Adobe Production Studio became part of the Creative Suite family. The equivalent version for Production Studio Premium is the Adobe Creative Suite Production Premium.

Macromedia Studio
Macromedia Studio was a suite of programs designed for web content creation designed and distributed by Macromedia. After Adobe's 2005 acquisition of Macromedia, Macromedia Studio 8 was replaced, modified, and integrated into two editions of the Adobe Creative Suite family of software from version 2.3 onwards. The closest relatives of Macromedia Studio 8 are now called Adobe Creative Suite Web Premium.

Core applications from Macromedia Studio have been merged with Adobe Creative Suite since CS3, including Flash, Dreamweaver, and Fireworks. Some Macromedia applications were absorbed into existing Adobe products, e.g. FreeHand has been replaced with Adobe Illustrator. Director and ColdFusion are not part of Adobe Creative Suite and will only be available as standalone products. The final version of Macromedia Studio released include:
 * Macromedia Studio MX Released May 29, 2002, internally it was version 6 and the first incarnation of the studio to use the "MX" suffix, which for marketing purposes was a shorthand abbreviation that meant "Maximize". Studio MX included Dreamweaver, Flash, FreeHand, Fireworks and a developer edition of ColdFusion.
 * Macromedia Studio MX Plus Released February 10, 2003, sometimes referred to as MX 1.1. MX Plus was a special edition release of MX that included Freehand MX (replacing Freehand 10), Contribute and DevNet Resource Kit Special Edition in addition to the existing MX suite of products.
 * Macromedia Studio MX 2004 Released September 10, 2003, despite its name, it is internally version 7. Studio MX 2004 included FreeHand along with updated versions of Dreamweaver, Flash and Fireworks. An alternate version of Studio MX 2004 included Flash Professional and a new interface for Dreamweaver.
 * Macromedia Studio 8 Released September 13, 2005, Studio 8 was the last version of Macromedia Studio. It comprised Dreamweaver 8, Flash 8, Flash 8 Video Converter, Fireworks 8, Contribute 3 and FlashPaper.

Creative Suite 3
Adobe Creative Suite 3 (CS3) was announced on March 27, 2007; it introduced universal binaries for all major programs for the Apple Macintosh, as well as including all of the core applications from Macromedia Studio and Production Studio.

Some Creative Suite programs also began using the Presto layout engine used in the Opera web browser.

Adobe began selling CS3 applications in six different combinations called "editions." Design Standard & Premium and Web Standard & Premium began shipping on April 16, 2007, and Production Premium and Master Collection editions began shipping on July 2, 2007. The latest released CS3 version was version 3.3, released on June 2, 2008. In this version Fireworks CS3 was included in Design Premium and all editions that had included Acrobat 8 Pro had it replaced with Acrobat 9 Pro. Below is a matrix of the applications included in each edition of CS3 version 3.3:

CS3 included several programs, including Dreamweaver, Flash Professional, and Fireworks that were developed by Macromedia, a former rival acquired by Adobe in 2005. It also included Adobe OnLocation and Adobe Ultra that were developed by Serious Magic, also a firm acquired by Adobe in 2006.

Adobe dropped the following programs (that were previously included in CS2) from the CS3 software bundles:
 * Adobe GoLive (replaced by Adobe Dreamweaver)
 * Adobe ImageReady (merged into Adobe Photoshop and replaced by Adobe Fireworks)
 * Adobe Audition (replaced by Adobe Soundbooth)

Adobe had announced that it would continue to develop Audition as a standalone product, while GoLive had been discontinued. Adobe GoLive 9 was released as a standalone product on June 10, 2007. Adobe Audition 3 was announced as a standalone product on September 6, 2007. Adobe had discontinued ImageReady and had replaced it with Fireworks, with some of ImageReady's features integrated into Photoshop. Audition became part of the Creative Suite again in CS5.5 when Soundbooth was discontinued.

Creative Suite 4
Adobe Creative Suite 4 (CS4) was announced on September 23, 2008, and officially released on October 15, 2008. All applications in CS4 featured the same user interface, with a new tabbed interface for working with concurrently running Adobe CS4 programs where multiple documents can be opened inside multiple tabs contained in a single window.

Adobe CS4 was also developed to perform better under 64-bit and multi-core processors. On MS Windows, Adobe Photoshop CS4 ran natively as a 64-bit application. Although they were not natively 64-bit applications, Adobe After Effects CS4 and Adobe Premiere Pro CS4 had been optimized for 64-bit computers. However, there were no 64-bit versions of CS4 available for Mac OS X. Additionally, CS4 was the last version of Adobe Creative Suite installable on the PowerPC architecture on Mac OS X, although not all applications in the suite are available for PowerPC. The unavailable products on PowerPC include the featured applications within the Production Premium collection (Soundbooth, Encore, After Effects, Premiere, and OnLocation). In early testing of 64-bit support in Adobe Photoshop CS4, overall performance gains ranged from 8% to 12%, due to the fact that 64-bit applications could address larger amounts of memory and thus resulted in less file swapping — one of the biggest factors that can affect data processing speed.

Two programs were dropped from the CS4 line-up: Adobe Ultra, a vector keying application which utilizes image analysis technology to produce high quality chroma key effects in less than ideal lighting environments and provides keying of a subject into a virtual 3D environment through virtual set technology, and Adobe Stock Photos. Below is a matrix of the applications that were bundled in each of the software suites for CS4:

Creative Suite 5
Adobe Creative Suite 5 (CS5) was released on April 30, 2010. From CS5 onwards, Windows versions of Adobe Premiere Pro CS5 and Adobe After Effects CS5 were 64-bit only and required at least Windows Vista 64-bit or a later 64-bit Windows version. Windows XP Professional x64 Edition was no longer supported. The Mac versions of the CS5 programs were rewritten using macOS's Cocoa APIs in an effort to modernize the codebase. These new Mac versions dropped support for PowerPC-based Macs and were 64-bit Intel-only. Adobe Version Cue, an application that enabled users to track and manipulate file metadata and automate the process of collaboratively reviewing documents among groups of people, and the Adobe Creative Suite Web Standard edition, previously available in CS4, were dropped from the CS5 line-up. Below is a matrix of the applications that were bundled in each of the software suites for CS5:

Creative Suite 5.5
Following the release of CS5 in April 2010, Adobe changed its release strategy to an every other year release of major number installments. CS5.5 was presented on April 12, 2011, as an in-between program until CS6. The update helped developers optimize websites for a variety of tablets, smart phones, and other devices. At the same time, Adobe announced a subscription-based pay service as an alternative to full purchase. On July 1, 2011, Adobe Systems announced its Switcher Program, which will allow people who had purchased any version of Apple's Final Cut Pro (or Avid Media Composer) to receive a 50 percent discount on Creative Suite CS5.5 Production Premium or Premiere Pro CS5.5.

Not all products were upgraded to CS5.5 in this release; applications that were upgraded to CS5.5 included Adobe InDesign, Adobe Flash Catalyst, Adobe Flash Professional, Adobe Dreamweaver, Adobe Premiere Pro, Adobe After Effects, and Adobe Device Central. Adobe Audition also replaced Adobe Soundbooth in CS5.5, Adobe Story was first offered as an AIR-powered screenwriting and preproduction application, and Adobe Acrobat X Pro replaced Acrobat 9.3 Pro. Below is a matrix of the applications that were bundled in each of the software suites for CS5.5:

Creative Suite 6
During an Adobe conference call on June 21, 2011, CEO Shantanu Narayen said that the April 2011 launch of CS5.5 was "the first release in our transition to an annual release cycle", adding, "We intend to ship the next milestone release of Creative Suite in 2012." On March 21, 2012, Adobe released a freely available beta version of Adobe Photoshop CS6. The final version of Adobe CS6 was launched on a release event April 23, 2012, and first shipped May 7. Adobe also launched a subscription-based offering named Adobe Creative Cloud where users are able to gain access to individual applications or the full Adobe Creative Suite 6 suite on a per-month basis, plus additional cloud storage spaces and services.

The native 64-bit Windows applications available in Creative Suite 6 were Photoshop, Illustrator, After Effects (64-bit only), Premiere Pro (64-bit only), Encore (64-bit only), SpeedGrade (64-bit only) and Bridge.

Discontinuation
On May 5, 2013, during the opening keynote of its Adobe MAX conference, Adobe announced that it was retiring the "Creative Suite" branding in favor of "Creative Cloud", and making all future feature updates to its software (now appended with "CC" instead of "CS", e.g. Photoshop CC) available via the Creative Cloud subscription service rather than through the purchasing of perpetual licenses.

Customers must pay a subscription fee and if they stop paying, they will lose access to the proprietary file formats, which are not backward-compatible with the Creative Suite (Adobe admitted that this is a valid concern ). Individual subscribers must have an Internet connection to download the software and to use the 2 GB of provided storage space (or the additionally purchased 20 GB ), and must validate the license monthly.

Adobe's decision to make the subscription service the only sales route for its creative software was met with strong criticism (see Creative Cloud controversy). Several online articles began offering replacements of Photoshop, Illustrator, and other programs, with free software such as GIMP and Inkscape or competing products such as Affinity Designer, CorelDRAW, PaintShop Pro, and Pixelmator directly offering alternatives.

In addition to many of the products formerly part of the Creative Suite (one product, Fireworks, was announced as having reached the end of its development cycle), Creative Cloud also offers subscription-exclusive products such as Adobe Muse and the Adobe Edge family, Web-based file and website hosting, Typekit fonts, and access to the Behance social media platform. The new CC versions of their applications, and the full launch of the updated Creative Cloud service, was announced for June 17, 2013. New versions with major feature updates have been released regularly, with a refresh of the file formats occurring in October 2014. Adobe also announced that it would continue to offer bug fixes for the CS6 products so that they will continue to run on the next versions of Microsoft Windows and Apple OS X. However, they have said there are no updates planned to enable CS6 to run in macOS Catalina.

title: Adobe Creative Suite


text:
Starve the beast

"Starve the beast" is a political strategy employed by American conservatives to limit government spending by cutting taxes, to deprive the federal government of revenue in a deliberate effort to force it to reduce spending. The term "the beast", in this context, refers to the United States federal government and the programs it funds, primarily with American tax money, particularly social programs such as education, welfare, Social Security, Medicare, and Medicaid.

On July 14, 1978, economist and future Federal Reserve chairman Alan Greenspan testified to the Senate Finance Committee: "Let us remember that the basic purpose of any tax cut program in today's environment is to reduce the momentum of expenditure growth by restraining the amount of revenue available and trust that there is a political limit to deficit spending."

Before his election as President, then-candidate Ronald Reagan foreshadowed the strategy during the 1980 US Presidential debates, saying "John Anderson tells us that first we've got to reduce spending before we can reduce taxes. Well, if you've got a kid that's extravagant, you can lecture him all you want to about his extravagance. Or you can cut his allowance and achieve the same end much quicker."

The earliest known use of "starve the beast" is in a 1979 newspaper article quoting Santa Rosa, California city councilman Jerry Wilhelm at a tax forum sponsored by the Libertarian Party.

Since 2000
The tax cuts and deficit spending of former US President George W. Bush's administration were attempts to "starve the beast". Bush said in 2001: "so we have the tax relief plan [...] that now provides a new kind—a fiscal straightjacket [sic] for Congress. And that's good for the taxpayers, and it's incredibly positive news if you're worried about a federal government that has been growing at a dramatic pace over the past eight years and it has been."

Republican presidential candidate Fred Thompson's tax-cut plan, incorporating a flat tax, also deferred paying for the larger deficits it would create. It "would most likely be funded by lower government spending on Social Security and Medicare benefits", according to the Wall Street Journal.

Political activist Grover Norquist authored an oath, the so-called "Taxpayer Protection Pledge", that 279 Senators and Congressman have signed. The oath states the signatories will never vote to raise taxes on anyone under any circumstances. It is viewed by some of the unsigned as a stumbling block to mutual fiscal negotiations to benefit the country.

Economic analysis
James M. Buchanan, a Nobel Prize-winning economist, helped develop the fiscal illusion hypothesis: "It's obvious, borrowing allows spending to be made that will yield immediate political payoffs without the incurring of any immediate political cost." In their book Democracy in Deficit (1977), Buchanan and Richard E. Wagner suggest that the complicated nature of the U.S. tax system causes fiscal illusion and results in greater public expenditure than would be the case in an idealized system in which everyone is aware in detail of what their share of the costs of government is.

Empirical evidence shows that Starve the Beast may be counterproductive, with lower taxes actually corresponding to higher spending. An October 2007 study by Christina D. Romer and David H. Romer of the National Bureau of Economic Research found: "[...] no support for the hypothesis that tax cuts restrain government spending; indeed, [the findings] suggest that tax cuts may actually increase spending. The results also indicate that the main effect of tax cuts on the government budget is to induce subsequent legislated tax increases."

William Niskanen, chairman emeritus of the libertarian Cato Institute, criticized "starve the beast". According to Niskanen, if deficits finance 20% of government spending, then citizens perceive government services as discounted; services that are popular at 20% off the listed price would be less popular at full price. He hypothesized that higher revenues could constrain spending, and found strong statistical support for that conjecture based on data from 1981 to 2005. Another Cato researcher, Michael New, tested Niskanen's model in different time periods and using a more restrictive definition of spending (non-defense discretionary spending) and arrived at a similar conclusion.

Professor Leonard E. Burman of Syracuse University testified to a U.S. Senate committee in July 2010 that: "My guess is that if President Bush had announced a new war surtax to pay for Iraq or an increase in the Medicare payroll tax rate to pay for the prescription drug benefit, both initiatives would have been less popular. Given that the prescription drug benefit only passed Congress by one vote after an extraordinary amount of arm-twisting, it seems unlikely that it would have passed at all if accompanied by a tax increase. Starve the beast doesn't work."

Economist Paul Krugman summarized: "Rather than proposing unpopular spending cuts, Republicans would push through popular tax cuts, with the deliberate intention of worsening the government's fiscal position. Spending cuts could then be sold as a necessity rather than a choice, the only way to eliminate an unsustainable budget deficit." He wrote that the "beast is starving, as planned" and that "Republicans insist that the deficit must be eliminated, but they're not willing either to raise taxes or to support cuts in any major government programs. And they're not willing to participate in serious bipartisan discussions, either, because that might force them to explain their plan—and there isn't any plan, except to regain power."

Historian Bruce Bartlett, former domestic policy adviser to President Ronald Reagan, referred to "starve the beast" as "the most pernicious fiscal doctrine in history", and blames it for the increase in US government debt since the 1980s.

Political advocacy
Former U.S. Senator Jon Kyl (R-AZ), a veteran of the Senate Finance Committee, stated "you should never have to offset the cost of a deliberate decision to reduce tax rates on Americans."

Lobbyist Grover Norquist is a well-known proponent of the strategy and has famously said, "My goal is to cut government in half in twenty-five years, to get it down to the size where we can drown it in the bathtub."

"Feed the beast"
A related idea known as "Feed the beast", refers to increasing taxes for the purported purpose of balancing the budget only to make the government spend those inflows. Writer Stephen Moore and economist Richard Vedder have written in the Wall Street Journal that every new dollar of new taxes leads to more than one dollar of new spending according to their research. In an op-ed, they both stated that "[t]he grand bargain so many in Washington yearn for—tax increases coupled with spending cuts—is a fool's errand" since "higher tax collections never resulted in less spending". Their conclusions have been disputed by economist and writer Bruce Bartlett in The Fiscal Times, who stated that tax increases in the early 1990s helped contribute to more austere budgets in the late 1990s.

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

title: Starve the beast


text:
John Boot

John Boot (October 1815 – 30 May 1860) was an English chemist and retail businessperson who was the sole founder of Boots the Chemists. Originally working in agriculture, he was forced by ill health to change careers and set up a shop to sell medicinal herbal remedies at Goose Gate, Nottingham. Although he had no formal qualification, he had learned the skills from his mother and from the Methodist book, Primitive Physic by John Wesley.

When Boot died in 1860, his wife Mary took over the business, and his son, Jesse, went on to expand the business by opening more stores in poor areas, eventually expanding it into the company Boots UK.

Early life
Boot was born in Radcliffe-on-Trent, England, in October 1815. He was the son of William Boot; his mother Sarah (née Fox) had practised the duty of herbal management; John was inspired by this.

Founding Boots
Originally a farm worker, he was forced to change career due to poor health. He set up a shop at Goose Gate, Nottingham, to sell medicinal herbal remedies, and called it "British and American Botanic Establishment".

In the store, he offered remedies and consultations to members of the public three days a week, in a poor area of Nottingham. The career had also appealed to Boot due to his Methodist roots, where he had studied the books of John Wesley, including Primitive Physic, a book about the fundamentals of herbal biology and remedies.

Personal life and death
Boot married Elizabeth Mills in 1838; she died in 1848. He married his second wife Mary Wills, in 1849, and the couple had one child, Jesse, on 2 June 1850.

Boot died on 30 May 1860, leaving his wife and business behind. Mary Boot carried on with the business, renaming it as M & J Boot, Herbalists. Boot's son, Jesse, would help bring the business to a much larger custom base, by opening further shops in other poor areas of the city, and eventually evolving into the national Boots UK empire.

title: John Boot


text:
Talk:Phone connector (audio)

History
I was surprised by a lack of a "Decline" section, considering their modern unavailability in many general consumer devices capable of playing audio, ranging from smartphones to some modern audio players. Perhaps someone familiar with the topic could add this? Gangweedersriseup (talk) 08:15, 23 May 2023 (UTC)

 * Done. See Phone connector (audio) section in History which links to a couple other sections discussing this a bit. Em3rgent0rdr (talk) 18:47, 15 December 2023 (UTC)

Comparison image with 4.4mm balanced jack
The current connector comparison image lacks the 4.4mm balanced jack, which is, as of 2023, now standard across all prosumer and professional audio equipment that offers/requires a balanced audio signal. I've taken a new photo that also includes the 4.4mm jack, however I've been unable to find any standalone 2.5mm TRS plugs anywhere in my house, apart from a Baofeng data cable. Any thoughts or suggestions? -- benlisquare T•C•E 12:06, 25 November 2023 (UTC)

 * We don't say much about this connector in the article so I'm not sure how important this update is. The old image shows some simple TS options which is nice. ~Kvng (talk) 23:23, 29 November 2023 (UTC)

Replace almost all "jack" with "socket"
In common usage, the word "jack" has confusingly too often been used to refer to the plug, even though it originally meant the female connector. "Socket" however hasn't been corrupted. So, I think jack should be avoided in this article. Except for "other uses" and the historical section talking about the origin from "jack-knife", this article should stick to using "socket" as much as possible. Em3rgent0rdr (talk) 10:19, 12 December 2023 (UTC)

 * I was concerned that phone jack is the WP:COMMONNAME and phone socket might not be a familiar term but I've done some quick image searches and determined that this change is unlikely to introduce additional confusion. ~Kvng (talk) 23:58, 12 December 2023 (UTC)

Design section needs to be rearranged
The design section is currently a messy arrangement...this is how it looks on my desktop:

I'm thinking maybe the A, B, C, D images can instead be placed inside a Table as one column and have their name as another column and their description in another column. That will help to be able to refer to the thing being discussed when its caption is near the image. And maybe move that into the section discussing springs. And the Tip-Ring-Sleeve image can probably be moved up to earlier section, maybe in history as it can be a picture of the modern standard. And then maybe this "Design" section will become too small that it can just be renamed "Cleaning contacts" or something, cause that is what it talks about. Em3rgent0rdr (talk) 19:10, 15 December 2023 (UTC)

Broken reference in Design section
Reference 79, to "Jack Schematics Table" PDF is broken. It points to http://www.switchcraft.com/documents/jack_schematics.pdf

I don't know which was the content of the original document but I bet it can be the PDF it is now available on https://www.mouser.com/datasheet/2/393/Jack_Schematics-310971.pdf since the document itself is marked as coming form Switchcraft. Anyway this PDF seems a reasonable reference to replace the broke one, even in the case it is not the same document.

I am quite new in editing Wikipedia so I ask if I can proceed in replacing the reference. Menegoz (talk) 15:24, 1 February 2024 (UTC)

 * I've just fixed by digging up the original pdf from archive.org and editing the citation to point to archive.org's copy. Thanks for reporting this dead link. Em3rgent0rdr (talk) 15:59, 1 February 2024 (UTC)

title: Talk:Phone connector (audio)


text:
Elisabeth Beskow

Elisabeth Maria Beskow (19November 1870 – 17October 1928) was a Swedish writer. Born in Stockholm, Sweden she went to the Beskow School and later studied at the Sabbatsberg Hospital as well as the Sophiahemmet. She wrote about fifty books under the pseudonym Runa. A number of her books are translated into Danish, Finnish, French, English, German and Dutch.

In her books she discussed the equal rights of men and women and spoke against animal testing and for vegetarianism.

Bibliography—a selection

 * Allt eller intet (1895)
 * Från skogarna och fjällen (Beijer, 1896)
 * På Elghyttan (Fosterlandsstift, 1902)
 * Nina (Fosterlandsstift, 1903)
 * Var rädd om din krona! (Stockholm Fosterlandsstift : Barnaserien, 1903)
 * Gamle prästen i Hornsjö och andra berättelser (Fosterlandsstiftelsen, 1904)
 * Sagor och berättelser för barn (Palmquist, 1904)
 * Med blicken mot det osynliga (Fosterlandsstift., 1906)
 * Katri berättelse (Fosterlandsstiftelsen, 1907, Bibliotek för de unga. Ungdomsserien ; 6)
 * Röster (A. V. Carlson, 1909)
 * Den ljusnande framtid (Fosterlandsstift, 1910, Bibliotek för de unga. Ungdomsserien ; 9)
 * Vildfågel (A. V. Carlson, 1911)
 * I vildmarken och andra berättelser från Lappland (A. V. Carlson, 1911)
 * Korsfararne, handling i dramatisk form, (A. V. Carlson, 1912)
 * Ljudande malm (Rock Island, Ill. : Augustana Book Concern, [1912?])
 * Vildfågels näste (A. V. Carlson, 1913)
 * En tonskapelse berättelse (A. V. Carlson, 1913)
 * Han och hans hustru (A. V. Carlson, 1915)
 * Grannarna i Västanfors (A. V. Carlson, 1916)
 * Sif (Carlson, 1917)
 * Lärobok i stenografi (Gumperts bokh. i distr., 1917)
 * Birger Löwing (A. V. Carlson, 1918)
 * Hans moders gud (A. V. Carlson, 1914)
 * Birger Löwing (A. V. Carlson, 1918)
 * Den lille väpnaren, sagor och berättelser för barn 2:a uppl, (Lindblad, 1919)
 * Fostersyskonen (Stockholm, 1922)
 * Hans ögons ljus (A. V. Carlson, 1923
 * Ekekronas (A. V. Carlson, 1924)
 * Fader och son (A. V. Carlson, 1925)
 * Gossar och flickor (Lindblad, 1925)
 * Ols Barbro (A. V. Carlson, 1921)
 * Skalunga I och II (Carlson 1919–25)
 * Skiftande dagrar berättelser (Lindblad, 1926)
 * Trettonåringar (A. V. Carlson, 1926)
 * Testamentet (A. V. Carlson, 1927)
 * Vårdrömmar (Uppsala, 1927)
 * Förnyelse, (A. V. Carlson, 1928)
 * Vardagsliv

title: Elisabeth Beskow


text:
Talk:Starve-the-beast

Started this page to watch for any comments or questions Bulatych Tue Nov 11 19:31:50 UTC 2003

"Cutting taxes"
Is it worth mentioning that the tax-cutting has to be done carefully? Some sources argue that Bush's tax cuts are only benefitting some people rather than boosting the economy.

 * Across the board rate cuts are not "tax cuts for the wealthy". The dollar amounts are of course the greatest at the top, but an across the board tax rate cut is not favoring any particular income group.  Politicians have been lying about this for decades.  Estate tax cuts, capital gains tax cuts - maybe you have an argument; but rate cuts help every taxpayer. Dubc0724 12:55, 7 June 2006 (UTC)

Choke the Beast is an alternative description
Isn't "Choke-the-Beast" a common enough usage to justify a redirect to this article? I sometimes hear or read only that and no mention of "Starve-the-Beast".

 * A quick google search made me think you were wrong at first, but then I excluded the 90,000 references to Wikipedia, and it's actually quite close (both around 400 entries). I'll add it. Dave (talk) 18:21, 24 December 2005 (UTC)

 * Actually, it looks like I formulated my search wrong. 90,000 Wikipedia mirrors did seem like way too many.  Anyway, Choke the beast redirects here now. Dave (talk) 21:48, 24 December 2005 (UTC)

"What empirical evidence"???
"Some empirical evidence shows that the strategy may actually be counterproductive, with higher taxes actually corresponding to lower spending: "Controlling for the unemployment rate, federal spending [from 1981 to 2000] increased by about one-half percent of GDP for each one percentage point decline in the relative level of federal tax revenues." The article (written by William Niskanen and Peter Van Doren of the Cato Institute) shows that "a tax increase may be the most effective policy to reduce the relative level of federal spending," though the authors oppose tax increases for other reasons.[1] Additionally, some economists and politicians see the budget deficits created by this strategy as harmful to the economy"

In 1980's the US federal military spending shot thou the roof, in order to force the USSR to try and match us while Region did a number of other things to help undermined them including getting the sautés to drop oil prices and general waging economic and political warfare on them.(not military) While taxes were dropped the spending level in the US government was necessary as to force the Communist Régime to outstretch it self. so of course Spending increased with tax depresses at that time, however, the economic comeback that resulted from the tax breaks earlier in his administration doubled revenue and the GDP but spending was still increased significantly more particular on the military side all as a result or indirect result of combating the Soviet union. How in direct result: The trouble in the US system with passing any bill thou congress regardless of what party controls it, is in order to get that bills passed congressmen must make a number of deals with other congressmen to get their support this usual involved what we call Pork barrel spending, and generally projects that those congressmen want done back in their own states. It is partially true when apposing parties are involved in spending on completely non related and often non-helpful issues such as social programs increases, as well as numerous other types of spending increases. Note: Spending is entirely in the hands of Congress Not the president, the president has a veto that can be overruled by congress but such veto such as was prior and after the passing and US Supreme court overruling of the Line item veto. Can only be used in vetoing an entire bill which typical contains numerous such compromising in spending and over spending, the results of such a veto would either force congress to overrule it with a supermajority in both houses or  reevaluated it. if it is the latter such that congress can not overrule the veto, then as it is typical done at the last imminent the new compromise would have to be rushed thou which is to say in all odds even more costly, as if it is not passed the US government will shut down due ot lack of funding. Which 200 years ago probably wasn’t that bad, but today with the huge dependencies since but partial in the last 100 years installed on that government that would be Catastrophic.

the problem with this type of spending as Ronald Regain pointed out, in many such speeches is unlike military spending it doesn’t get cut realty easily, in fact it general tends to sick around and grow indefinably. That’s the nature of government social programs once you create them they become political candy upon which significant numbers of constituents become depended upon and thus provide you with a reliable voter base. This also opens the door to enormous amounts of corruption. Military and general most other forums of US government spending do not have this effect as their effect on the people themselves is far less direct and rarely felts, In other words its pretty hard to become depended upon it on a Daly bases unless you actually needed it. because the Military does not preformed basic everyday services for you nor does it take those services jobs away from others.

Fortunately for the USA It runs a great deal against the cultural foundations of this nation in being in anyway depended upon big government. Although unfortunately it still exist in and has continued to grow thou out the years for the same reason it does everywhere else.

Needless to say once established social program spending never goes away, in fact it just keeps growing and growing and growing, until it bankrupts you. Which is ultimately what Ronald forced the Soviet Union into dealing with at its end. By cutting it off from all other escape routs.

If you really get down to it, the whole point of “starving the beast” is to help create a situation not unlike that of when you try and get your kid to walk on his or her own for the first time. Basically you put publicans and the people in a situation where they can morally if not finically be forced to move off this addictive drunk of government socialism, and move on to their own. This takes a long time, and general it works under the presumption that ultimately your other programs such as military can be cut leaving you only with the social programs causing almost all of the problems, and using the prospect of taxing higher as the political leverage upon which you can pull the addictive drug down.

As it is in the USA Federal budget most of it including (that of military spending even right now) is that of Social programs specifically just Social security and Medicare. Both account for more than 1 trillion US dollars in spending a year. They are also even with the US Military spending in the War on Terror, in Iraq, Afghanistan and around the rest of the world, is the fastest growing part of the US federal government spending as well. These social programs will as they have continue to grow under previous laws and basic nature, ever increasingly especial with the retirement of the baby-boomer until they make up the entire federal budget and then some.

title: Talk:Starve-the-beast


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Edwin Smith (photographer)

Edwin George Herbert Smith (15 May 1912 – 29 December 1971) was an English photographer. He is best known for his distinctive vignettes of English gardens, landscapes, and architecture. On his own or in partnership with his wife, the artist and writer Olive Cook, he authored or contributed to numerous books during his lifetime and his photographs are still regularly used today.

Biography
He was born in Canonbury, Islington, London, the only child of Edwin Stanley Smith, a clerk, and his wife Lily Beatrice, (née Gray). After leaving school he was educated at the Northern Polytechnic, transferring to the architectural school at the age of 16. He then won a scholarship to the Architectural Association, but gave up his course and worked as a draughtsman for several years. He became a freelance photographer in 1935, working briefly for Vogue as a fashion photographer. However he concentrated his artistic efforts on subjects such as the mining community of Ashington in Northumberland, the docks of Newcastle, and circuses and fairgrounds around London.

In 1935 Smith married Rosemary Ansell, but the marriage ended in divorce two years later. By this time Smith was living with Olive Cook, whom he married in 1954. Smith was also a writer, producing photographic handbooks, including All the Photo Tricks (1940), for Focal Press. But it is for his photograph books he is best remembered. These include: English Parish Churches (1952), English Cottages and Farmhouses (1954), The English House Through Seven Centuries (1968), Pompeii and Herculanaeum (1960), Ireland (with Micheal Mac Liammoir) (1966), Scotland (with Eric Linklater) (1967), Rome: From its Foundation to the Present (1971) and England (with Angus Wilson) (1971). Several of these titles were collaborations with his wife; Cook providing the text beside Smith's photography.

Smith was also a prolific artist. He produced water and oil paintings, drawings, linocuts and woodcuts throughout his life, and in later years at Saffron Walden, he drew up architectural plans for local properties.

He became ill in the spring of 1971, but cancer was not diagnosed until a few weeks before his death on 29 December. It was only after his death that exhibitions of Smith's work appeared, with a monograph finally being published in 1984.

After Cook's own death in 2002, her papers and some of those of her husband were placed in Newnham College Archives, Cambridge. Smith's photographic archive was bequeathed to the Royal Institute of British Architects, as were his notebooks containing detailed records of the photographs taken on his travels throughout Britain and Europe. Edwin Smith was also an avid collector and creator of Toy Theatre. On his wife's death, the collection passed to the Pollock's Toy Museum Trust.

A retrospective of Smith's work was presented at RIBA's new Architecture Gallery from 10 September 2014.

title: Edwin Smith (photographer)


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Long QT syndrome

Long QT syndrome (LQTS) is a condition affecting repolarization (relaxing) of the heart after a heartbeat, giving rise to an abnormally lengthy QT interval. It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. These episodes can be triggered by exercise or stress. Some rare forms of LQTS are associated with other symptoms and signs including deafness and periods of muscle weakness.

Long QT syndrome may be present at birth or develop later in life. The inherited form may occur by itself or as part of larger genetic disorder. Onset later in life may result from certain medications, low blood potassium, low blood calcium, or heart failure. Medications that are implicated include certain antiarrhythmics, antibiotics, and antipsychotics. LQTS can be diagnosed using an electrocardiogram (EKG) if a corrected QT interval of greater than 450–500 milliseconds is found, but clinical findings, other EKG features, and genetic testing may confirm the diagnosis with shorter QT intervals.

Management may include avoiding strenuous exercise, getting sufficient potassium in the diet, the use of beta blockers, or an implantable cardiac defibrillator. For people with LQTS who survive cardiac arrest and remain untreated, the risk of death within 15 years is greater than 50%. With proper treatment this decreases to less than 1% over 20 years.

Long QT syndrome is estimated to affect 1 in 7,000 people. Females are affected more often than males. Most people with the condition develop symptoms before they are 40 years old. It is a relatively common cause of sudden death along with Brugada syndrome and arrhythmogenic right ventricular dysplasia. In the United States it results in about 3,500 deaths a year. The condition was first clearly described in 1957.

Signs and symptoms
Many people with long QT syndrome have no signs or symptoms. When symptoms occur, they are generally caused by abnormal heart rhythms (arrhythmias), most commonly a form of ventricular tachycardia called Torsades de pointes (TdP). If the arrhythmia reverts to a normal rhythm spontaneously the affected person may experience lightheadedness (known as presyncope) or faint which may be preceded by a fluttering sensation in the chest. If the arrhythmia continues, the affected person may experience a cardiac arrest, which if untreated may lead to sudden death. Those with LQTS may also experience seizure-like activity (non-epileptic seizure) as a result of reduced blood flow to the brain during an arrhythmia. Epilepsy is also associated with certain types of long QT syndrome.

The arrhythmias that lead to faints and sudden death are more likely to occur in specific circumstances, in part determined by which genetic variant is present. While arrhythmias can occur at any time, in some forms of LQTS arrhythmias are more commonly seen in response to exercise or mental stress (LQT1), in other forms following a sudden loud noise (LQT2), and in some forms during sleep or immediately upon waking (LQT3).

Some rare forms of long QT syndrome affect other parts of the body, leading to deafness in the Jervell and Lange-Nielsen form of the condition, and periodic paralysis in the Andersen–Tawil (LQT7) form.

Risk for arrhythmias
While those with long QT syndrome have an increased risk of developing abnormal heart rhythms, the absolute risk of arrhythmias is very variable. The strongest predictor of whether someone will develop TdP is whether they have experienced this arrhythmia or another form of cardiac arrest in the past. Those with LQTS who have experienced syncope without an ECG having been recorded at the time are also at higher risk, as syncope in these cases is frequently due to an undocumented self-terminating arrhythmia.

In addition to a history of arrhythmias, the extent to which the QT is prolonged predicts risk. While some have QT intervals that are very prolonged, others have only slight QT prolongation, or even a normal QT interval at rest (concealed LQTS). Those with the longest QT intervals are more likely to experience TdP, and a corrected QT interval of greater than 500 ms is thought to represent those at higher risk. Despite this, those with only subtle QT prolongation or concealed LQTS still have some risk of arrhythmias. Overall, every 10 ms increase in the corrected QT interval is associated with a 15% increase in arrhythmic risk.

As the QT prolonging effects of both genetic variants and acquired causes of LQTS are additive, those with inherited LQTS are more likely to experience TdP if given QT prolonging drugs or if they experience electrolyte problems such as low blood levels of low potassium (hypokalaemia). Similarly, those taking QT prolonging medications are more likely to experience TdP if they have a genetic tendency to a prolonged QT interval, even it this tendency is concealed. Arrhythmias occur more commonly in drug-induced LQTS if the medication in question has been rapidly given intravenously, or if high concentrations of the drug are present in the person's blood. The risk of arrhythmias is also higher if the person receiving the drug has heart failure, is taking digitalis, or has recently been cardioverted from atrial fibrillation. Other risk factors for developing torsades de pointes among those with LQTS include female sex, increasing age, pre-existing cardiovascular disease, and abnormal liver or kidney function.

Causes
There are several subtypes of long QT syndrome. These can be broadly split into those caused by genetic mutations which those affected are born with, carry throughout their lives, and can pass on to their children (inherited or congenital long QT syndrome), and those caused by other factors which cannot be passed on and are often reversible (acquired long QT syndrome).

Inherited
Inherited, or congenital long QT syndrome, is caused by genetic abnormalities. LQTS can arise from variants in several genes, leading in some cases to quite different features. The common thread linking these variants is that they affect one or more ion currents leading to prolongation of the ventricular action potential, thus lengthening the QT interval. Classification systems have been proposed to distinguish between subtypes of the condition based on the clinical features (and named after those who first described the condition) and subdivided by the underlying genetic variant. The most common of these, accounting for 99% of cases, is Romano–Ward syndrome (genetically LQT1-6 and LQT9-16), an autosomal dominant form in which the electrical activity of the heart is affected without involving other organs. A less commonly seen form is Jervell and Lange-Nielsen syndrome, an autosomal recessive form of LQTS combining a prolonged QT interval with congenital deafness. Other rare forms include Andersen–Tawil syndrome (LQT7) with features including a prolonged QT interval, periodic paralysis, and abnormalities of the face and skeleton; and Timothy syndrome (LQT8) in which a prolonged QT interval is associated with abnormalities in the structure of the heart and autism spectrum disorder.

Romano–Ward syndrome
LQT1 is the most common subtype of Romano–Ward syndrome, responsible for 30 to 35% of all cases. The gene responsible, KCNQ1, has been isolated to chromosome 11p15.5 and encodes the alpha subunit of the KvLQT1 potassium channel. This subunit interacts with other proteins (in particular, the minK beta subunit) to create the channel, which carries the delayed potassium rectifier current IKs responsible for the repolarisation phase of the cardiac action potential. Variants in KCNQ1 that decrease IKs (loss of function variants) slow the repolarisation of the action potential. This causes the LQT1 subtype of Romano–Ward syndrome when a single copy of the variant is inherited (heterozygous, autosomal dominant inheritance). Inheriting two copies of the variant (homozygous, autosomal recessive inheritance) leads to the more severe Jervell and Lange–Nielsen syndrome. Conversely, variants in KCNQ1 that increase IKs lead to more rapid repolarisation and the short QT syndrome.

The LQT2 subtype is the second-most common form of Romano–Ward syndrome, responsible for 25 to 30% of all cases. It is caused by variants in the KCNH2 gene (also known as hERG) on chromosome 7 which encodes the potassium channel that carries the rapid inward rectifier current IKr. This current contributes to the terminal repolarisation phase of the cardiac action potential, and therefore the length of the QT interval.

The LQT3 subtype of Romano–Ward syndrome is caused by variants in the SCN5A gene located on chromosome 3p22–24. SCN5A encodes the alpha subunit of the cardiac sodium channel, NaV1.5, responsible for the sodium current INa which depolarises cardiac cells at the start of the action potential. Cardiac sodium channels normally inactivate rapidly, but the mutations involved in LQT3 slow their inactivation leading to a small sustained 'late' sodium current. This continued inward current prolongs the action potential and thereby the QT interval. While some variants in SCN5A cause LQT3, other variants can cause quite different conditions. Variants causing a reduction in the early peak current can cause Brugada syndrome and cardiac conduction disease, while other variants have been associated with dilated cardiomyopathy. Some variants which affect both the early and late sodium current can cause overlap syndromes which combine aspects of both LQT3 and Brugada syndrome.

Rare Romano–Ward subtypes (LQT4-6 and LQT9-16)
LQT5 is caused by variants in the KCNE1 gene responsible for the potassium channel beta subunit MinK. This subunit, in conjunction with the alpha subunit encoded by KCNQ1, is responsible for the potassium current IKs which is decreased in LQTS. LQT6 is caused by variants in the KCNE2 gene responsible for the potassium channel beta subunit MiRP1 which generates the potassium current IKr. Variants that decrease this current have been associated with prolongation of the QT interval. However, subsequent evidence such as the relatively common finding of variants in the gene in those without long QT syndrome, and the general need for a second stressor such as hypokalaemia to be present to reveal the QT prolongation, has suggested that this gene instead represents a modifier to susceptibility to QT prolongation. Some therefore dispute whether variants in KCNE2 are sufficient to cause Romano-Ward syndrome by themselves.

LQT9 is caused by variants in the membrane structural protein, caveolin -3. Caveolins form specific membrane domains called caveolae in which voltage-gated sodium channels sit. Similar to LQT3, these caveolin variants increase the late sustained sodium current, which impairs cellular repolarization.

LQT10 is an extremely rare subtype, caused by variants in the SCN4B gene. The product of this gene is an auxiliary beta-subunit (NaVβ4) forming cardiac sodium channels, variants in which increase the late sustained sodium current. LQT13 is caused by variants in GIRK4,  a protein involved in the parasympathetic modulation of the heart. Clinically, the patients are characterized by only modest QT prolongation, but an increased propensity for atrial arrhythmias. LQT14, LQT15 and LQT16 are caused by variants in the genes responsible for calmodulin (CALM1, CALM2, and CALM3 respectively). Calmodulin interacts with several ion channels and its roles include modulation of the L-type calcium current in response to calcium concentrations, and trafficking the proteins produced by KCNQ1 and thereby influencing potassium currents. The precise mechanisms by which means these genetic variants prolong the QT interval remain uncertain.

Jervell and Lange–Nielsen syndrome
Jervell and Lange–Nielsen syndrome (JLNS) is a rare form of LQTS inherited in an autosomal recessive manner. In addition to severe prolongation of the QT interval, those affected are born with severe sensorineural deafness affecting both ears. The syndrome is caused by inheriting two copies of certain variant in the KCNE1 or KCNQ1 genes. The same genetic variants lead to the LQT5 and LQT1 forms of Romano-Ward syndrome if only a single copy of the variant is inherited. JLNS is generally associated with a higher risk of arrhythmias than most other forms of LQTS.

Andersen–Tawil syndrome (LQT7)
LQT7, also known as Andersen–Tawil syndrome, is characterised by a triad of features – in addition to a prolonged QT interval, those affected may experience intermittent weakness often occurring at times when blood potassium concentrations are low (hypokalaemic periodic paralysis), and characteristic facial and skeletal abnormalities such as a small lower jaw (micrognathia), low set ears, and fused or abnormally angled fingers and toes (syndactyly and clinodactyly). The condition is inherited in an autosomal-dominant manner and is caused by mutations in the KCNJ2 gene which encodes the potassium channel protein Kir2.1.

Timothy syndrome (LQT8)
LQT8, also known as Timothy syndrome combines a prolonged QT interval with fused fingers or toes (syndactyly). Abnormalities of the structure of the heart are commonly seen including ventricular septal defect, tetralogy of Fallot, and hypertrophic cardiomyopathy. The condition presents early in life and the average life expectancy is 2.5 years with death most commonly caused by ventricular arrhythmias. Many children with Timothy syndrome who survive longer than this have features of autism spectrum disorder. Timothy syndrome is caused by variants in the calcium channel Cav1.2 encoded by the gene CACNA1c.

Table of associated genes
The following is a list of genes associated with Long QT syndrome:

Acquired
Although long QT syndrome is often a genetic condition, a prolonged QT interval associated with an increased risk of abnormal heart rhythms can also occur in people without a genetic abnormality, commonly due to a side effect of medications. Drug-induced QT prolongation is often a result of treatment by antiarrhythmic drugs such as amiodarone and sotalol, antibiotics such as erythromycin, or antihistamines such as terfenadine. Other drugs which prolong the QT interval include some antipsychotics such as haloperidol and ziprasidone, and the antidepressant citalopram. Lists of medications associated with prolongation of the QT interval such as the CredibleMeds database can be found online.

Other causes of acquired LQTS include abnormally low levels of potassium (hypokalaemia) or magnesium (hypomagnesaemia) within the blood. This can be exacerbated following a sudden reduction in the blood supply to the heart (myocardial infarction), low levels of thyroid hormone (hypothyroidism), and a slow heart rate (bradycardia).

Anorexia nervosa has been associated with sudden death, possibly due to QT prolongation. The malnutrition seen in this condition can sometimes affect the blood concentration of salts such as potassium, potentially leading to acquired long QT syndrome, in turn causing sudden cardiac death. The malnutrition and associated changes in salt balance develop over a prolonged period of time, and rapid refeeding may further disturb the salt imbalances, increasing the risk of arrhythmias. Care must therefore be taken to monitor electrolyte levels to avoid the complications of refeeding syndrome.

Factors which prolong the QT interval are additive, meaning that a combination of factors (such as taking a QT-prolonging drug and having low levels of potassium) can cause a greater degree of QT prolongation than each factor alone. This also applies to some genetic variants which by themselves only minimally prolong the QT interval but can make people more susceptible to significant drug-induced QT prolongation.

Mechanisms
The various forms of long QT syndrome, both congenital and acquired, produce abnormal heart rhythms (arrhythmias) by influencing the electrical signals used to coordinate individual heart cells. The common theme is a prolongation of the cardiac action potential – the characteristic pattern of voltage changes across the cell membrane that occur with each heart beat. Heart cells when relaxed normally have fewer positively charged ions on the inner side of their cell membrane than on the outer side, referred to as the membrane being polarised. When heart cells contract, positively charged ions such as sodium and calcium enter the cell, equalising or reversing this polarity, or depolarising the cell. After a contraction has taken place, the cell restores its polarity (or repolarises) by allowing positively charged ions such as potassium to leave the cell, restoring the membrane to its relaxed, polarised state. In long QT syndrome it takes longer for this repolarisation to occur, shown in individual cells as a longer action potential while being marked on the surface ECG as a long QT interval.

The prolonged action potentials can lead to arrhythmias through several mechanisms. The arrhythmia characteristic of long QT syndrome, Torsades de Pointes, starts when an initial action potential triggers further abnormal action potentials in the form of afterdepolarisations. Early afterdepolarisations, occurring before the cell has fully repolarised, are particularly likely to be seen when action potentials are prolonged, and arise due to reactivation of calcium and sodium channels that would normally switch off until the next heartbeat is due. Under the right conditions, reactivation of these currents, facilitated by the sodium-calcium exchanger, can cause further depolarisation of the cell. The early afterdepolarisations triggering arrhythmias in long QT syndrome tend to arise from the Purkinje fibres of the cardiac conduction system. Early afterdepolarisations may occur as single events, but may occur repeatedly leading to multiple rapid activations of the cell.

Some research suggests that delayed afterdepolarisations, occurring after repolarisation has completed, may also play a role in long QT syndrome. This form of afterdepolarisation originates from the spontaneous release of calcium from the intracellular calcium store known as the sarcoplasmic reticulum, forcing calcium out of cell through the sodium calcium exchanger in exchange for sodium, generating a net inward current.

While there is strong evidence that the trigger for Torsades de Pointes comes from afterdepolarisations, it is less certain what sustains this arrhythmia. Some lines of evidence suggest that repeated afterdepolarisations from many sources contribute to the continuing arrhythmia. However, some suggest that the arrhythmia sustains through a mechanism known as re-entry. According to this model, the action potential prolongation occurs to a variable extent in different layers of the heart muscle with longer action potentials in some layers than others. In response to a triggering impulse, the waves of depolarisation will spread through regions with shorter action potentials but block in regions with longer action potentials. This allows the depolarising wavefront to bend around areas of block, potentially forming a complete loop and self-perpetuating. The twisting pattern on the ECG can be explained by movement of the core of the re-entrant circuit in the form of a meandering spiral wave.

Diagnosis
Diagnosing long QT syndrome is challenging. Whilst the hallmark of LQTS is prolongation of the QT interval, the QT interval is highly variable among both those who are healthy and those who have LQTS. This leads to overlap between the QT intervals of those with and without LQTS. 2.5% of those with genetically proven LQTS have a QT interval within the normal range. Conversely, given the normal distribution of QT intervals, a proportion of healthy people will have a longer QT interval than any arbitrary cutoff. Other factors beyond the QT interval should therefore be taken into account when making a diagnosis, some of which have been incorporated into scoring systems.

Electrocardiogram
Long QT syndrome is principally diagnosed by measuring the QT interval corrected for heart rate (QTc) on a 12-lead electrocardiogram (ECG). Long QT syndrome is associated with a prolonged QTc, although in some genetically proven cases of LQTS this prolongation can be hidden, known as concealed LQTS. The QTc is less than 450 ms in 95% of normal males, and less than 460 ms in 95% of normal females. LQTS is suggested if the QTc is longer than these cutoffs. However, as 5% of normal people also fall into this category, some suggest cutoffs of 470 and 480 ms for males and females respectively, corresponding with the 99th centiles of normal values.

The major subtypes of inherited LQTS are associated with specific ECG features. LQT1 is typically associated with broad-based T-waves, whereas the T-waves in LQT2 are notched and of lower amplitude, whilst in LQT3 the T-waves are often late onset, being preceded by a long isoelectric segment.

Schwartz score
The Schwartz score has been proposed as a method of combining clinical and ECG factors to assess how likely an individual is to have an inherited form of LQTS. The table below lists the criteria used to calculate the score.

Other investigations
In cases of diagnostic uncertainty, other investigations may be helpful to unmask a prolonged QT. In addition to prolonging the resting QT interval, LQTS may affect how the QT changes in response to exercise and stimulation by catecholamines such as adrenaline. Provocation tests, in the form of exercise tolerance tests or direct infusion of adrenaline, can be used to detect these abnormal responses. These investigations are most useful for identifying those with concealed congenital Type 1 LQTS 1 (LQT1) who have a normal QT interval at rest. While in healthy persons the QT interval shortens during exercise, in those with concealed LQT1 exercise or adrenaline infusion may lead to paradoxical prolongation of the QT interval, revealing the underlying condition.

Guideline cutoffs
International consensus guidelines differ on the degree of QT prolongation required to diagnose LQTS. The European Society of Cardiology recommends that, with or without symptoms or other investigations, LQTS can be diagnosed if the corrected QT interval is longer than 480ms. They recommend that a diagnosis can be considered in the presence of a QTc of greater than 460 ms if unexplained syncope has occurred. The Heart Rhythm Society guidelines are more stringent, recommending QTc cutoff of greater than 500 ms in the absence of other factors that prolong the QT, or greater than 480 ms with syncope. Both sets of guidelines agree that LQTS can also be diagnosed if an individual has a Schwartz score of greater than 3 or if a pathogenic genetic variant associated with LQTS is identified, regardless of QT interval.

Treatment
Those diagnosed with LQTS are usually advised to avoid drugs that can prolong the QT interval further or lower the threshold for TDP, lists of which can be found in public access online databases. In addition to this, two intervention options are known for individuals with LQTS: arrhythmia prevention and arrhythmia termination.

Arrhythmia prevention
Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with LQTS. Since the cause of arrhythmias in LQTS is early afterdepolarizations (EADs), and they are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include administration of beta receptor blocking agents, which decreases the risk of stress-induced arrhythmias. Nadolol, a powerful non-selective beta blocker, has been shown to reduce the arrhythmic risk in all three main genotypes (LQT1, LQT2, and LQT3).

Genotype and QT interval duration are independent predictors of recurrence of life-threatening events.
 * Sodium channel blocking drugs such as mexiletine have been used to prevent arrhythmias in long QT syndrome. While the most compelling indication is for those whose long QT syndrome is caused by defective sodium channels producing a sustained late current (LQT3), mexiletine also shortens the QT interval in other forms of long QT syndrome including LQT1, LQT2 and LQT8. As the predominant action of mexiletine is on the early peak sodium current, there are theoretical reasons why drugs which preferentially suppress the late sodium current such as ranolazine may be more effective, although evidence that this is the case in practice is limited.
 * Amputation of the cervical sympathetic chain (left stellectomy). This therapy is typically reserved for LQTS caused by JLNS, but may be used as an add-on therapy to beta blockers in certain cases. In most cases, modern therapy favors ICD implantation if beta blocker therapy fails.
 * In patients considered at high risk of life-threatening arrhythmic events, ICD implantation may be considered as a preventive step.

Arrhythmia termination
Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Also, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with fainting episodes despite beta blocker therapy, and in patients having experienced a cardiac arrest. As mentioned earlier, ICDs may be used also in patients considered at high risk of life-threatening arrhythmic events.

With better knowledge of the genetics underlying LQTS, more precise treatments hopefully will become available.

Outcomes
Genotype and QTc interval duration are the strongest predictors of outcome for patients with LQTS. 2022 European Society of Cardiology clinical practice guidelines have endorsed the use of independently validated risk score calculator, called 1-2-3-LQTS-Risk Calculator, which allows to calculate individual 5-year risk of life-threatening arrhythmic events.

For people who experience cardiac arrest or fainting caused by LQTS and who are untreated, the risk of death within 15 years is around 50%. With careful treatment this decreases to less than 1% over 20 years. Those who exhibit symptoms before the age of 18 are more likely to experience a cardiac arrest.

Epidemiology
Inherited LQTS is estimated to affect between one in 2,500 and 7,000 people.

History
The first documented case of LQTS was described in Leipzig by Meissner in 1856, when a deaf girl died after her teacher yelled at her. Soon after being notified, the girl's parents reported that her older brother, also deaf, had previously died after a terrible fright. This was several decades before the ECG was invented, but is likely the first described case of Jervell and Lange-Nielsen syndrome. In 1957, the first case documented by ECG was described by Anton Jervell and Fred Lange-Nielsen, working in Tønsberg, Norway. Italian pediatrician Cesarino Romano, in 1963, and Irish pediatrician Owen Conor Ward, in 1964, separately described the more common variant of LQTS with normal hearing, later called Romano-Ward syndrome. The establishment of the International Long-QT Syndrome Registry in 1979 allowed numerous pedigrees to be evaluated in a comprehensive manner. This helped in detecting many of the numerous genes involved. Transgenic animal models of the LQTS helped define the roles of various genes and hormones involved, and recently experimental pharmacological therapies to normalize the abnormal repolarization in animals were published.

title: Long QT syndrome


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User talk:Bulatych

You can leave messages for me here. Bulatych Tue Nov 11 19:38:55 UTC 2003

Greetings
Welcome,

You have done a good job so far in Wikipedia (WP). I can see that you're a serious Wikipedian interested in improving our project. If you stay for a while, you'll discovered that collectively, we're a cooperative and friendly community. We are all here to learn, and hopefully can give something back. If you have questions or doubts of any sort, do not hesitate to post them on the Village Pump, somebody will respond ASAP. Other helpful pages include:
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title: User talk:Bulatych


text:
Talk:Brown ale

Comments
I nearly wrote: "English commercial examples include Newcastle Brown Ale, which is truly hideous, and Samuel Smith's Nut Brown Ale, which is quite pleasant.", but I thought better of it. ;) Stewartadcock 19:40, 11 Nov 2003 (UTC)

Nut Brown
Is there any technical or official meaning of nut brown as opposed to just brown? Or is the usage entirely poetic? VermillionBird 21:39, 29 October 2005 (UTC)

 * Nut browns typically include a high roasted malt such as victory or biscuit malt into the grist which gives the beer a slight toasted nut note to it. This is definitely not a "poetic" usage and is in fact a pretty good descriptor.  Garyfoster 15:46, 9 October 2007 (UTC)

 * Thank you for your response. What would a just brown label indicate, as opposed to a nut brown?  VermillionBird (talk) 04:02, 20 May 2008 (UTC)

''Nut browns typically include a high roasted malt such as victory or biscuit malt into the grist which gives the beer a slight toasted nut note to it. This is definitely not a "poetic" usage and is in fact a pretty good descriptor.''

Garyfoster, you're making that up. Where's you're evidence? "Nut brown" is brewer marketingspeak, and has no independent meaning at all. Zythophile (talk) 00:30, 12 February 2011 (UTC)

Mann's
There seem to be a lot of mentions of Mann's, including a rather prominent picture at the top of the page. Additionally, only one external link is provided - to Mann's website. Seems like there's a bit of advertising going on. Am I right, or is it just me? —The preceding unsigned comment was added by LordDimwit (talk • contribs) 02:13, 9 May 2007 (UTC).

As Mann´s Brown Ale was the original modern Brown Ale (first brewed in the 1890s), it seems perfectly reasonable for it to be featured prominently in the article.Patto1ro 07:02, 9 May 2007 (UTC)

Fair use rationale for Image:Manns logo new sm.jpg
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BetacommandBot 23:16, 13 September 2007 (UTC)

Styles
I fleshed out the style descriptions and variations with descriptions of the major styles of brown ale as recognized by the BJCP. I included reference links to the BJCP online style documentation. Garyfoster 15:46, 9 October 2007 (UTC)

Restored the styles section that I put in, which was removed without explanation. If you're going to undo my work, which I consider a pretty good addition to the article, please at least have the courtesy to give an explanation and open a discussion. Garyfoster 21:41, 11 October 2007 (UTC)

We've had this discussion several times before. The BJCP is not an authority on European beer styles.'06:44, 12 October 2007 (UTC) —Preceding unsigned comment added by Patto1ro (talk • contribs)

Could you try looking at the many discussions we've had about the bjcp and European beer styles. They are not an authority on Eurpean beer styles. They are an American homebrewers' organisation. I'm going to take out the references to them again, because that is what was agreed after a long debate. Patto1ro 16:06, 13 October 2007 (UTC)

And furthermore, User:Garyfoster, when discussing whether to include information which may be helpful to readers or excluding it, User:Patto1ro always advocates excluding it — unless it is an external link to his website. — goethean ॐ 16:35, 17 October 2007 (UTC)

Dead Link
Note that the link to the Manns site is dead. —Preceding unsigned comment added by 209.115.153.68 (talk) 21:50, 13 December 2007 (UTC)

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BJCP
Without objections, I shall link this aticle to the BJCP. BJCP (talk) 22:41, 6 April 2009 (UTC)

 * I object.Patto1ro (talk) 05:42, 7 April 2009 (UTC)

 * Editors, please give reasons, there is too much adding and reverting going on. 1Z (talk)

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title: Talk:Brown ale


text:
Apostle (Latter Day Saints)

In the Latter Day Saint movement, an apostle is a "special witness of the name of Jesus Christ who is sent to teach the principles of salvation to others." In many Latter Day Saint churches, an apostle is a priesthood office of high authority within the church hierarchy. In many churches, apostles may be members of the Quorum of the Twelve and First Presidency of the church. In most Latter Day Saint churches, modern-day apostles are considered to have the same status and authority as the Biblical apostles.

In the Latter Day Saint tradition, apostles and prophets are believed to be the foundation of the church, Jesus Christ himself being the chief cornerstone. The "Articles of Faith", written by Joseph Smith, mentions apostles:

"'We believe in the same organization that existed in the Primitive Church, namely, apostles, prophets, pastors, teachers, evangelists, and so forth.'"

History
Joseph Smith and Oliver Cowdery were both designated apostles by 1830. The founding articles and covenants of the Church of Christ stated an "apostle is an elder" and, as such, had the same responsibilities as an elder, though an apostle's primary responsibility was preaching. Other church members with proselytizing responsibilities were also referred to as apostles. A June 1829 revelation appointed Cowdery and David Whitmer to designate twelve apostles.

Subsequently, the Quorum of the Twelve Apostles was organized February 14, 1835, with the selection of twelve men. After the appointment of a quorum of apostles, the term became increasingly restricted to members of that quorum, but members of the quorums of the seventy were also sometimes referred to as apostles.

Apostles in The Church of Jesus Christ of Latter-day Saints
In the Church of Jesus Christ of Latter-day Saints (LDS Church), apostle is the highest priesthood office of the Melchizedek priesthood. The President of the Church is always an apostle, as are the members of the Quorum of the Twelve Apostles. In practice, counselors in the First Presidency are almost always apostles as well. There are usually at least twelve apostles in the LDS Church, though at times there has been as many as 21.

Some apostles have been ordained to that office without being included within the Quorum of the Twelve. Alvin R. Dyer, for example, was ordained an apostle in 1967; although he served as a counselor in the First Presidency between 1968 and 1970, upon the death of David O. McKay, he returned to his previous position as an Assistant to the Quorum of the Twelve. Joseph Angell Young was ordained an apostle in 1864 but was never a member of either the Quorum of the Twelve Apostles or the First Presidency. Joseph F. Smith, Brigham Young, Jr., and Sylvester Q. Cannon had each been ordained as apostles before eventually being called into the Quorum of the Twelve.

Due to a precedent established after the succession crisis which occurred after the death of Joseph Smith, the senior apostle, the President of the Quorum of the Twelve, becomes the new President of the Church upon the death of his predecessor. On these occasions, it is at the next church general conference that the president of the Quorum of the Twelve is formally sustained by the members of the church as the "prophet, seer, and revelator" and president of the church. The next most senior apostle becomes president of the Quorum of the Twelve.

Following their calling to the apostleship, members of the Quorum are sustained in general conference as apostles and prophets, seers, and revelators. This procedure also takes place at other meetings of church members such as ward and stake conferences. Each member of the First Presidency and Quorum of the Twelve is sustained by name.

Usually, the president of the church ordains a new apostle, although any other apostle may ordain a person to the priesthood office. If the president of the church is unable due to infirmity to ordain a new apostle, the ordination is usually performed by an apostle who is a member of the First Presidency or by the president of the Quorum of the Twelve.

The Bible Dictionary of the LDS Church defines apostle as meaning "one sent forth" and elaborates as follows:

"[Apostle] was the title Jesus gave to the twelve whom he chose and ordained to be his closest disciples during his ministry on earth, and whom he sent forth to represent him after his ascension into heaven. The calling of an apostle is to be a special witness of the name of Jesus Christ in all the world, particularly of his divinity and of his bodily resurrection from the dead . Twelve men with this high calling constitute an administrative council in the work of the ministry. When a vacancy occurred with the death of Judas Iscariot, Matthias was divinely appointed to that special office as a member of the council . Today twelve men with this same divine calling and ordination constitute the Quorum of the Twelve Apostles in The Church of Jesus Christ of Latter-day Saints. The title was also applied to others who, though not of the number of the original twelve, yet were called to serve as special witnesses of the Lord. Paul repeatedly spoke of himself as an apostle. He applied the titles to James, the Lord's brother, and also to Barnabas (cf. ). The New Testament does not inform us whether these three brethren also served in the council of the Twelve as vacancies occurred therein, or whether they were apostles strictly in the sense of being special witnesses for the Lord Jesus Christ. Jesus is referred to as an apostle in, a designation meaning that he is the personal and select representative of the Father."

Bruce R. McConkie also describes each elder and member of the church as an apostle: "Every elder in the Church is or should be an apostle; that is, as a minister of the Lord and as a recipient of personal revelation from the Holy Ghost, every elder has the call to bear witness of the truth on all proper occasions. Indeed, every member should have apostolic insight and revelation, and is under obligation to raise the warning voice."

McConkie also explained the meaning of the word "in the ordained sense": "an apostle is one who is ordained to the office of the Melchizedek Priesthood. Ordinarily those so ordained are also set apart as members of the Council of the Twelve and are given all of the keys of the kingdom of God on earth. This apostleship carries the responsibility of proclaiming the gospel in all the world and also of administering the affairs of the Church. Christ 'chose twelve, whom also he named apostles', and upon their shoulders the burden of the kingdom rested after he ascended to his Father (.) The original Twelve in latter-days were selected by revelation by the Three Witnesses to the Book of Mormon (.)"

title: Apostle (Latter Day Saints)


text:
Paolo Savi

Paolo Savi (11 July 1798 – 5 April 1871) was an Italian geologist and ornithologist.

Biography
Savi was born in Pisa, the son of Gaetano Savi, professor of botany at the University of Pisa. The younger Savi became assistant lecturer in zoology at the university in 1820, was appointed professor in 1823, and lectured also on geology. He devoted great attention to the museum of the university, the Natural History Museum of the University of Pisa, and formed one of the finest natural history collections in Europe.

Savi was regarded as the father of Italian geology. He studied the geology of it:Monti Pisani and the Apuan Alps, explaining the metamorphic origin of the Carrara marble; he also contributed essays on the Miocene strata and fossils of Monte Bamboli, the iron ores of Elba and other subjects. With Giuseppe Meneghini (1811–1889) he published memoirs on the stratigraphy and geology of Tuscany (1850–1851).

Savi also became eminent as an ornithologist, and was the author of Ornitologia Toscana (1827–1831) and Ornitologia Italiana (1873–1876). In the autumn of 1821 he obtained specimens of an unstreaked, dark, rufous-brown warbler which was new to science. He published a full description of the bird in 1824, and it became commonly known as Savi's warbler.

Personal
Savi was buried in Pisa cemetery and his statue now stands in the Orto botanico di Pisa.

Major works

 * Osservazioni sopra la Blarta acervorum di panzee. Gryllus Myrmocophilus nob. Memoria (inedita) del dott. Paolo Savi, con tavola in rame, Biblioteca Italiana ossia Giornale di letteratura scienze ed arti (1819 ago), Volume 15, Fascicolo
 * Sulla Salvinia natans. Memoria inedita del dottor Paolo Savi, aiuto del professore di botanica dell'università di Pisa, con tavola in rame, Biblioteca Italiana ossia Giornale di letteratura scienze ed arti (1820 dic, Volume 20, Fascicolo)
 * Ornitologia Toscana, ossia descrizione e storia degli uccelli che trovansi nella Toscana con l'aggiunta delle descrizioni di tutti gli altri propri al rimanente d'Italia, 3 volumi (Pisa, Dalla tipografia Nistri 1827-1831). L'opera, di notevole importanza per la storia dell'ornitologia italiana, contiene 31 figure incise in rame. Venne ristampata postuma nel 1873 a Firenze (sempre in 3 voll.), con il titolo "Ornitologia italiana", a cura del figlio Adolfo. [Ornitologia italiana (opera postuma) Firenze :Successori Le Monnier, 1873-1876] online online at BHL
 * Sul Mischio di Serravezza (Nuovo Giornale d. Lett., XX, Pisa 1830);
 * Catalogo ragionato di una collezione geognostica contenente le rocce più caratteristiche della formazione del Macigno della Toscana, quelle di trabocco, cioè Dolomitiche, Porfiriche e Granitiche le quali hanno disordinato le stratificazioni delle prime e quelle alterate dal contatto delle straboccate (ibid., 1830);
 * Carta geologica dei Monti Pisani levata dal vero (Pisa 1832);
 * Tagli geologici delle Alpi Apuane e del Monte pisano e cenno sull’isola d’Elba (Nuovo Giornale d. Lett., XXVI, 1833);
 * Sulla miniera di ferro dell’Isola d'Elba (ibid., XXXI, 1835);
 * Sui terreni stratificati dipendenti o annessi alle masse serpentinose della Toscana (ibid., XXXIV e XXXV, 1837);
 * Sui vari sollevamenti e abbassamenti che hanno dato alla Toscana l’attuale configurazione (ibid., XXXV, 1837);
 * Del carbon fossile in Italia. Estratto dalla Memoria sulla Scorza del Globo Terrestre, del prof. P. Savi Annali universali di statistica economia pubblica, storia, viaggi e commercio (1838 apr, Serie 1, Volume 56, Fascicolo 166)
 * Delle rocce ofiolitiche della Toscana e delle masse metalliche in esse contenute (ibid., 1839);
 * Sopra i carboni fossili dei terreni miocenici della Maremma Toscana (Pisa 1843);
 * Considerazioni geologiche sull'Appennino Pistoiese (Firenze 1845);
 * Sulla catena metallifera delle Alpi Apuane e sulla costituzione geologica dei Monti Pisani (Pisa 1846);
 * Considerazioni sulla geologia della Toscana, in collaborazione con G. Meneghini (Firenze 1851);
 * Saggio sulla costituzione geologica della Provincia di Pisa (Statist. della provincia di Pisa, Pisa 1863).

title: Paolo Savi


text:
User:Orthogonal

orthogonal was a Wikipedia editor from November 2003 to September 2004.

I won't be logging in again, so I'm afraid that I'll have to let someone else have the last word. ;)

Best wishes to (most -- I won't prevaricate) everyone -- and those of you for whom I've felt a special affection know who you are, so anything I would have to say to you goes without saying --, and I hope and fervently trust Wikipedia will continue to be a great success.

I won't be checking what was my Talk page, or anything else on Wikipedia, so there's no point in leaving messages for me -- and anything I had to say, I've said.

As to any orphan pages I've left behind or any other loose ends, those belong to the community (after all, they were released under the GFDL, weren't they), so do with them as you think best -- which probably means deleting them, but again, they are yours now, not mine, so do what you will.

-- orthogonal 03:12, 29 Sep 2004 (UTC)

title: User:Orthogonal