ACM ICPC Dhaka Site

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ACM ICPC Dhaka Site
Data
Established	1997
Region	Asia
Abbreviation	ACM ICPC

ACM International Collegiate Programming Contest (abbreviated as ACM-ICPC or just ICPC) is an annual multi-tiered competition among the universities of the world. There are thirteen different sites in Asia that host Asia Regional Final and Dhaka is one of them. Each year winner of the Asia Regional Final Dhaka Site Contest advances to the ACM-ICPC World Final. Like other sites of ICPC, Dhaka site contest is also sponsored by IBM and operated under the auspices of the Association for Computing Machinery (ACM).

Contents 1 History 2 Past events 2.1 1997 2.2 1998 2.3 1999 2.4 2000 2.5 2001 2.6 2002 2.7 2003 2.8 2004 2.9 2005 2.10 2006 2.11 2007 2.12 2008 2.13 2009 3 Dhaka site local teams in the world final 4 ACM ICPC Dhaka site hosts 4.1 Host Universities 5 Current event 5.1 Dates of event 6 References 7 External links

History

BUET Bengal Tiger, first champion, ACM ICPC Dhaka site contest and also the first team from Bangladesh to participate in the ACM ICPC World Final.

ACM ICPC Dhaka site contest started in 1997 with the initiative of Professor A. L. Haque of North South University (NSU). Its first event was held on 18 November 1997 with the participation of 18 teams from 11 institutions. Bangladesh University of Engineering and Technology – BUET Bengal Tigers team became the champion and moved to the world final which was held on 28 February 1998 at Atlanta, Georgia, USA. Champion BUET team of Suman Kumar Nath (now at Microsoft Research), Rezaul Alam Chowdhury (UT Austin) and Tarique Mesbaul Islam (Waterloo) occupied 24th position in the world final among 54 teams tying with Stanford University. Same year, NSU team received a wild card for being the host of the Dhaka site regional contest and participated in the world final.

North South University hosted this event 7 times from 1997-1999 and 2004-2006 and 2008 while Bangladesh University of Engineering and Technology hosted thrice from 2001-2003. East West University hosted the event in 2007.

Past events

1997

• Champion: Bangladesh University of Engineering and Technology
• Host: North South University
• Champion’s position at the world final: 24th
• Notes: Bangladesh University of Engineering and Technology also secured 2nd, 3rd and 4th place.

1998

• Champion: Bangladesh University of Engineering and Technology
• Host: North South University
• Champion’s position at the world final: Honorable Mention
• Notes: Bangladesh University of Engineering and Technology also secured 3rd and 4th place. Sherif University of Tehran and IIT Kanpur secured 7th and 11th place respectively.

1999

• Champion: Chinese University of Hong Kong
• Host: North South University
• Champion’s position at the world final: 8th
• Notes: Bangladesh University of Engineering and Technology secured 2nd, 3rd and 4th place.

2000

• Not Hosted

2001

• Champion: Bangladesh University of Engineering and Technology
• Host: Bangladesh University of Engineering and Technology
• Champion’s position at the world final: Honorable Mention
• Notes: Bangladesh University of Engineering and Technology and ZongShan University of China secured 2nd and 3rd place respectively.

2002

• Champion: Bangladesh University of Engineering and Technology
• Host: Bangladesh University of Engineering and Technology
• Champion’s position at the world final: Honorable Mention
• Notes: Nanyang Technological University of Singapore secured 2nd place.

2003

• Champion: Fudan University
• Maximum problem solved: 6
• Host: Bangladesh University of Engineering and Technology
• Champion’s position at the world final: 15th
• Notes:Bangladesh University of Engineering and Technology secured 2nd and 3rd place. Dhaka University became 4th.

2004

• Champion:Fudan University
• Maximum problem solved: 6
• Host:North South University
• Champion’s position at the world final: 6th
• Notes: Bangladesh University of Engineering and Technology secured 2nd place. National University of Singapore and IIT Bombay secured 3rd and 6th place respectively.

2005

• Champion:Fudan University
• Maximum problem solved: 6
• Host:North South University
• Champion’s position at the world final: 39th
• Notes: Dhaka University and Bangladesh University of Engineering and Technology secured 2nd and 3rd place respectively. Multimedia University of Malaysia received an honorable mention.

2006

• Champion:Fudan University

• Host:North South University

• Champion’s position at the world final: 26th
• Notes: Bangladesh University of Engineering and Technology secured 2nd place. American International University – Bangladesh and North South University jointly secured 3rd place.

2007

• Champion: Bangladesh University of Engineering and Technology
• Host: East West University
• Maximum problem solved: 7
• Notes: Fudan University and East West University secured 2nd and 3rd place respectively. Total 86 Teams from 33 Universities competed to take the pride to qualify for ACM ICPC world final 2008.

2008

• Champion: Fudan University
• Host: North South University
• Maximum problem solved: 9
• Notes; Bangladesh University of Engineering and Technology secured 2nd place and received wild card for participating in the world finals. A total of 83 teams competed.

2009

• Champion: Fudan University
• Host: North South University
• Maximum problem solved: 7
• Notes; Bangladesh University of Engineering and Technology secured 2nd place and Dhaka University was place 3rd. A total of 89 teams participated.

Dhaka site local teams in the world final

Each year at least one local team from Dhaka site takes part in the world final either as the regional champion or by wild card. On few occasions Dhaka site local teams made it by winning ACM ICPC Kanpur site regional. In 2005, Fudan University became champion at two different sites and withdrawn their championship from Dhaka site. As a result, 2nd ranked team, Dhaka University who was supposed to get a wild card got the direct entry to the world final and Bangladesh University of Engineering and Technology got the wild card. Summery of all the Dhaka site local team results in the world final are illustrated in the following table:

World Final	Date	Place	University	Team Name	Contestant	Result	Entry
22nd	Feb 28, 1998	Atlanta, Georgia	Bangladesh University of Engineering and Technology	Bengal Tigers	Suman Kumar Nath, Rezaul Alam Chowdhury, Tarique Mesbaul Islam	24th	Dhaka site champion
			North South University	NSU Dream	Tarique Zaman Chowdhury, Mehrin Shahed, Salman Ahmed Awan	H.M.	Dhaka site wild card
23rd	April 12, 1999	Eindhoven, the Netherlands	Bangladesh University of Engineering and Technology	The Balloon Counters	Rezaul Alam Chowdhury, Mojahedul Hoque Abul Hasanat, Mehedy Masood, Farah Farzana	H.M.	Dhaka site champion
24th	March 18, 2000	Orlando, Florida	Bangladesh University of Engineering and Technology	BUET Backtrackers	Mustaq Ahmed, Munirul Abedin, M Rubaiyat Ferdous Jewel	11th	Kanpur site champion
25th	March 10, 2001	Vancouver, Canada	Bangladesh University of Engineering and Technology	BUET Loopers	Mustaq Ahmed, Munirul Abedin, Abdullah Al Mahmud	29th	Kanpur site champion
26th	March 23, 2002	Honolulu, Hawaii	Bangladesh University of Engineering and Technology	BUET Ackermanns	Md Kamruzzaman, Abdullah Al Mahmud, Mushfiqur Rouf	H.M	Dhaka site champion
			American International University – Bangladesh	AIUB-A	Adib Hasan Manob, Md. Mahabub Alam, Md. Nurul Amin	H.M.	Kanpur site wild card
27th	March 25, 2003	Beverly Hills, California	Bangladesh University of Engineering and Technology	BUET Loopers	Asif-ul Haque, Mehedi Bakht, Md Saifur Rahman	H.M	Dhaka site champion
28th	March 31, 2004	Prague,Czech Republic	Bangladesh University of Engineering and Technology	BUET Phonix	Asif-ul Haque, Mehedi Bakht, Md Saifur Rahman	27th	Dhaka site wild card
29th	April 16, 2005	Shanghai, China	Bangladesh University of Engineering and Technology	BUET Explorer	Mushfiqur Rouf, Abdullah Al Mahmud, Manzurur Rahman Khan	29th	Dhaka site wild card
30th	April 12, 2006	San Antonio, Texas	University of Dhaka	DU Gryffindor	Quazi Sarfaraz Hussain, Ariful Islam Siddiqi, Mainul Islam	H.M.	Dhaka site direct entry
			Bangladesh University of Engineering and Technology	BUET BUET Exceed	Istiaque Ahmed, Manzurur Khan, Omar Haider	39th	Dhaka site wild card
31st	March 15, 2007	Tokyo, Japan	Bangladesh University of Engineering and Technology	BUET xC33d	Istiaque Ahmed, Sabbir Yousuf Sanny, Mohammad Mahmudur Rahman	H.M.	Dhaka site wild card
32nd	April 9, 2008	Banff, Canada	Bangladesh University of Engineering and Technology	BUET Sprinter	Sabbir Yousuf Sanny, Mahbubul Hasan, Shahriar Rouf	31st	Dhaka site champion
			East West University	EWU Dream of Twilight	Sohel Hafiz, Mahbub Mozadded, Md. Arifuzzaman Arif	H.M.	Dhaka site wild card
33rd	April 21, 2009	Stockholm, Sweden	Bangladesh University of Engineering and Technology	BUET Falcon	Mahbubul Hasan, Shahriar Rouf, Tanaeem M. Moosa	34th	Dhaka site Runner-up
			University of Dhaka	DU Dark Knights	Syed Zubair Hossain, Jane Alam Jan, Iqram Mahmud	49th	Kanpur site Runner-up
			North South University	NSU ARCTURUS	Samee Zahur, M. Mustafijur Rahman Faysal, Md. Ameer Hamza	H.M.	Kuala Lumpur site
34rd	February 5, 2010	Harbin, China	Bangladesh University of Engineering and Technology	BUET Rand Ecliptic	Tanaeem M. Moosa, Tasnim Imran Sunny, Muntasir Mashuq	36th	Dhaka site Runner-up

ACM ICPC Dhaka site hosts

Past nine ACM ICPC Dhaka site contests have been hosted by North South University and Bangladesh University of Engineering and Technology. In 2007, East West University granted the permission from the ACM ICPC authority to host next three contests in 2007-2009.

Host Universities

• 1997 – North South University
• 1998 – North South University
• 1999 – North South University
• 2000 – Not hosted
• 2001 – Bangladesh University of Engineering and Technology
• 2002 – Bangladesh University of Engineering and Technology
• 2003 – Bangladesh University of Engineering and Technology
• 2004 – North South University
• 2005 – North South University
• 2006 – North South University
• 2007 – East West University
• 2008 – North South University
• 2009 – North South University

Current event

This year ACM ICPC Dhaka site contest was held at the new campus of North South University at Bashundhara on 24 October 2009.

Dates of event

October 23 (Friday) & 24 (Saturday), 2009

References

1. ^ Professor M Kaykobad, “Do You Know ACM ICPC World Finals Tit bits?“, ACM ICPC Dhaka Site Magazine 2006, pp-12
2. ^ Professor M Kaykobad, “Programming Contest and Bangladeshi Students“, National Computer Programming Contest Magazine 2004, pp-12
3. ^ ^{a b} Professor M Kaykobad, “Do You Know ACM ICPC World Finals Tit bits?“, ACM ICPC Dhaka Site Magazine 2006, pp-13
4. ^ Professor M Kaykobad, “Programming Contest and Bangladeshi Students“, National Computer Programming Contest Magazine 2004, pp-14
5. ^ ACM ICPC World Final 1998, Official Standing
6. ^ ^{a b c d e} Magazine, ACM ICPC Dhaka Site 2003, BUET.
7. ^ Official Rank List, ACM ICPC Dhaka Site, 2003 from Baylor University server
8. ^ ACM ICPC World Final 2004, Official Standing
9. ^ Official Rank List, ACM ICPC Dhaka Site, 2004 from Baylor University server
10. ^ ACM ICPC World Final 2005, Official Standing
11. ^ Official Rank List, ACM ICPC Dhaka Site, 2005 from Baylor University server
12. ^ ACM ICPC World Final 2006, Official Standing
13. ^ Official Rank List, ACM ICPC Dhaka Site, 2006 from Baylor University server
14. ^ ACM ICPC World Final 2007, Official Standing
15. ^ View Standings
16. ^ Professor Dr. MD. Shamsul Alam, Former Head, Dept of CSE, BUET, BUET in ACM ICPC Regional Contests, ACM ICPC 2003 Magazine
17. ^ Professor M. Kaykobad, History of Computer Programming Contest(in Bangladesh), ACM ICPC Dhaka Site Magazine 2004
18. ^ BUET at ACM ICPC, from the official site of the Department of CSE, BUET

External links

• ACM ICPC Dhaka Site Home page from Baylor University server
• ACM ICPC 2007 Dhaka Site Home page from East West University server
• Hall of Champion, ACM ICPC

v • d • e ACM ICPC Dhaka Site Contests Host Institution ACM ICPC Asia Regional Dhaka Site Events North South University 1997, 1998, 1999, 2004, 2005, 2006, 2008, 2009 Bangladesh University of Engineering and Technology 2001, 2002, 2003 East West University 2007

Retrieved from “http://en.wikipedia.org/wiki/ACM_ICPC_Dhaka_Site”
Categories: Programming contests | Computer science competitions

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Honda NT650

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Honda NT650 GT

Manufacturer	Honda
Also called	Hawk GT, Bros, RC31
Production	1988–1991
Class	naked bike
Engine	647cc Four-stroke V-Twin
Transmission	5 speed manual
Wheelbase	56.3 in.
Seat height	30.4 in.
Weight	393 lb. (dry), 412 lb. (wet)
Fuel capacity	2.9 gal

This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (December 2009)

The Honda HawkGT NT650 motorcycle has been called a cult bike; an “unmitigated sales disaster” which nonetheless attracted a loyal following. Designated as model RC31, it was designed by Toshiaki Kishi, and was the second Honda with “Pro-Arm” suspension after the RC30 VFR750R. The Japanese model was named the Bros. The RC model designation is for bikes up to 750cc, though the Honda Pacific Coast (PC800) has an engine of more than 750 cc and a model designation of RC34.

650cc Honda Hawk GT

The bike’s main distinction is in its frame and single-sided swingarm. The dual spar aluminum frame and single sided swingarm (licensed from ELF) was technologically advanced in 1988. The mildly tuned engine is descended from the VT500 and has been seen, in one guise or another, in several other models.

The bike was ahead of its time in many regards and as a result was not a strong seller despite the bike having grown to cult status. The Hawk GT was one of the first modern naked bikes along with the Yamaha SRX, which were both released several years before the Ducati Monster and eventually the Suzuki SV650. The Hawk GT is often described as a cult bike.

Contents 1 North American model 2 Europe model 3 Japan model 4 Notes 5 References

North American model

The US model NT650, Hawk GT 647, RC31 was introduced in 1988 and produced through 1991. In 1988 the bike was sold in the colors “Tempest Gray Metallic” and “Candy Flair Blue”. For the remainder of the bikes production run it was only sold in red. There are only very minor changes between the 1988 model year and the 1989-91 model years. In 1989, the front suspension damper rods were changed to have only 2 (rather than 4 for the ‘88) holes. The front brake calipers were also changed to have screw-on covers over the mounting pins. In 1991, the oil lines were run internally through the engine, rather than externally and only a handful of 1991 model year bikes actually made it into the United States, making the 1991 the rarest vintage Hawk in America.

The Canadian model was identical to the US model except for the colors.

Europe model

A cousin to the Hawk GT, the Revere was available in Europe from 1988. The steel frame, shaft-drive, larger petrol tank, main stand, and longer rear end differentiate it from the Hawk GT. The NTV650 replaced the Revere in 1993. It was a revised version of the early model with no main stand, different carburetor, tube handlebar and longer exhaust. The engine power dropped in 3 steps from 60 HP to 50 HP. The NTV650 was replaced in 1997 by the Deauville, basically an NTV650 with full bodywork and hard saddlebags – not too different in general appearance from the PC800.

Japan model

400cc Honda Bros

Named the Bros in Japan, the NT came in 400cc and 650cc versions. After Honda stopped exporting the Hawk in 1992, they continued the Bros in Japan for one more year. A close ratio gear box (which drops into the Hawk) different wheels, and lower clip-ons were the major changes.

Notes

1. ^ “Cult Bikes; A legend in your own mind?”, American Motorcyclist: 23–26, February 1996, http://books.google.com/books?id=O_YDAAAAMBAJ&pg=PT23 
2. ^ “1989 Honda NT650 Hawk GT; The bike that changed my life”, Motorcyclist: 15, October 2009, http://www.motorcyclistonline.com/newsandupdates/122_0910_1989_honda_nt650_hawk_gt/index.html 
3. ^ “Honda CB-1, 1989-1990″, Motorcyclist: 95, Dec. 2000 
4. ^ “Cult Bike!”, American Motorcyclist: 22, June 2007, http://books.google.com/books?id=RvYDAAAAMBAJ&pg=PA22 

References

document with red question mark.svg” src=”http://upload.wikimedia.org/wikipedia/commons/thumb/a/a4/Text_document_with_red_question_mark.svg/40px-Text_document_with_red_question_mark.svg.png” width=”40″ height=”40″ />

This Section includes a list of references, related reading or external links, but its sources remain unclear because it lacks inline citations. Please improve this article by introducing more precise citations where appropriate. (December 2009)

• Matthew Miles, “Going British on a budget. (customizing a Honda Hawk GT 647 motorcycle)”, Cycle World 30 (9 (Sept 1991):): 54 
• Allan Girdler (July 1990), “Standard time. (motorcycles) (evaluation)”, Cycle World 29 (7): 26 
• “The 10 best motorcycles of 1988. (evaluation)”, Cycle World 27 (10): 27, October 1988 
• “Honda Hawk GT; bird of a different feather. (evaluation)”, Cycle World 27 (6): 34(6, June 1988 
• David Edwards (June 1988), “The view from the real world. (3 Cycle World readers try out the Honda Hawk GT)”, Cycle World 27 (6): 40 

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• This page was last modified on 4 March 2010 at 21:18.
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Cave of Archedemos the Nympholept

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Cave of Archedemos the Nympholept ?????? ??? ????????? ?????? ??? ???????????
View towards the north of part of the sculpted decoration in the cave of the Nypholept
Location
Coordinates	and other data for this location”>37°51?30?N 23°48?6?E? / ?37.85833°N 23.80167°E? / 37.85833; 23.80167Coordinates: 37°51?30?N 23°48?6?E? / ?and other data for this location”>37.85833°N 23.80167°E? / 37.85833; 23.80167
Period	Archaic to Early Christian
Country	Greece
Region	Attica
Elevation	269 m (880 ft)

The Cave of Archedemos the Nympholept is a small cave near Vari in Attica, Greece. The cave is an archaeological site (meaning that access is restricted – the location given in the infobox is not exact). It was excavated in the first quarter of the 20th century by an American team of archaeologists. The cave is unique in Greece in that there exist ancient sculptures hewn into the living rock of the cave. In fact, the sculptures are carved into a calcite column and flowstone within the cave. The cave was used from the Archaic period and reused in Early Christian times.

The marble votive tablets from the cave are now exhibited at the National Archaeological Museum of Athens.

References

The Cave at Vari. I. Description, Account of Excavation, and History, Charles Heald Weller, American Journal of Archaeology, Vol. 7, No. 3 (Jul. – Sep., 1903), pp. 263-288

This article relating to archaeology in Europe is a stub. You can help Wikipedia by expanding it. v • d • e

Retrieved from “http://en.wikipedia.org/wiki/Cave_of_Archedemos_the_Nympholept”
Categories: Caves of Greece | Ancient Attica | Ancient Greek art | European archaeology stubs

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Frederick Abberline

  (Redirected from Frederick George Abberline)
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An illustration of Abberline from an 1888 newspaper

Frederick George Abberline (8 January 1843 in Blandford Forum, Dorset – 10 December 1929) was a Chief Inspector for the London Metropolitan Police and was a prominent police figure in the investigation into the Jack the Ripper murders of 1888.

Contents 1 Early life 2 Police career 3 Personal life 4 Abberline in popular culture 5 References 6 External links

Early life

Frederick Abberline was the son of Edward Abberline, a saddlemaker and Sheriff’s Officer and Clerk of the Market, minor local government positions, and his wife Hannah (née Chinn). Edward Abberline died in 1849, and his widow opened a small shop and brought up her four children, Emily, Harriett, Edward and Frederick, alone.

Police career

Frederick was a clockmaker until he left home to go to London, where he enlisted in the Metropolitan Police on 5 January 1863, being appointed to N Division (Islington) with the Warrant Number 43519. PC Abberline so impressed his superiors that they promoted him to Sergeant two years later on 19 August 1865. On his promotion he moved to Y Division (Highgate). Throughout 1867 he investigated Fenian activities as a plain clothes officer. He was promoted to Inspector on 10 March 1873, and three days later, on 13 March transferred to H Division in Whitechapel. On 8 April 1878 Abberline was appointed Local Inspector in charge of H Division’s CID.

On 26 February 1887 Abberline transferred to A Division (Whitehall), and then moved to CO Division (Central Office) at Scotland Yard on 19 November 1887, being promoted to Inspector First-Class on 9 February 1888 and to Chief Inspector on 22 December 1890. Following the murder of Mary Ann Nichols on 31 August 1888, Abberline was seconded back to Whitechapel due to his extensive experience in the area. He was placed in charge of the various detectives investigating the Ripper murders. Chief Inspector Walter Dew, then a detective constable in Whitechapel’s H Division in 1888, knew Abberline and, while describing him as sounding and looking like a bank manager, also stated that his knowledge of the area made him one of the most important members of the Whitechapel murder investigation team.

Among the many suspects in the case, Abberline’s primary suspect was Severin Antoniovich Klosowski, aka George Chapman.

Abberline was subsequently involved in the investigation of the Cleveland Street scandal in 1889. Chief Inspector Abberline retired from the police on 8 February 1892, having received 84 commendations and awards, and worked as a private enquiry agent, including three seasons at Monte Carlo, before taking over the European Agency of the famous Pinkerton National Detective Agency of America, for whom he worked for 12 years.

Personal life

Abberline was married twice: once in March 1868 to 25-year-old Martha Mackness, the daughter of a labourer, from Elton, Northamptonshire; she died of tuberculosis two months after the marriage. On 17 December 1876, a decade before the Ripper murders, Abberline married 32-year-old Emma Beament, the daughter of a merchant, from Hoxton New Town, Shoreditch. Although they had no children, there is no credible evidence that the couple were unhappy, and the marriage lasted until Frederick’s death over 50 years later. On his retirement from the Pinkerton Detective Agency in 1904 Abberline retired to Bournemouth.

Frederick George Abberline died in 1929 aged 86 at his home, “Estcourt”, 195 Holdenhurst Road, Bournemouth, and was buried in Bournemouth at Wimborne Road Cemetery. In 2007, following a campaign for Abberline’s unmarked grave to be recognised, and with the approval of his surviving relatives, a black granite headstone, inscribed and donated by a local stonemason, was erected on the grave where Abberline and his second wife Emma are buried . A blue plaque commemorating Abberline was unveiled at 195 Holdenhurst Road (now divided into flats) on 29 September 2001.

Abberline in popular culture

Several fictional retellings of the events surrounding the Jack the Ripper murders have cast Abberline in a central role. The suggestion is often but erroneously made for the sake of drama that Abberline was unmarried and formed an attachment to one of the women connected to the events. The two most popular film depictions have also cast him as an addict, for which there is no known historical basis.

• Abberline was played by Michael Caine in a 1988 television film called Jack the Ripper. Here, the character was an aging alcoholic whose quest to solve the murder gives him the strength to give up drinking.

• A fictionalized Abberline was featured as a central figure in Alan Moore and Eddie Campbell’s graphic novel From Hell (1991-1999), and subsequently portrayed by Johnny Depp in the very liberal film adaptation of that work (2001). The graphic novel paints him as a sulky but sympathetic policeman, different from his peers only in his moralism and being overweight, and takes pains to include little-known details of his life such as his involvement with the Pinkerton National Detective Agency. The film’s version of Abberline was portrayed as an intelligent detective who is ahead of his time in his deductive techniques. He is also portrayed as being clairvoyant, allowing the filmmakers to ascribe to Abberline the contributions of spiritualist and psychic Robert James Lees. Although Abberline is addicted to opium and absinthe, he is a decent man who ultimately goes on a crusade against very powerful governmental and upper-class figures to stop the grotesque murders of Jack the Ripper. In the film Abberline dies of an overdose in his late 30s; in reality,he died of natural causes aged 86.

• Abberline was played by Gordon Christie in the 1973 TV miniseries Jack the Ripper.

• In “The Ripper”, an episode of the TV series The Collector, Abberline was played by Robert Wisden.

• Abberline appears as a character in several of the Inspector Lestrade novels by M. J. Trow. He is generally depicted as incompetent and obstructive. The first novel in the series, The Adventures of Inspector Lestrade (1985), ISBN 0333384474, deals with the aftermath of the Ripper case.

• Abberline was used as a model for the character “Fred Abberline” in Kuroshitsuji.

• A Scotland Yard inspector called Francis Aberline plays a key role in the 2010 horror thriller The Wolfman. Francis Aberline, played by Hugo Weaving, is a fictionalized Frederick Abberline, who comes to investigate the savage killings occurring in the fictional English village of Blackmoor. Lawrence Talbot, played by Benicio del Toro, makes a mocking reference to Aberline’s investigation of the Ripper case. “Francis” was Frederick Abberline’s real-life nickname.

References

1. ^ The Jack the Ripper A to Z by Paul Begg, Martin Fido and Keith Skinner. Pub. by Headline Book Publishing Plc (1992) pg 5
2. ^ Dew, Walter ‘I Caught Crippen’ Blackie & Son Ltd (1938)
3. ^ Begg, Fido and Skinner, pg5
4. ^ “Headstone for Ripper-hunt officer”, BBC News 4 July 2007
5. ^ http://www.casebook.org/images/Abberline%20Plaque.pdf

External links

• Brief profile from Casebook.org
• Casebook.org message board thread discussing the Abberline grave project
• Photograph of Abberline’s grave with its granite headstone in situ

v • d • e Jack the Ripper Canonical victims Mary Ann Nichols · Annie Chapman · Elizabeth Stride · Catherine Eddowes · Mary Jane Kelly Police Frederick Abberline · Robert Anderson · Thomas Arnold · Walter Dew · George Godley · Donald Swanson · Charles Warren Letters and clues Dear Boss letter · Saucy Jacky postcard · From Hell letter · Openshaw letter · Goulston Street graffito Conspiracy theories · Fiction · Suspects · Whitechapel murders

Retrieved from “http://en.wikipedia.org/wiki/Frederick_Abberline”
Categories: Jack the Ripper | 1843 births | 1929 deaths | Metropolitan Police officers | People from Blandford Forum

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Tim O’Brien

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Tim O’Brien may refer to:

• Tim O’Brien (author), American author
• Timothy O’Brien, professor
• Timothy L. O’Brien, American journalist
• Tim O’Brien (musician), American musician
• Sir Tim O’Brien, Irish-born cricketer
• Tim O’Brien (politician), legislator in the Connecticut House of Representatives
• Tim O’Brien (illustrator)
• Timothy O’Brien (theatre designer)

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This disambiguation page lists articles associated with the same personal name. If an internal link led you here, you may wish to change the link to point directly to the intended article.

Retrieved from “http://en.wikipedia.org/wiki/Tim_O%27Brien”
Categories: Human name disambiguation pagesHidden categories: All article disambiguation pages | All disambiguation pages

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Bihar Regiment

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The Bihar Regiment
Active	1941–Present
Country	India
Branch	Army
Type	Infantry
Size	17 Battalions
Regimental Centre	Danapur, Bihar
Motto	Karam Hi Dharam (Work is Worship)
War Cry	Jai Bajrang Bali (Victory to Bajrang Bali) Birsa Munda Ki Jai (Victory to Birsa Munda)
Engagements	]
Decorations	3 Ashoka Chakras
Battle honours	Post Independence Haka , Gangaw and Batalik. Theatre honours=Akhaura.
Commanders
Current commander	Lieutenant General Rajeev Rai
Notable commanders	Lieutenant General Sant Singh, Lt Gen K S Mann, Lt Gen A R K Reddy, Lt Gen O S Lohchab, Lt Gen Balbir Singh
Insignia
Regimental Insignia	The Ashoka Lion

The Bihar Regiment is a regiment of the Indian Army. The regiment can trace its origins back to the British Indian Army.

History

Hindu, Buddhist and Muslim influences intermingled to produce a soldiery which was traditionally arms bearing, disciplined and deeply religious. The Bihar Regiment claims its origins from the sepoy battalions raised in 1757 by Clive at Patna. These were formed by the men from the Bhojpur region of Bihar. Their success in combat had impressed the local ruler Mir Kasim, to begin raising units trained in western combat techniques. The Bihari battalions raised by Mir Kasim had not only done well, but beaten the British in some engagements. The Bihari, or poorbia/purviah soldier thereafter continued to provide the backbone of The Bengal Infantry of the British.

The Bihar Regiment was formed in 1941 by regularising the 11th (Territorial) Battalion, 19th Hyderabad Regiment, and raising new battalions. The Bihari was not only an excellent soldier, he was also quick to learn and apply the tactical drills with initiative. He was disciplined when led by good officers, but capable of hostility when his beliefs and customs were disregarded. The 1857 revolt against the introduction of greased cartridges, was led by Bihari troops, who preferred being blown by the guns to losing their faith. Biharis thereafter were not encouraged to enter military service by British until after the Great War (World War I), when they were accepted in the Hyderabad Regiment which then later became the Kumaon Regiment. 1st Bihar owes its origins to the Kumaonis. The 2nd was raised in 1942 as part of the Bihar Regiment.

On 15 December 1971 a Seaborne expedition was launched against Cox’s Bazar after reports of had reached Army HQ that some Pakistani troops were escaping into Burma that way. The Task force consisted of the HQ of 2 Artillery Brigade, the 1st Battalion, 3 Gorkha Rifles Regiment, 11th Battalion, Bihar Regiment and troops of support services.

Pakistan sponsored intruders crossed the L.O.C. in Kargil and entered the Indian Territory. “Operation Vijay” was launched by Indian Army to flush out intruders from the Indian Territory More than 10,000 Jawans and Officers serving in Bihar Regiment and other regiments were on the war front. In a well planned operation in the Batalik Sector, the soldiers of the Bihar Regiment, in a fierce fight with the Pakistan Army, captured Point 4268 and Jubar Ridge on night 06/7 July 99. 7 July 1999 is a red letter day when it was announced that Jawans of Bihar Regiment pushed back intruders from Jubar Hills and point 4268 in Kuker Thang area in Batalik sector.

Units

Regimental Battalions:

• 1st Battalion
• 2nd Battalion
• 3rd Battalion
• 4th Battalion
• 5th Battalion
• 6th Battalion
• 7th Battalion
• 8th Battalion
• 9th Battalion
• 10th Battalion
• 11th Battalion
• 12th Battalion
• 14th Battalion
• 15th Battalion
• 16th Battalion
• 17th Battalion
• 21st Battalion

---

References

Bihar Regiment on Bharat-Rakshak

Bihar Regiment on Global Security

v • d • e Indian Army Infantry Regiments Brigade of the Guards • The Parachute Regiment • Mechanised Infantry Regiment • Punjab Regiment • Madras Regiment • The Grenadiers • Maratha Light Infantry • Rajputana Rifles • Rajput Regiment • Jat Regiment • Sikh Regiment • Sikh Light Infantry • Dogra Regiment • Garhwal Rifles• Kumaon Regiment • Assam Regiment • Bihar Regiment • Mahar Regiment • Jammu & Kashmir Rifles • Jammu & Kashmir Light Infantry • Naga Regiment • 1 Gorkha Rifles (The Malaun Regiment) • 3 Gorkha Rifles • 4 Gorkha Rifles • 5 Gorkha Rifles (Frontier Force) • 8 Gorkha Rifles • 9 Gorkha Rifles • 11 Gorkha Rifles • Ladakh Scouts

Retrieved from “http://en.wikipedia.org/wiki/Bihar_Regiment”
Categories: Indian Army | Regiments of the Indian ArmyHidden categories: All articles with unsourced statements | Articles with unsourced statements from February 2009

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Angelman syndrome

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Angelman Syndrome
Classification and external resources
ICD-10	Q93.5
ICD-9	759.89
OMIM	105830
DiseasesDB	712
MeSH	D017204

Angelman syndrome (AS) is a neuro-genetic disorder characterized by intellectual and developmental delay, sleep disturbance, seizures, jerky movements especially hand-flapping, frequent laughter or smiling, and usually a happy demeanor.

AS is a classic example of genetic imprinting in that it is usually caused by deletion or inactivation of genes on the maternally inherited chromosome 15 while the paternal copy, which may be of normal sequence, is imprinted and therefore silenced. The sister syndrome, Prader-Willi syndrome, is caused by a similar loss of paternally-inherited genes and maternal imprinting. AS is named after a British pediatrician, Dr. Harry Angelman, who first described the syndrome in 1965. An older, alternative term for AS, happy puppet syndrome, is generally considered pejorative and stigmatizing so it is no longer used, though it remains useful as a diagnostic heuristic. People with AS are sometimes known as “angels”, both because of the syndrome’s name and because of their youthful, happy appearance.

Contents 1 History 2 Prevalence 3 Pathophysiology 4 Clinical features in Angelman Syndrome 5 Diagnosis 6 Treatment 7 Living with Angelman syndrome 8 Prognosis 9 See also 10 References 11 External links

History

“Boy with a Puppet” or “A child with a drawing” by Giovanni Francesco Caroto.

Dr. Harry Angelman, a pediatrician working in Warrington (then in Lancashire) first reported three children with this condition in 1965. Angelman later described his choice of the title “Puppet Children” to describe these cases as being related to an oil painting he had seen while vacationing in Italy:

Case reports from the United States first began appearing in the medical literature in the early 1980s. In 1987, it was first noted that around half of the children with AS have a small piece of chromosome 15 missing (chromosome 15q partial deletion).

Prevalence

Though the prevalence of Angelman syndrome is not precisely known, there are some estimates. The best data available are from studies of school age children, ages 6–13 years, living in Sweden and from Denmark where the diagnosis of AS children in medical clinics was compared to an 8 year period of about 45,000 births. The Swedish study showed an AS prevalence of about 1/20,000 and the Danish study showed a minimum AS prevalence of about 1/10,000.

Pathophysiology

Angelman syndrome is caused by the loss of the normal maternal contribution to a region of chromosome 15, most commonly by deletion of a segment of that chromosome. Other causes include uniparental disomy, translocation, or single gene mutation in that region. A healthy person receives two copies of chromosome 15, one from the mother, the other from the father. However, in the region of the chromosome that is critical for Angelman syndrome, the maternal and paternal contribution express certain genes very differently. This is due to sex-related epigenetic imprinting; the biochemical mechanism is DNA methylation. In a normal individual, the maternal allele is expressed and the paternal allele is silenced. If the maternal contribution is lost or mutated, the result is Angelman syndrome. (When the paternal contribution is lost, by similar mechanisms, the result is Prader-Willi syndrome.) It should be noted that the methylation test that is performed for Angelman syndrome (a defect in UBE3A) is actually looking for the gene’s neighbour SNRPN (which has the opposite pattern of methylation).

Angelman syndrome can also be the result of mutation of a single gene. This gene (UBE3A, part of the ubiquitin pathway) is present on both the maternal and paternal chromosomes, but differs in the pattern of methylation (Imprinting). The paternal silencing of the UBE3A gene occurs in a brain region-specific manner; in the hippocampus and cerebellum, the maternal allele is almost exclusively the active one. The most common genetic defect leading to Angelman syndrome is an ~4Mb (mega base) maternal deletion in chromosomal region 15q11-13 causing an absence of UBE3A expression in the paternally imprinted brain regions. UBE3A codes for an E6-AP ubiquitin ligase, which chooses its substrates very selectively and the four identified E6-AP substrates have shed little light on the possible molecular mechanisms underlying the human Angelman syndrome mental retardation state.

Initial studies of mice that do not express maternal UBE3A show severe impairments in hippocampal memory formation. Most notably, there is a deficit in a learning paradigm that involves hippocampus-dependent contextual fear conditioning. In addition, maintenance of long-term synaptic plasticity in hippocampal area CA1 in vitro is disrupted in Ube3a^-/- mice. These results provide links amongst hippocampal synaptic plasticity in vitro, formation of hippocampus-dependent memory in vivo, and the molecular pathology of Angelman syndrome.

Clinical features in Angelman Syndrome

The following list features of Angelman Syndrome and their relative frequency in affected individuals.

Consistent (100%)

• Developmental delay, functionally severe
• Speech impairment, none or minimal use of words; receptive and non-verbal communication skills higher than verbal ones
• Movement or balance disorder, usually ataxia of gait and/or tremulous movement of limbs
• Behavioral uniqueness: any combination of frequent laughter/smiling; apparent happy demeanor; easily excitable personality, often with hand flapping movements; hypermotoric behavior; short attention span

Frequent (more than 80%)

• Delayed, disproportionate growth in head circumference, usually resulting in microcephaly (absolute or relative) by age 2
• Seizures, onset usually < 3 years of age
• Abnormal EEG, characteristic pattern with large amplitude slow-spike waves

Associated (20 – 80%)

• Strabismus
• Hypopigmented skin and eyes
• Tongue thrusting; suck/swallowing disorders
• Hyperactive tendon reflexes
• Feeding problems during infancy
• Uplifted, flexed arms during walking
• Prominent mandible
• Increased sensitivity to heat
• Wide mouth, wide-spaced teeth
• Sleep disturbance
• Frequent drooling, protruding tongue
• Attraction to/fascination with water
• Excessive chewing/mouthing behaviors
• Flat back of head
• Enlarged toes
• Smooth Palms

Diagnosis

The diagnosis of Angelman syndrome is based on:

• A history of delayed motor milestones and then later a delay in general development, especially of speech
• Unusual movements including fine tremors, jerky limb movements, hand flapping and a wide-based, stiff-legged gait.
• Characteristic facial appearance (but not in all cases).
• A history of epilepsy and an abnormal EEG tracing.
• A happy disposition with frequent laughter
• A deletion on chromosome 15

Diagnostic criteria for the disorder were initially established in 1995 in collaboration with the Angelman Syndrome Foundation (USA); these criteria have undergone revision in 2005.

Treatment

There is currently no cure available. The epilepsy can be controlled by the use of one or more types of anticonvulsant medications. However, there are difficulties in ascertaining the levels and types of anticonvulsant medications needed to establish control, because AS is usually associated with having multiple varieties of seizures, rather than just the one as is normal cases of epilepsy. Many families use melatonin to promote sleep in a condition which often affects sleep patterns. Many individuals with Angelman Syndrome sleep for a maximum of 5 hours at any one time. Mild laxatives are also used frequently to encourage regular bowel movements and early intervention with physiotherapy is important to encourage joint mobility and prevent stiffening of the joints.

Living with Angelman syndrome

Although Angelman syndrome is life-changing, it does not need to be life-destroying. Those with the syndrome are generally happy and contented people, who like human contact and play. People with AS exhibit a profound desire for personal interaction with others. Communication can be difficult at first, but as a child with AS develops, there is a definite character and ability to make themselves understood. It is widely accepted that their understanding of communication directed to them is much larger than their ability to return conversation. Most afflicted people will not develop more than 5-10 words, if any at all.

Seizures are a consequence, but so is excessive laughter, which is a major hindrance to early diagnosis.

Actor Colin Farrell, author Ian Rankin, professional baseball player Dave Henderson, and professional hockey player Peter McDuffe have sons with AS.

Prognosis

The severity of the symptoms associated with Angelman Syndrome varies significantly across the population of those affected. Some speech and a greater degree of self-care are possible among the least profoundly affected. Unfortunately, walking and the use of simple sign language may be beyond the reach of the more profoundly affected. Early and continued participation in physical, occupational (related to the development of fine-motor control skills), and communication (speech) therapies are believed to improve significantly the prognosis (in the areas of cognition and communication) of individuals affected by AS. Further, the specific genetic mechanism underlying the condition is thought to correlate to the general prognosis of the affected person. On one end of the spectrum, a mutation to late to the least affected, whereas larger deletions on chromosome 15 are thought to correspond to the most affected.

The clinical features of Angelman syndrome alter with age. As adulthood approaches, hyperactivity and poor sleep patterns improve. The seizures decrease in frequency and often cease altogether and the EEG abnormalities are less obvious. Medication is typically advisable to those with seizure disorders. Often overlooked is the contribution of the poor sleep patterns to the frequency and/or severity of the seizures. Medication may be worthwhile in order to help deal with this issue and improve the prognosis with respect to seizures and sleep. Also noteworthy are the reports that the frequency and severity of seizures temporarily escalate in pubescent Angelman Syndrome girls but do not seem to affect long-term health.

The facial features remain recognizable but many adults with AS look remarkably youthful for their age.

Puberty and menstruation begin at around the average age. Sexual development is thought to be unaffected, as evidenced by a single reported case of a woman with Angelman syndrome conceiving a female child who also had Angelman syndrome.

The majority of those with AS achieve continence by day and some by night. Angelman Syndrome is not a degenerative syndrome. Many people with AS improve their living skills with support.

Dressing skills are variable and usually limited to items of clothing without buttons or zippers. Most adults are able to eat with a knife or spoon and fork and can learn to perform simple household tasks. General health is fairly good and life-span near average. Particular problems which have arisen in adults are a tendency to obesity (more in females), and worsening of scoliosis if it is present. The affectionate nature which is also a positive aspect in the younger children may also persist into adult life where it can pose a problem socially, but this problem is not insurmountable.

See also

• Genomic Imprinting
• Prader-Willi Syndrome
• Epigenetics

References

1. ^ ^{a b} Angelman, Harvey (1965). “‘Puppet’ Children: A report of three cases”. Dev Med Child Neurol. 7: 681–688. 
2. ^ Angelman H. Personal communication with Dr. Charles Williams (1991), cited at Facts about Angelman Syndrome, Angelman Syndrome Foundation (USA) http://www.angelman.org/stay-informed/facts-about-angelman-syndrome/ accessed December 18, 2008
3. ^ Dooley, JM; Berg JM, Pakula Z, MacGregor DL. (1981). “The puppet-like syndrome of Angelman.”. Am J Dis Child 135 (7): 621–4. 
4. ^ Williams, CA; Frias JL (1982). “The Angelman (”happy puppet”) syndrome.”. Am J Med Genet. 11 (4): 453–60. doi:10.1002/ajmg.1320110411. 
5. ^ Magenis, RE; Brown MG, Lacy DA, Budden S, LaFranchi S. (1987). “Is Angelman syndrome an alternate result of del(15)(q11q13)?”. Am J Med Genet. 28 (4): 829–38. doi:10.1002/ajmg.1320280407. 
6. ^ Steffenburg S, Gillberg CL, Steffenburg U, Kyllerman M (1996). “Autism in Angelman syndrome: a population-based study”. Pediatr. Neurol. 14 (2): 131–6. doi:10.1016/0887-8994(96)00011-2. PMID 8703225. 
7. ^ Petersen MB, Brøndum-Nielsen K, Hansen LK, Wulff K (1995). “Clinical, cytogenetic, and molecular diagnosis of Angelman syndrome: estimated prevalence rate in a Danish county; the disorder predominantly affects Anglo-Saxons.”. Am. J. Med. Genet. 60 (3): 261–2. doi:10.1002/ajmg.1320600317. PMID 7573182. 
8. ^ White HE, Durston VJ, Harvey JF, Cross NC (2006). “Quantitative analysis of SNRPN(correction of SRNPN) gene methylation by pyrosequencing as a diagnostic test for Prader-Willi syndrome and Angelman syndrome”. Clin. Chem. 52 (6): 1005–13. doi:10.1373/clinchem.2005.065086. PMID 16574761. 
9. ^ Weeber E, Levenson J, Sweatt J (2002). “Molecular genetics of human cognition.”. Mol Interv 2 (6): 376–91, 339. doi:10.1124/mi.2.6.376. PMID 14993414. 
10. ^ Facts about Angelman Syndrome. Anonymous. Angelman Syndrome Foundation (USA) website. Accessed December 19, 2008.
11. ^ Williams CA, Angelman H, Clayton-Smith J, et al. (1995). “Angelman syndrome: consensus for diagnostic criteria. Angelman Syndrome Foundation”. Am. J. Med. Genet. 56 (2): 237–8. doi:10.1002/ajmg.1320560224. PMID 7625452. 
12. ^ Williams CA, Beaudet AL, Clayton-Smith J, et al. (2006). “Angelman syndrome 2005: updated consensus for diagnostic criteria”. Am. J. Med. Genet. A 140 (5): 413–8. doi:10.1002/ajmg.a.31074. PMID 16470747. 
13. ^ Andersen WH, Rasmussen RK, Strømme P (2001). “Levels of cognitive and linguistic development in Angelman syndrome: a study of 20 children”. Logopedics, phoniatrics, vocology 26 (1): 2–9. doi:10.1080/140154301300109044. PMID 11432411. 
14. ^ Buntinx IM, Hennekam RC, Brouwer OF, et al. (March 1995). “Clinical profile of Angelman syndrome at different ages”. American Journal of Medical Genetics 56 (2): 176–83. doi:10.1002/ajmg.1320560213. PMID 7625442. 
15. ^ Timesonline
16. ^ Lossie A, Driscoll D. “Transmission of Angelman syndrome by an affected mother.”. Genet Med 1 (6): 262–6. PMID 11258627. 
17. ^ Laan LA, den Boer AT, Hennekam RC, Renier WO, Brouwer OF (1996). “Angelman syndrome in adulthood”. Am. J. Med. Genet. 66 (3): 356–60. doi:10.1002/(SICI)1096-8628(19961218)66:3<356::AID-AJMG21>3.0.CO;2-K. PMID 9072912. 

External links

• Angelman Syndrome Foundation USA
• Angelman Syndrome Association AUS
• Angelman Syndrome Support Education & Research Trust – UK
• Angelman syndrome at the Open Directory Project
• Angelman Syndrome at NIH/UW GeneTests
• Foundation for Angelman Syndrome Therapeutics

v • d • e Pathology: chromosome abnormalities (Q90-Q99 · 758) Autosomal Trisomies Down syndrome (21) · Edwards syndrome (18) · Patau syndrome (13) Trisomy 9 · Warkany syndrome 2 (8) · Trisomy 22/Cat eye syndrome (22) · Trisomy 16 Monosomies/deletions Wolf-Hirschhorn syndrome (4) · Cri du chat/Chromosome 5q deletion syndrome (5) · Williams syndrome (7) · Jacobsen syndrome (11) · Miller-Dieker syndrome/Smith-Magenis syndrome (17) · Di George’s syndrome (22) genomic imprinting (Angelman syndrome/Prader–Willi syndrome (15)) X/Y linked Monosomy Turner syndrome (XO) Trisomy/tetrasomy, other karyotypes/mosaics Klinefelter’s syndrome (47,XXY) · 48,XXYY · 49,XXXXY Triple X syndrome (47,XXX) · 48,XXXX · 49,XXXXX 47,XYY Translocations Leukemia/lymphoma Lymphoid Burkitt’s lymphoma t(8 MYC;14 IGH) · Follicular lymphoma t(14 IGH;18 BCL2) · Mantle cell lymphoma/Multiple myeloma t(11 CCND1:14 IGH) · Anaplastic large cell lymphoma t(2 ALK;5 NPM1) · Acute lymphoblastic leukemia Myeloid Philadelphia chromosome t(9 ABL; 22 BCR) · Acute myeloblastic leukemia with maturation t(8 RUNX1T1;21 RUNX1) · Acute promyelocytic leukemia t(15 PML,17 RARA) · Acute megakaryoblastic leukemia t(1 RBM15;22 MKL1) Other Ewing’s sarcoma t(11 FLI1; 22 EWS) · Synovial sarcoma t(x SYT;18 SSX) · Dermatofibrosarcoma protuberans t(17 COL1A1;22 PDGFB) · Myxoid liposarcoma t(12 DDIT3; 16 FUS) · Desmoplastic small round cell tumor t(11 WT1; 22 EWS) · Alveolar rhabdomyosarcoma t(2 PAX3; 13 FOXO1) t (1 PAX7; 13 FOXO1) Gonadal dysgenesis Mixed gonadal dysgenesis · XX gonadal dysgenesis Other Fragile X syndrome · Uniparental disomy

v • d • e Non-Mendelian inheritance: genomic imprinting Chromosome 15 Angelman syndrome · Prader-Willi syndrome Chromosome 11 Beckwith-Wiedemann syndrome · Silver-Russell dwarfism · Myoclonic dystonia

Retrieved from “http://en.wikipedia.org/wiki/Angelman_syndrome”
Categories: Disability | Genetic disorders | Neurological disorders | Rare diseases | SyndromesHidden categories: All articles with unsourced statements | Articles with unsourced statements from November 2009

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Earl Loreburn

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This article does not cite any references or sources. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2009)

The title Earl Loreburn was created in the Peerage of the United Kingdom in 1911 for Robert Reid, 1st Baron Loreburn, the Lord Chancellor. The title became extinct upon his death in 1923.

Lord Loreburn held the subsidiary title Baron Loreburn, of Dumfries in the County of Dumfries (1906).

Earls Loreburn (1911)

• Robert Threshie Reid, 1st Earl Loreburn (1846–1923)

Retrieved from “http://en.wikipedia.org/wiki/Earl_Loreburn”
Categories: Earldoms | Extinct earldomsHidden categories: Articles lacking sources from December 2009 | All articles lacking sources

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Age of Renaissance

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The Age of Renaissance game box

Age of Renaissance is a board game designed by Don Greenwood and Jared Scarborough and published by Avalon Hill in 1996. The game is for 3-6 players and the box claims that the game should take 2-6 hours to play, though as with any serious multiplayer strategy game, this can entirely depend on the players. Age of Renaissance is somewhat of a sequel to Civilization. In 1997, Age of Renaissance won the Origins Award for Best Pre-20th Century Board Game of 1996.

Game play

In Age of Renaissance, each player takes the role of one of six commercial capitals of Europe: Venice, Genoa, Barcelona, London, Paris, and Hamburg. Initially each player controls one city, their capital. As the game progresses, each player’s financial empire grows to a larger number of cities which provide income each turn. Each region where a city can be established also produces one of a number of different commodities: stone, wool, timber, grain, wine, cloth, metal, fur, silk, spice, gold, or ivory. Control of commodities doesn’t do anything alone, but when a commodity card is played, every player with stakes in that commodity cashes in. Commodities and income from cities provide players with their two main sources of income. Players then use that money to buy counters to expand their empire, and to buy civilization advances that have various effects on the game.

There is a deck of cards that players draw from. Once the deck is depleted, a new batch of cards (and some of the used cards) are shuffled in and the game progresses to the second epoch. Once the deck is depleted again, more new cards (and again some of the used cards) are shuffled to form a new deck for the third epoch. Once the deck is depleted a third time, the game ends and the player with the highest score wins. Score is determined by adding up the values of a player’s advances and cash, less a penalty for the “misery” of their people. The rules also suggest shorter versions of the game that end after either one or two epochs.

The game has many complexities and interesting rules that add to the gameplay. For instance, each player secretly bids for the number of units they want to control in a given turn. The player with the fewest units goes first, and the player with the most goes last. However, the rules for combat give a significant advantage in effectiveness to the players going early in a turn rather than later, leaving players with an interesting choice. Another noteworthy rule is the clever requirement that all diplomacy take place in the open at the table, which dramatically improves gameplay by keeping things moving.

Strategically, it is critical in a game of Age of Renaissance to recognize the player in the lead. There are many cards that can significantly hurt a specific player, and these are best used to keep the leader(s) in check lest they run away with the game.

References

1. ^ “Origins Award Winners (1996)”. Academy of Adventure Gaming Arts & Design. http://www.originsgamefair.com/awards/1996/list-of-winners. 

External links

• Age of Renaissance at BoardGameGeek

Retrieved from “http://en.wikipedia.org/wiki/Age_of_Renaissance”
Categories: Avalon Hill games | Historical board games | Don Greenwood games

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• This page was last modified on 7 May 2009 at 21:44.
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Arthur B. Williams

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Arthur Bruce Williams (January 27, 1872 – May 1, 1925) was a politician from the U.S. state of Michigan.

Williams was born in Ashland, Ohio, and attended the common schools of Eaton County, Michigan. He graduated from Olivet College, in that county, in 1892. He was admitted to the bar in 1894 and commenced practice in Battle Creek. He was interested in agricultural pursuits at his summer home in Gull Lake. He served as director of the Old National Bank in Battle Creek, and also as vice president and general counsel of the Postum Cereal Company. He also served as president of the Michigan Manufacturers’ Association.

On June 19, 1923, Williams was elected as a Republican from Michigan’s 3rd congressional district to the 68th United States Congress to fill the vacancy caused by the death of John M. C. Smith. In 1924 he was re-elected to the 69th Congress and served until his death in Baltimore, Maryland. He was interred in Maple Hill Cemetery in Charlotte, Michigan.

References

• Arthur B. Williams at the Biographical Directory of the United States Congress
• The Political Graveyard

United States House of Representatives
Preceded by John M. C. Smith	United States Representative for the 3rd Congressional District of Michigan June 19, 1923 – May 1, 1925	Succeeded by Joseph L. Hooper

Retrieved from “http://en.wikipedia.org/wiki/Arthur_B._Williams”
Categories: 1872 births | 1925 deaths | Members of the United States House of Representatives from Michigan | People from Ashland County, Ohio

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