document_title: I Put a Spell on You

question_text: who sang i put a spell on you in hocus pocus

text: I Put a Spell on You

text: The original composition[edit]

text: Hawkins had originally intended to record "I Put a Spell on You" as "a refined love song, a blues ballad". However, the producer "brought in ribs and chicken and got everybody drunk, and we came out with this weird version ... I don't even remember making the record. Before, I was just a normal blues singer. I was just Jay Hawkins. It all sort of just fell in place. I found out I could do more destroying a song and screaming it to death."[7]

text: Hawkins first recorded "I Put a Spell on You" as a ballad during his stint with Grand Records in late 1955. However, that version was not released at the time (it has since been reissued on Hawkins' UK Rev-Ola CD The Whamee 1953–55). The following year, Hawkins re-recorded the song for Columbia's Okeh Records – the notorious screaming version, which was released in October 1956. This version was banned from radio for its outrageous style. A truncated version was released but the ban remained. The record still sold over a million copies.[8]

text: The hit brought Hawkins together with Cleveland disc jockey Alan Freed who promptly added him to his "Rock and Roll Revue." Up to this time, Hawkins had been a blues performer: emotional, but not wild. Freed suggested a gimmick to capitalize on the "demented" sound of "I Put a Spell on You": Hawkins wore a long cape, and appeared onstage by rising out of a coffin in the midst of smoke and fog.[9] The act was a sensation, later bolstered by tusks worn in Hawkins' nose, on-stage snakes and fireworks, and a cigarette-smoking skull named "Henry".

text: This theatrical act was one of the first shock rock performances.[10]

text: Personnel[edit]

text:
Guitar – Mickey Baker
Piano – Ernie Hayes
Tenor Saxophone – Sam "The Man" Taylor
Baritone Saxophone – Bud Johnson
Bass – Al Lucas
Drums – David "Panama" Francis
Arranged By – Leroy Kirkland
Recorded 12 September 1956[11]

text: Covers and samples[edit]

text: "I Put a Spell on You" has been covered by other artists extensively; there are several hundred versions available on online stores like iTunes. Most of the covers treat the song seriously; few attempt to duplicate Hawkins's bravura performance. Although Hawkins' version did not make any charts, several later cover versions have.

text:
Nina Simone's version reached No. 23 on the U.S. Billboard R&B chart in 1965; it also reached No. 49 on the UK singles chart that year, and No. 28 when it was reissued in 1969.[12]
The version by The Alan Price Set reached No. 9 in the UK in 1966[13] and No. 80 on the Billboard Hot 100.
Creedence Clearwater Revival's version reached No. 58 on the U.S. Hot 100 in 1968. The band later performed it at the Woodstock Festival in 1969.[14]
A disco version by Dutch singer Dee Dee (Anna Dekkers) reached No. 16 on the Dutch charts in 1978 and was also released in Belgium (where it peaked on No. 12), France, Germany, Spain, and Australia.
In the UK, Bryan Ferry's version reached No. 18 in 1993.[15]
The version by Sonique reached No. 36 in 1998 and No. 8 on reissue in 2000.[5][6][16]

text: Other versions of note:

text:
Marilyn Manson covered the song on the 1995 EP Smells Like Children
The Crazy World of Arthur Brown covered the track on their self-titled album.
Manfred Mann released a version on their U.K. EP No Living Without Loving in November 1965 (also appeared on the band's 1966 U.S. album 'Pretty Flamingo').
The 2010 version by Jeff Beck featuring Joss Stone was nominated for the Grammy Award for Best Rock Performance by a Duo or Group with Vocal at the 53rd Grammy Awards.[17]
Bette Midler covered the song in the film Hocus Pocus in an elaborate song and dance sequence. Midler performed the song again during her 2015 Divine Intervention Tour, wearing a costume similar to the one she wore in Hocus Pocus.
Annie Lennox included a version of the song on her 2014 album Nostalgia.


document_title: List of Star Wars films and television series

question_text: when was the first star wars film released

root

text: Feature films[edit]

text: Film series[edit]

text:
Film trilogies

Film
Release date
Director(s)
Screenwriter(s)
Story by
Producer(s)
Initial distributor(s)

Original trilogy

Episode IV –
A New Hope
May 25, 1977 (1977-05-25)
George Lucas
Gary Kurtz
20th Century Fox[a]

Episode V –
The Empire Strikes Back
May 21, 1980 (1980-05-21)
Irvin Kershner
Leigh Brackett and Lawrence Kasdan
George Lucas

Episode VI –
Return of the Jedi
May 25, 1983 (1983-05-25)
Richard Marquand
Lawrence Kasdan and George Lucas
Howard Kazanjian

Prequel trilogy

Episode I –
The Phantom Menace
May 19, 1999 (1999-05-19)
George Lucas
George Lucas
Rick McCallum
20th Century Fox[a]

Episode II –
Attack of the Clones
May 16, 2002 (2002-05-16)
George Lucas and
Jonathan Hales
George Lucas

Episode III –
Revenge of the Sith
May 19, 2005 (2005-05-19)
George Lucas

Sequel trilogy

Episode VII –
The Force Awakens
December 18, 2015 (2015-12-18)
J. J. Abrams
Lawrence Kasdan & J. J. Abrams and Michael Arndt
Kathleen Kennedy, J. J. Abrams and Bryan Burk
Walt Disney Studios Motion Pictures

Episode VIII –
The Last Jedi
December 15, 2017 (2017-12-15)
Rian Johnson
Kathleen Kennedy and Ram Bergman

Episode IX
December 20, 2019 (2019-12-20)[1]
J. J. Abrams
J. J. Abrams & Chris Terrio[2][3]
Kathleen Kennedy, Michelle Rejwan and J. J. Abrams

tag: table

text:
Standalone films

Film
Release date
Director(s)
Screenwriter(s)
Story by
Producer(s)
Initial distributor(s)

Animated film

Star Wars:
The Clone Wars
August 15, 2008 (2008-08-15)
Dave Filoni
Henry Gilroy, Steven Melching & Scott Murphy
George Lucas and Catherine Winder
Warner Bros.

Anthology films

Rogue One:
A Star Wars Story
December 16, 2016 (2016-12-16)
Gareth Edwards
Chris Weitz and Tony Gilroy
John Knoll and Gary Whitta
Kathleen Kennedy, Allison Shearmur and Simon Emanuel
Walt Disney Studios Motion Pictures

Solo:
A Star Wars Story
May 25, 2018 (2018-05-25)[4]
Ron Howard
Jon Kasdan & Lawrence Kasdan

text: Cast[edit]

text: Technical information[edit]

text: All seven films of the Star Wars series were shot in an aspect ratio of 2.39:1. The original and sequel trilogies were shot with anamorphic lenses. Episodes IV, V, and VII were shot in Panavision, while Episode VI was shot in Joe Dunton Camera (JDC) scope. Episode I was shot with Hawk anamorphic lenses on Arriflex cameras, and Episodes II and III were shot with Sony's CineAlta high-definition digital cameras.[5]

tag: p

text: Music and sound effects[edit]

text: Lucas hired Ben Burtt to oversee the sound effects on the original 1977 film. Burtt's accomplishment was such that the Academy of Motion Picture Arts and Sciences presented him with a Special Achievement Award because it had no award at the time for the work he had done.[6] Lucasfilm developed the THX sound reproduction standard for Return of the Jedi.[7] John Williams composed the scores for all eight films. Lucas's design for Star Wars involved a grand musical sound, with leitmotifs for different characters and important concepts. Williams's Star Wars title theme has become one of the most famous and well-known musical compositions in modern music history.[8]

text: Stunts[edit]

text: Lucas hired 'the Dean of Special Effects' John Stears, who created R2-D2, Luke Skywalker's Landspeeder, the Jedi Knights' lightsabers, and the Death Star.[9][10] The technical lightsaber choreography for the original trilogy was developed by leading filmmaking sword-master Bob Anderson. Anderson trained actor Mark Hamill (Luke Skywalker) and performed all the sword stunts as Darth Vader during the lightsaber duels in The Empire Strikes Back and Return of the Jedi, wearing Vader's costume. Anderson's role in the original Star Wars trilogy was highlighted in the film Reclaiming the Blade, where he shares his experiences as the fight choreographer developing the lightsaber techniques for the movies.[11]

text: Re-releases[edit]

text: Box office performance[edit]

text:
Film
Release date
Budget
Box office revenue
Box office ranking
Refs.

North America
Other
territories
Worldwide
Adjusted for
inflation
(North America)[b]
All-time
North America
All-time
worldwide

Star Wars
May 25, 1977
$11 million
$460,998,007
$314,400,000
$775,398,007
$1,359,782,041
#11
#77
[13]

The Empire Strikes Back
May 21, 1980
$11–$33 million
$290,475,067
$257,493,937
$547,969,004
$776,875,106
#84
#166
[14][15]

Return of the Jedi
May 25, 1983
$32.5–42.7 million
$309,306,177
$165,800,000
$475,106,177
$748,807,361
#68
#198
[16]

Original trilogy total
$54.5–86.7 million
$7009106077925100000♠1,060,779,251
$7008728100000000000♠728,100,000
$7009178887925100000♠1,788,879,251
$2,885,464,508

The Phantom Menace
May 19, 1999
$115 million
$474,544,677
$552,500,000
$1,027,044,677
$722,955,556
#12
#29
[17]

Attack of the Clones
May 16, 2002
$115 million
$310,676,740
$338,721,588
$649,398,328
$429,035,543
#66
#117
[18]

Revenge of the Sith
May 19, 2005
$113 million
$380,270,577
$468,484,191
$848,754,768
$476,488,298
#29
#61
[19]

Prequel trilogy total
$343 million
$7009116549199400000♠1,165,491,994
$7009135970577900000♠1,359,705,779
$7009252519777300000♠2,525,197,773
$1,628,479,397

The Force Awakens
December 18, 2015
$245 million
$936,662,225
$1,131,516,000
$2,068,178,225
$955,104,548
#1
#3
[20]

The Last Jedi
December 15, 2017
$200 million
$620,164,565
$712,484,660
$1,332,649,225
$620,164,565
#7
#9
[21]

Sequel trilogy total
$445 million
$7009153266838300000♠1,532,668,383
$7009180651870100000♠1,806,518,701
$7009333918708400000♠3,339,187,084
$1,551,110,706

The Clone Wars
August 15, 2008
$8.5 million
$35,161,554
$33,121,290
$68,282,844
$35,679,744
#2,187

[22]

Rogue One
December 16, 2016
$200 million
$532,177,324
$523,879,949
$1,056,057,273
$532,091,909
#9
#24
[23]

All films total
$1 billion
$3,950,319,348
$4,006,323,018
$7,956,642,366
$7009569086667300000♠5,690,866,673
#2
#3

text: Critical and public response[edit]

text:
Film
Rotten Tomatoes
Metacritic
CinemaScore

Star Wars
93% (8.6/10 average rating) (113 reviews)[24]
90 (24 reviews)[25]

The Empire Strikes Back
94% (8.9/10 average rating) (90 reviews)[26]
82 (25 reviews)[27]

Return of the Jedi
80% (7.2/10 average rating) (86 reviews)[28]
58 (24 reviews)[29]

Star Wars: Episode I – The Phantom Menace
55% (6/10 average rating) (216 reviews)[30]
51 (36 reviews)[31]
A−[32]

Star Wars: Episode II – Attack of the Clones
66% (6.7/10 average rating) (245 reviews)[33]
54 (39 reviews)[34]
A−[32]

Star Wars: Episode III – Revenge of the Sith
79% (7.3/10 average rating) (287 reviews)[35]
68 (40 reviews)[36]
A−[32]

Star Wars: The Clone Wars
18% (4.2/10 average rating) (168 reviews)[37]
35 (30 reviews)[38]
B−[32]

Star Wars: The Force Awakens
93% (8.2/10 average rating) (383 reviews)[39]
81 (54 reviews)[40]
A[32]

Rogue One
85% (7.5/10 average rating) (379 reviews)[41]
65 (51 reviews)[42]
A[32]

Star Wars: The Last Jedi
91% (8.1/10 average rating) (374 reviews)[43]
85 (56 reviews)[44]
A[32]

List indicator(s)

A dark grey cell indicates the information is not available for the film.

text: Academy Awards[edit]

text: The nine live-action films together have been nominated for 36 Academy Awards, of which they won seven. The films were also awarded a total of three Special Achievement Awards. Star Wars received seven awards and four nominations,[45] The Empire Strikes Back received one award, one Special Achievement Award and two nominations,[46] Return of the Jedi received one Special Achievement Award and four nominations,[47] The Phantom Menace received three nominations,[48] Attack of the Clones and Revenge of the Sith received one nomination each,[49][50] The Force Awakens received five nominations,[51] Rogue One received two nominations[52] and The Last Jedi received four nominations.[53]

text: Five films in the franchise (Return of the Jedi,[47] The Phantom Menace,[48] The Force Awakens,[51] Rogue One[52] and The Last Jedi[53]) were nominated for Best Sound Mixing; two films (Star Wars[45] and The Empire Strikes Back[46]) won the award. Five films (The Phantom Menace,[48] Attack of the Clones,[49] The Force Awakens,[51] Rogue One[52] and The Last Jedi[53]) were nominated for Best Visual Effects; Star Wars[45] won the award, while The Empire Strikes Back[46] and Return of the Jedi[47] received Special Achievement Awards for their visual effects and Star Wars[45] received a Special Achievement Award for its alien, creature and robot voices. Four films (The Empire Strikes Back,[46] Return of the Jedi,[47] The Force Awakens[51] and The Last Jedi[53]) were nominated for Best Original Score; Star Wars[45] won the award. The Force Awakens[51] was nominated for Best Film Editing and Star Wars[45] won the award. The Empire Strikes Back[46] and Return of the Jedi[47] were nominated for Best Art Direction-Set Decoration and Star Wars[45] won the award. Four films (Return of the Jedi,[47] The Phantom Menace,[48] The Force Awakens[51] and The Last Jedi[53]) were nominated for Best Sound Editing. Star Wars[45] won Best Costume Design and it also received nominations for Best Supporting Actor (Alec Guinness), Best Director (George Lucas), Best Picture and Best Original Screenplay. Revenge of the Sith[50] received a nomination for Best Makeup.

text: National Film Registry[edit]

text: In 1989, the Library of Congress selected the original Star Wars film for preservation in the U.S. National Film Registry, as being "culturally, historically, or aesthetically significant."[54] Its sequel, The Empire Strikes Back, was selected in 2010.[55][56] Despite these callings for archival, it is unclear whether copies of the 1977 and 1980 theatrical sequences of Star Wars and Empire—or copies of the 1997 Special Edition versions—have been archived by the NFR, or indeed if any copy has been provided by Lucasfilm and accepted by the Registry.[57][58]

text: Television and internet[edit]

text: Animated series[edit]

text:
Title
Seasons
Episodes
Release year
Supervising Director
Production company
Network
Setting
Canon

Droids
1
13
1985–86

Nelvana
ABC
Between Revenge of the Sith and A New Hope
No

Ewoks
2
35
1985–86

Before Return of the Jedi

Clone Wars (2003)
3
25
2003–05
Genndy Tartakovsky
Cartoon Network Studios
Cartoon Network
Between Attack of the Clones and Revenge of the Sith

The Clone Wars (2008)
6
121
2008–14
Dave Filoni
Lucasfilm Animation
Cartoon Network (Season 1–5) and Netflix (Season 6)
Between Attack of the Clones and Revenge of the Sith
Yes

Rebels
4
75
2014–18
Dave Filoni (Season 1 and 2) and Justin Ridge (Season 3 and 4)
Disney XD
Between Revenge of the Sith and A New Hope

Forces of Destiny
2
16
2017

YouTube
Across all eras

text: Television films and specials[edit]

text:
Film
Release date
Director(s)
Screen writer(s)
Network
Setting
Canon

Holiday Special

Holiday Special
November 17, 1978
David Acomba and Steve Binder
Bruce Vilanch
CBS
Between A New Hope and The Empire Strikes Back
No

Ewok television films

Caravan of Courage: An Ewok Adventure
November 25, 1984
John Korty
Bob Carrau

Story by: George Lucas
ABC
Between The Empire Strikes Back and Return of the Jedi
No

Ewoks: The Battle for Endor
November 24, 1985
Jim Wheat and Ken Wheat
Jim Wheat and Ken Wheat

Story by: George Lucas

text: Critical and public response[edit]

text:
Film
Rotten Tomatoes
Metacritic
CinemaScore

Holiday Special
43% (7 reviews)[59]

Caravan of Courage: An Ewok Adventure
25% (12 reviews)[60]

Ewoks: The Battle for Endor

List indicator(s)

A dark grey cell indicates the information is not available for the film.
No critical consensus has been reached for either film.

text: Parodies[edit]

text: Lucasfilm Star Wars parodies[edit]

text: The following parodies were directly produced by Lucasfilm.

text:
Title
Release year
Notes

Mockumentaries

Return of the Ewok
1982
24-minute fictional mockumentary-style movie, focusing on the decision of Warwick Davis to become an actor and act as Wicket the Ewok in Return of the Jedi.[61]

R2-D2: Beneath the Dome
2002
20-minute mockumentary-style movie, focusing on the "true" story of R2-D2's life. It was made as a fun side-project by some of the crew of Star Wars Episode II: Attack of the Clones, but was later released for television and its own DVD.[62]

Animated series

Star Wars Detours
N/A
Produced between 2012 and 2013, this animated animated Star Wars parody series from the creators of Robot Chicken was never released. Star Wars Detours was produced prior to the Disney acquisition,[63] but its release was postponed in 2013 and it ultimately never aired,[64] despite 39 episodes having been completed and 62 additional scripts finished.[65]

text: Lego Star Wars[edit]

text: To promote its sets, Lego has created multiple short films, television specials, and animated series that parody the Star Wars saga. Lego versions of Han Solo, Chewbacca, C-3PO, and Lando cameo aboard the Millennium Falcon in The Lego Movie.[66]

text: Short films[edit]

text:
Title
Release date
Notes

Lego Star Wars: Revenge of the Brick
2005
Short film based on Revenge of the Sith

Lego Star Wars: The Quest for R2-D2
2009
Short film based on Star Wars: The Clone Wars

Lego Star Wars: Bombad Bounty
2010
Short film that follows up The Quest for R2-D2

text: Television specials[edit]

text:
Title
Release year
Notes

Lego Star Wars: The Padawan Menace
2011
Half hour TV special

Lego Star Wars: The Empire Strikes Out
2012
Half hour TV special

text: Animated series[edit]

text:
Title
Release year
Episodes
Notes

Lego Star Wars: The Yoda Chronicles
2013–14
7
Comic television series also known as Star Wars: The New Yoda Chronicles.

Lego Star Wars: Droid Tales
2015
5
Comic television series retelling Episodes I-VI and Star Wars Rebels episode "Droids in Distress".

Lego Star Wars: The Freemaker Adventures
2016–present
26
Comic television series set between Empire Strikes Back and Return of the Jedi.

text: Other licensed Star Wars parodies[edit]

text: Parody Star Wars themed TV specials[edit]

text:
Robot Chicken series have produced three television specials satirizing the Star Wars films ("Robot Chicken: Star Wars", "Episode II", and "III"), the success of the specials led to the development animated parody series Star Wars Detours.[67]
Family Guy series have also produced three Star Wars specials titled "Blue Harvest", "Something, Something, Something, Dark Side" and "It's a Trap!".[68]
Phineas and Ferb parody of Star Wars aired in the summer of 2014, soon after Disney's acquisition of the franchise.[69]

tag: ul

text: Notes[edit]

text:
^ Jump up to: a b Until the deal between 21st Century Fox and The Walt Disney Company has been finalized
Jump up ^ Adjusting for inflation is complicated by the fact that the first four films have had multiple releases in different years, so their earnings cannot be simply adjusted by the initial year of release. Inflation adjusted figures for 2005 can be found in Block, Alex Ben; Wilson, Lucy Autrey, eds. (2010). George Lucas's Blockbusting: A Decade-By-Decade Survey of Timeless Movies Including Untold Secrets of Their Financial and Cultural Success. HarperCollins. p. 519. ISBN 978-0061778896.  Adjustment to constant dollars is undertaken in conjunction with the United States Consumer Price Index provided by the Federal Reserve Bank of Minneapolis, using 2005 as the base year.[12]

tag: ol


document_title: Ted Levine

question_text: who was the bad guy in silence of the lambs

text: Ted Levine

text: Early life and career[edit]

text: Levine was born in Bellaire, Ohio, the son of Charlotte Virginia (Clark) and Milton Dmitri Levine,[1] who were both doctors and members of Physicians for Social Responsibility. Levine's father was of Russian Jewish descent and his mother had Welsh ancestry. He describes himself as a "hillbilly Jew".[2] He grew up in Oak Park, Illinois. In 1975, he enrolled at Marlboro College. He became a fixture in the Chicago theatre scene and joined the Remains Theatre which was co-founded by Gary Cole and William Petersen. After his stage experience, Levine began to devote most of his energy during the 1980s toward finding roles in film and television.

text: Mainstream success[edit]

text: After his breakout role in The Silence of the Lambs (as primary antagonist Buffalo Bill), there was a period where he was typecast in villainous roles. Levine was able to remedy this by playing more positive characters, such as a member of Al Pacino's police unit in Heat, astronaut Alan Shepard in the HBO mini-series From the Earth to the Moon, and Paul Walker's police superior Sergeant Tanner in The Fast and the Furious. In the drama Georgia, he played Mare Winningham's husband, one of his most sympathetic roles. His résumé also includes an uncredited role as the voice of the sociopathic trucker "Rusty Nail" in 2001's Joy Ride, and his performance as Detective Sam Nico in the 2003 film Wonderland, based on the gruesome murders in the Hollywood Hills. From 2002 to 2009, he co-starred as Captain Leland Stottlemeyer on USA Network's detective series Monk, starring Tony Shalhoub.

text: Levine provided the voice of the supervillain Sinestro in Superman: The Animated Series, Static Shock, Justice League, and Justice League Unlimited. Levine also appeared as a patriarch whose family takes a turn for the worse in the remake of The Hills Have Eyes (2006). In 2007, he portrayed local Sheriff James Timberlake in The Assassination of Jesse James by the Coward Robert Ford and appeared in Ridley Scott's American Gangster, alongside Denzel Washington and Russell Crowe. In 2010, he appeared as the warden of the island prison in Shutter Island, starring Leonardo DiCaprio. In 2012, he appeared as Sheriff Bloom Towne in Deep Dark Canyon, alongside Spencer Treat Clark and Nick Eversman, who portray Sheriff Towne's sons, Nate and Skylar, respectively. In 2013, he had a major supporting role in the FX murder mystery series The Bridge as Lieutenant Hank Wade, commander of a police homicide unit in a Texas border city.[3] In 2014 he portrayed General Underwood in the British-Finnish action film Big Game.[4] In February 2017, Levine was cast in Jurassic World: Fallen Kingdom as Ken Wheatley.[5]

text: Filmography[edit]

text: Feature films[edit]

text:
Year
Title
Role
Notes

1986
One More Saturday Night
Cop in Station

1987
Ironweed
Pocono Pete

1988
Betrayed
Wes

1989
Next of Kin
Willy Simpson

1990
Love at Large
Frederick King/James McGraw

1991
The Silence of the Lambs
Jame "Buffalo Bill" Gumb

1992
The Paint Job
Kenny the D.J.

1993
Nowhere to Run
Mr. Dunston

1994
Todo cambia
Vince

1995
The Mangler
Officer John Hunton

1995
Georgia
Jake

1995
Heat
Det. Mike Bosko

1996
Bullet
Louis Stein

1997
Mad City
Lemke

1997
Switchback
Deputy Nate Booker

1997
Flubber
Wesson

1998
You Can Thank Me Later
Eli Cooperberg

1999
Wild Wild West
General 'Bloodbath' McGrath

2001
Evolution
General Russell Woodman

2001
The Fast and the Furious
Sgt. Tanner

2001
Joy Ride
Rusty Nail
Voice role

2001
Ali
Joe Smiley

2002
The Truth About Charlie
Emil Zadapec

2003
Wonderland
Sam Nico

2004
The Manchurian Candidate
Colonel Howard

2004
Birth
Mr. Conte

2005
The L.A. Riot Spectacular
Tom Saltine

2005
Memoirs of a Geisha
Colonel Derricks

2006
The Hills Have Eyes
Big Bob Carter

2007
The Assassination of Jesse James by the Coward Robert Ford
Sheriff James Timberlake

2007
American Gangster
Capt. Lou Toback

2010
Shutter Island
Warden

2012
Deep Dark Canyon
Bloom Towne

2013
Jimmy
James Lee Mitchell

2013
A Single Shot
Cecile

2013
Banshee Chapter
Thomas Blackburn

2014
Big Game
General Underwood

2014
Dig Two Graves
Sheriff Waterhouse

2014
Gutshot Straight
Lewis

2015
Little Boy
Sam

2016
Bleed for This
Lou Duva

2017
Bottom of the World
The Preacher

2018
Jurassic World: Fallen Kingdom
Ken Wheatley
Post-production

2018
A Violent Separation
Quinn
filming

text: Television[edit]

text:
Year
Title
Role
Notes

1983
Through Naked Eyes
Patrolman
Movie

1985
Two Fathers' Justice
Bennett
Movie

1985
American Playhouse
Commander
Episode: "The Killing Floor"

1986
Crime Story
Frank Holman
Movie

1986–87
Crime Story
Frank Holman
13 episodes

1989
The Fulfillment of Mary Gray
Jonathan
Movie

1991
Murder in High Places
Carson Russell
Movie

1991
Dead and Alive: The Race for Gus Farace
Charles Rose
Movie

1993
Death Train
Alex Tierney
Movie

1993
The Last Outlaw
Potts
Movie

1993
Broken Promises: Taking Emily Back
Gary Ward
Movie

1995
Nowhere Man
Dave 'Eddie' Powers
2 episodes (voice)

1996
Wiseguy
Paul Callendar
Movie

1997
1999
Superman: The Animated Series
Karkull
Sinestro
"Absolute Zero"
"In Brightest Day"

1997
Ellen Foster
Bill Hammond
Movie

1998
From the Earth to the Moon
Alan Shepard
2 episodes

1998
Moby Dick
Starbuck
Movie

2000
Harlan County War
Silas Kincaid
Movie

2000
Wonderland
Dr. Robert Banger
8 Episodes

2002
Third Watch
Brian O’Malley
Episode: "Falling"

2002–06
Justice League
Bulldozer / Sinestro
6 Episodes (voice)

2002–09
Monk
Captain Leland Stottlemeyer
125 Episodes

2004
Static Shock
Sinestro
Episode: "Fallen Hero"

2011
Hell on Wheels
Captain Daniel Johnson
Recurring

2011
Luck
Isadore Cohen
5 episodes

2013–14
The Bridge
Lt. Hank Wade
Main role (26 episodes)

2014
Child of Grace
Chief Edwards
Movie

2015
The Spoils Before Dying
Gerhart Moll
Episode: "The Trip Trap"

2016
Mad Dogs
Conrad Tull
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document_title: Epidemiology

question_text: epidemiologists attempt to explain the link between health and variables such as

question_tokens: epidemiologists attempt to explain the link between health and variables such as

text: Epidemiology

text: Etymology[edit]

text: Epidemiology, literally meaning "the study of what is upon the people", is derived from Greek epi, meaning 'upon, among', demos, meaning 'people, district', and logos, meaning 'study, word, discourse', suggesting that it applies only to human populations. However, the term is widely used in studies of zoological populations (veterinary epidemiology), although the term "epizoology" is available, and it has also been applied to studies of plant populations (botanical or plant disease epidemiology).[2]

text: The distinction between "epidemic" and "endemic" was first drawn by Hippocrates,[3] to distinguish between diseases that are "visited upon" a population (epidemic) from those that "reside within" a population (endemic).[4] The term "epidemiology" appears to have first been used to describe the study of epidemics in 1802 by the Spanish physician Villalba in Epidemiología Española.[4] Epidemiologists also study the interaction of diseases in a population, a condition known as a syndemic.

text: The term epidemiology is now widely applied to cover the description and causation of not only epidemic disease, but of disease in general, and even many non-disease, health-related conditions, such as high blood pressure and obesity. Therefore, this epidemiology is based upon how the pattern of the disease cause changes in the function of everyone.

text: History[edit]

text: The Greek physician Hippocrates is known as the father of medicine,[5][6] sought a logic to sickness; he is the first person known to have examined the relationships between the occurrence of disease and environmental influences.[7] Hippocrates believed sickness of the human body to be caused by an imbalance of the four humors (air, fire, water and earth “atoms”). The cure to the sickness was to remove or add the humor in question to balance the body. This belief led to the application of bloodletting and dieting in medicine.[8] He coined the terms endemic (for diseases usually found in some places but not in others) and epidemic (for diseases that are seen at some times but not others).[9]

text: Modern era[edit]

text: In the middle of the 16th century, a doctor from Verona named Girolamo Fracastoro was the first to propose a theory that these very small, unseeable, particles that cause disease were alive. They were considered to be able to spread by air, multiply by themselves and to be destroyable by fire. In this way he refuted Galen's miasma theory (poison gas in sick people). In 1543 he wrote a book De contagione et contagiosis morbis, in which he was the first to promote personal and environmental hygiene to prevent disease. The development of a sufficiently powerful microscope by Antonie van Leeuwenhoek in 1675 provided visual evidence of living particles consistent with a germ theory of disease.

text: Wu Youke (1582–1652) developed the concept that some diseases were caused by transmissible agents, which he called liqi (pestilential factors). His book Wenyi Lun (Treatise on Acute Epidemic Febrile Diseases) can be regarded as the main etiological work that brought forward the concept, ultimately attributed to Westerners, of germs as a cause of epidemic diseases (source: http://baike.baidu.com/view/143117.htm). His concepts are still considered in current scientific research in relation to Traditional Chinese Medicine studies (see: http://apps.who.int/medicinedocs/en/d/Js6170e/4.html).

text: Another pioneer, Thomas Sydenham (1624–1689), was the first to distinguish the fevers of Londoners in the later 1600s. His theories on cures of fevers met with much resistance from traditional physicians at the time. He was not able to find the initial cause of the smallpox fever he researched and treated.[8]

text: John Graunt, a haberdasher and amateur statistician, published Natural and Political Observations ... upon the Bills of Mortality in 1662. In it, he analysed the mortality rolls in London before the Great Plague, presented one of the first life tables, and reported time trends for many diseases, new and old. He provided statistical evidence for many theories on disease, and also refuted some widespread ideas on them.

text: John Snow is famous for his investigations into the causes of the 19th century cholera epidemics, and is also known as the father of (modern) epidemiology.[10][11] He began with noticing the significantly higher death rates in two areas supplied by Southwark Company. His identification of the Broad Street pump as the cause of the Soho epidemic is considered the classic example of epidemiology. Snow used chlorine in an attempt to clean the water and removed the handle; this ended the outbreak. This has been perceived as a major event in the history of public health and regarded as the founding event of the science of epidemiology, having helped shape public health policies around the world.[12][13] However, Snow’s research and preventive measures to avoid further outbreaks were not fully accepted or put into practice until after his death.

text: Other pioneers include Danish physician Peter Anton Schleisner, who in 1849 related his work on the prevention of the epidemic of neonatal tetanus on the Vestmanna Islands in Iceland.[14][15] Another important pioneer was Hungarian physician Ignaz Semmelweis, who in 1847 brought down infant mortality at a Vienna hospital by instituting a disinfection procedure. His findings were published in 1850, but his work was ill-received by his colleagues, who discontinued the procedure. Disinfection did not become widely practiced until British surgeon Joseph Lister 'discovered' antiseptics in 1865 in light of the work of Louis Pasteur.

text: In the early 20th century, mathematical methods were introduced into epidemiology by Ronald Ross, Janet Lane-Claypon, Anderson Gray McKendrick, and others.[16][17][18][19]

text: Another breakthrough was the 1954 publication of the results of a British Doctors Study, led by Richard Doll and Austin Bradford Hill, which lent very strong statistical support to the link between tobacco smoking and lung cancer.

text: In the late 20th century, with advancement of biomedical sciences, a number of molecular markers in blood, other biospecimens and environment were identified as predictors of development or risk of a certain disease. Epidemiology research to examine the relationship between these biomarkers analyzed at the molecular level, and disease was broadly named “molecular epidemiology”. Specifically, "genetic epidemiology" has been used for epidemiology of germline genetic variation and disease. Genetic variation is typically determined using DNA from peripheral blood leukocytes. Since the 2000s, genome-wide association studies (GWAS) have been commonly performed to identify genetic risk factors for many diseases and health conditions.

text: While most molecular epidemiology studies are still using conventional disease diagnosis and classification systems, it is increasingly recognized that disease evolution represents inherently heterogeneous processes differing from person to person. Conceptually, each individual has a unique disease process different from any other individual (“the unique disease principle”),[20][21] considering uniqueness of the exposome (a totality of endogenous and exogenous / environmental exposures) and its unique influence on molecular pathologic process in each individual. Studies to examine the relationship between an exposure and molecular pathologic signature of disease (particularly cancer) became increasingly common throughout the 2000s. However, the use of molecular pathology in epidemiology posed unique challenges including lack of research guidelines and standardized statistical methodologies, and paucity of interdisciplinary experts and training programs.[22] Furthermore, the concept of disease heterogeneity appears to conflict with the long-standing premise in epidemiology that individuals with the same disease name have similar etiologies and disease processes. To resolve these issues and advance population health science in the era of molecular precision medicine, “molecular pathology” and “epidemiology” was integrated to create a new interdisciplinary field of “molecular pathological epidemiology” (MPE),[23][24] defined as “epidemiology of molecular pathology and heterogeneity of disease”. In MPE, investigators analyze the relationships between; (A) environmental, dietary, lifestyle and genetic factors; (B) alterations in cellular or extracellular molecules; and (C) evolution and progression of disease. A better understanding of heterogeneity of disease pathogenesis will further contribute to elucidate etiologies of disease. The MPE approach can be applied to not only neoplastic diseases but also non-neoplastic diseases.[25] The concept and paradigm of MPE have become widespread in the 2010s.[26][27][28][29][30][31][32]

text: Types of studies[edit]

text: Epidemiologists employ a range of study designs from the observational to experimental and generally categorized as descriptive, analytic (aiming to further examine known associations or hypothesized relationships), and experimental (a term often equated with clinical or community trials of treatments and other interventions). In observational studies, nature is allowed to “take its course," as epidemiologists observe from the sidelines. Conversely, in experimental studies, the epidemiologist is the one in control of all of the factors entering a certain case study.[33] Epidemiological studies are aimed, where possible, at revealing unbiased relationships between exposures such as alcohol or smoking, biological agents, stress, or chemicals to mortality or morbidity. The identification of causal relationships between these exposures and outcomes is an important aspect of epidemiology. Modern epidemiologists use informatics as a tool.

text: Observational studies have two components, descriptive and analytical. Descriptive observations pertain to the “who, what, where and when of health-related state occurrence”. However, analytical observations deal more with the ‘how’ of a health-related event.[33] Experimental epidemiology contains three case types: randomized controlled trials (often used for new medicine or drug testing), field trials (conducted on those at a high risk of contracting a disease), and community trials (research on social originating diseases).[33]

text: The term 'epidemiologic triad' is used to describe the intersection of Host, Agent, and Environment in analyzing an outbreak.

text: Case series[edit]

text: Case-series may refer to the qualitative study of the experience of a single patient, or small group of patients with a similar diagnosis, or to a statistical factor with the potential to produce illness with periods when they are unexposed.

text: The former type of study is purely descriptive and cannot be used to make inferences about the general population of patients with that disease. These types of studies, in which an astute clinician identifies an unusual feature of a disease or a patient's history, may lead to formulation of a new hypothesis. Using the data from the series, analytic studies could be done to investigate possible causal factors. These can include case control studies or prospective studies. A case control study would involve matching comparable controls without the disease to the cases in the series. A prospective study would involve following the case series over time to evaluate the disease's natural history.[34]

text: The latter type, more formally described as self-controlled case-series studies, divide individual patient follow-up time into exposed and unexposed periods and use fixed-effects Poisson regression processes to compare the incidence rate of a given outcome between exposed and unexposed periods. This technique has been extensively used in the study of adverse reactions to vaccination, and has been shown in some circumstances to provide statistical power comparable to that available in cohort studies.

text: Case-control studies[edit]

text: Case-control studies select subjects based on their disease status. It is a retrospective study. A group of individuals that are disease positive (the "case" group) is compared with a group of disease negative individuals (the "control" group). The control group should ideally come from the same population that gave rise to the cases. The case-control study looks back through time at potential exposures that both groups (cases and controls) may have encountered. A 2×2 table is constructed, displaying exposed cases (A), exposed controls (B), unexposed cases (C) and unexposed controls (D). The statistic generated to measure association is the odds ratio (OR), which is the ratio of the odds of exposure in the cases (A/C) to the odds of exposure in the controls (B/D), i.e. OR = (AD/BC).

text:
Cases
Controls

Exposed
A
B

Unexposed
C
D

text: If the OR is significantly greater than 1, then the conclusion is "those with the disease are more likely to have been exposed," whereas if it is close to 1 then the exposure and disease are not likely associated. If the OR is far less than one, then this suggests that the exposure is a protective factor in the causation of the disease. Case-control studies are usually faster and more cost effective than cohort studies, but are sensitive to bias (such as recall bias and selection bias). The main challenge is to identify the appropriate control group; the distribution of exposure among the control group should be representative of the distribution in the population that gave rise to the cases. This can be achieved by drawing a random sample from the original population at risk. This has as a consequence that the control group can contain people with the disease under study when the disease has a high attack rate in a population.

text: A major drawback for case control studies is that, in order to be considered to be statistically significant, the minimum number of cases required at the 95% confidence interval is related to the odds ratio by the equation:

text: where N is the ratio of cases to controls. As the odds ratio approached 1, approaches 0; rendering case control studies all but useless for low odds ratios. For instance, for an odds ratio of 1.5 and cases = controls, the table shown above would look like this:

text:
Cases
Controls

Exposed
103
84

Unexposed
84
103

text: For an odds ratio of 1.1:

text:
Cases
Controls

Exposed
1732
1652

Unexposed
1652
1732

text: Cohort studies[edit]

text: Cohort studies select subjects based on their exposure status. The study subjects should be at risk of the outcome under investigation at the beginning of the cohort study; this usually means that they should be disease free when the cohort study starts. The cohort is followed through time to assess their later outcome status. An example of a cohort study would be the investigation of a cohort of smokers and non-smokers over time to estimate the incidence of lung cancer. The same 2×2 table is constructed as with the case control study. However, the point estimate generated is the relative risk (RR), which is the probability of disease for a person in the exposed group, Pe = A / (A + B) over the probability of disease for a person in the unexposed group, Pu = C / (C + D), i.e. RR = Pe / Pu.

text:
.....
Case
Non-case
Total

Exposed
A
B
(A + B)

Unexposed
C
D
(C + D)

text: As with the OR, a RR greater than 1 shows association, where the conclusion can be read "those with the exposure were more likely to develop disease."

text: Prospective studies have many benefits over case control studies. The RR is a more powerful effect measure than the OR, as the OR is just an estimation of the RR, since true incidence cannot be calculated in a case control study where subjects are selected based on disease status. Temporality can be established in a prospective study, and confounders are more easily controlled for. However, they are more costly, and there is a greater chance of losing subjects to follow-up based on the long time period over which the cohort is followed.

text: Cohort studies also are limited by the same equation for number of cases as for cohort studies, but, if the base incidence rate in the study population is very low, the number of cases required is reduced by ½.

text: Outbreak investigation[edit]

text: Causal inference[edit]

text: Although epidemiology is sometimes viewed as a collection of statistical tools used to elucidate the associations of exposures to health outcomes, a deeper understanding of this science is that of discovering causal relationships.

text: "Correlation does not imply causation" is a common theme for much of the epidemiological literature. For epidemiologists, the key is in the term inference. Correlation, or at least association between two variables, is a necessary but not sufficient criteria for inference that one variable causes the other. Epidemiologists use gathered data and a broad range of biomedical and psychosocial theories in an iterative way to generate or expand theory, to test hypotheses, and to make educated, informed assertions about which relationships are causal, and about exactly how they are causal.

text: Epidemiologists emphasize that the "one cause – one effect" understanding is a simplistic mis-belief.[citation needed] Most outcomes, whether disease or death, are caused by a chain or web consisting of many component causes.[35] Causes can be distinguished as necessary, sufficient or probabilistic conditions. If a necessary condition can be identified and controlled (e.g., antibodies to a disease agent, energy in an injury), the harmful outcome can be avoided (Robertson, 2015).

text: Bradford Hill criteria[edit]

text: In 1965, Austin Bradford Hill proposed a series of considerations to help assess evidence of causation,[36] which have come to be commonly known as the "Bradford Hill criteria". In contrast to the explicit intentions of their author, Hill's considerations are now sometimes taught as a checklist to be implemented for assessing causality.[37] Hill himself said "None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required sine qua non."[36]

text:
Strength of Association: A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.[36]
Consistency of Data: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.[36]
Specificity: Causation is likely if a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.[36]
Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).[36]
Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.[36]
Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).[36]
Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that "... lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations".[36]
Experiment: "Occasionally it is possible to appeal to experimental evidence".[36]
Analogy: The effect of similar factors may be considered.[36]

text: Legal interpretation[edit]

text: Epidemiological studies can only go to prove that an agent could have caused, but not that it did cause, an effect in any particular case:

text: "Epidemiology is concerned with the incidence of disease in populations and does not address the question of the cause of an individual's disease. This question, sometimes referred to as specific causation, is beyond the domain of the science of epidemiology. Epidemiology has its limits at the point where an inference is made that the relationship between an agent and a disease is causal (general causation) and where the magnitude of excess risk attributed to the agent has been determined; that is, epidemiology addresses whether an agent can cause a disease, not whether an agent did cause a specific plaintiff's disease."[38]

text: In United States law, epidemiology alone cannot prove that a causal association does not exist in general. Conversely, it can be (and is in some circumstances) taken by US courts, in an individual case, to justify an inference that a causal association does exist, based upon a balance of probability.

text: The subdiscipline of forensic epidemiology is directed at the investigation of specific causation of disease or injury in individuals or groups of individuals in instances in which causation is disputed or is unclear, for presentation in legal settings.

text: Population-based health management[edit]

text: Epidemiological practice and the results of epidemiological analysis make a significant contribution to emerging population-based health management frameworks.

text: Population-based health management encompasses the ability to:

text:
Assess the health states and health needs of a target population;
Implement and evaluate interventions that are designed to improve the health of that population; and
Efficiently and effectively provide care for members of that population in a way that is consistent with the community's cultural, policy and health resource values.

text: Modern population-based health management is complex, requiring a multiple set of skills (medical, political, technological, mathematical etc.) of which epidemiological practice and analysis is a core component, that is unified with management science to provide efficient and effective health care and health guidance to a population. This task requires the forward looking ability of modern risk management approaches that transform health risk factors, incidence, prevalence and mortality statistics (derived from epidemiological analysis) into management metrics that not only guide how a health system responds to current population health issues, but also how a health system can be managed to better respond to future potential population health issues.[39]

text: Examples of organizations that use population-based health management that leverage the work and results of epidemiological practice include Canadian Strategy for Cancer Control, Health Canada Tobacco Control Programs, Rick Hansen Foundation, Canadian Tobacco Control Research Initiative.[40][41][42]

text: Each of these organizations use a population-based health management framework called Life at Risk that combines epidemiological quantitative analysis with demographics, health agency operational research and economics to perform:

text:
Population Life Impacts Simulations: Measurement of the future potential impact of disease upon the population with respect to new disease cases, prevalence, premature death as well as potential years of life lost from disability and death;
Labour Force Life Impacts Simulations: Measurement of the future potential impact of disease upon the labour force with respect to new disease cases, prevalence, premature death and potential years of life lost from disability and death;
Economic Impacts of Disease Simulations: Measurement of the future potential impact of disease upon private sector disposable income impacts (wages, corporate profits, private health care costs) and public sector disposable income impacts (personal income tax, corporate income tax, consumption taxes, publicly funded health care costs).

text: Applied field epidemiology[edit]

text: Applied epidemiology is the practice of using epidemiological methods to protect or improve the health of a population. Applied field epidemiology can include investigating communicable and non-communicable disease outbreaks, mortality and morbidity rates, and nutritional status, among other indicators of health, with the purpose of communicating the results to those who can implement appropriate policies or disease control measures.

text: Humanitarian context[edit]

text: As the surveillance and reporting of diseases and other health factors becomes increasingly difficult in humanitarian crisis situations, the methodologies used to report the data are compromised. One study found that less than half (42.4%) of nutrition surveys sampled from humanitarian contexts correctly calculated the prevalence of malnutrition and only one-third (35.3%) of the surveys met the criteria for quality. Among the mortality surveys, only 3.2% met the criteria for quality. As nutritional status and mortality rates help indicate the severity of a crisis, the tracking and reporting of these health factors is crucial.

text: Vital registries are usually the most effective ways to collect data, but in humanitarian contexts these registries can be non-existent, unreliable, or inaccessible. As such, mortality is often inaccurately measured using either prospective demographic surveillance or retrospective mortality surveys. Prospective demographic surveillance requires lots of manpower and is difficult to implement in a spread-out population. Retrospective morality surveys are prone to selection and reporting biases. Other methods are being developed, but are not common practice yet.

text: WHO, “Health topics: Epidemiology.” http://www.who.int/topics/epidemiology/en/ Accessed: October 30, 2017.

text: Porta, Miquel. “A Dictionary of Epidemiology.” Sixth Edition. International Epidemiological Society. Oxford University Press. 2014. Accessed: October 30, 2017.

text: Prudhon, C & Spiegel, P. “A review of methodology and analysis of nutrition and mortality surveys conducted in humanitarian emergencies from October 1993 to April 2004” Emerging Themes in Epidemiology 2007, 4:10. http://www.ete-online.com/content/4/1/10 Accessed: October 30, 2017.

text: Roberts, B et al. “A new method to estimate mortality in crisis-affected and resource-poor settings: validation study.” International Journal of Epidemiology 2010;39:1584–1596. Accessed: October 30, 2017.

text: Validity: precision and bias[edit]

text: Different fields in epidemiology have different levels of validity. One way to assess the validity of findings is the ratio of false-positives (claimed effects that are not correct) to false-negatives (studies which fail to support a true effect). To take the field of genetic epidemiology, candidate-gene studies produced over 100 false-positive findings for each false-negative. By contrast genome-wide association appear close to the reverse, with only one false positive for every 100 or more false-negatives.[43] This ratio has improved over time in genetic epidemiology as the field has adopted stringent criteria. By contrast other epidemiological fields have not required such rigorous reporting and are much less reliable as a result.[43]

text: Random error[edit]

text: Random error is the result of fluctuations around a true value because of sampling variability. Random error is just that: random. It can occur during data collection, coding, transfer, or analysis. Examples of random error include: poorly worded questions, a misunderstanding in interpreting an individual answer from a particular respondent, or a typographical error during coding. Random error affects measurement in a transient, inconsistent manner and it is impossible to correct for random error.

text: There is random error in all sampling procedures. This is called sampling error.

text: Precision in epidemiological variables is a measure of random error. Precision is also inversely related to random error, so that to reduce random error is to increase precision. Confidence intervals are computed to demonstrate the precision of relative risk estimates. The narrower the confidence interval, the more precise the relative risk estimate.

text: There are two basic ways to reduce random error in an epidemiological study. The first is to increase the sample size of the study. In other words, add more subjects to your study. The second is to reduce the variability in measurement in the study. This might be accomplished by using a more precise measuring device or by increasing the number of measurements.

text: Note, that if sample size or number of measurements are increased, or a more precise measuring tool is purchased, the costs of the study are usually increased. There is usually an uneasy balance between the need for adequate precision and the practical issue of study cost.

text: Systematic error[edit]

text: A systematic error or bias occurs when there is a difference between the true value (in the population) and the observed value (in the study) from any cause other than sampling variability. An example of systematic error is if, unknown to you, the pulse oximeter you are using is set incorrectly and adds two points to the true value each time a measurement is taken. The measuring device could be precise but not accurate. Because the error happens in every instance, it is systematic. Conclusions you draw based on that data will still be incorrect. But the error can be reproduced in the future (e.g., by using the same mis-set instrument).

text: A mistake in coding that affects all responses for that particular question is another example of a systematic error.

text: The validity of a study is dependent on the degree of systematic error. Validity is usually separated into two components:

text:
Internal validity is dependent on the amount of error in measurements, including exposure, disease, and the associations between these variables. Good internal validity implies a lack of error in measurement and suggests that inferences may be drawn at least as they pertain to the subjects under study.
External validity pertains to the process of generalizing the findings of the study to the population from which the sample was drawn (or even beyond that population to a more universal statement). This requires an understanding of which conditions are relevant (or irrelevant) to the generalization. Internal validity is clearly a prerequisite for external validity.

text: Selection bias[edit]

text: Selection bias occurs when study subjects are selected or become part of the study as a result of a third, unmeasured variable which is associated with both the exposure and outcome of interest.[44] For instance, it has repeatedly been noted that cigarette smokers and non smokers tend to differ in their study participation rates. (Sackett D cites the example of Seltzer et al., in which 85% of non smokers and 67% of smokers returned mailed questionnaires.)[45] It is important to note that such a difference in response will not lead to bias if it is not also associated with a systematic difference in outcome between the two response groups.

text: Information bias[edit]

text: Information bias is bias arising from systematic error in the assessment of a variable.[46] An example of this is recall bias. A typical example is again provided by Sackett in his discussion of a study examining the effect of specific exposures on fetal health: "in questioning mothers whose recent pregnancies had ended in fetal death or malformation (cases) and a matched group of mothers whose pregnancies ended normally (controls) it was found that 28% of the former, but only 20% of the latter, reported exposure to drugs which could not be substantiated either in earlier prospective interviews or in other health records".[45] In this example, recall bias probably occurred as a result of women who had had miscarriages having an apparent tendency to better recall and therefore report previous exposures.

text: Confounding[edit]

text: Confounding has traditionally been defined as bias arising from the co-occurrence or mixing of effects of extraneous factors, referred to as confounders, with the main effect(s) of interest.[46][47] A more recent definition of confounding invokes the notion of counterfactual effects.[47] According to this view, when one observes an outcome of interest, say Y=1 (as opposed to Y=0), in a given population A which is entirely exposed (i.e. exposure X = 1 for every unit of the population) the risk of this event will be RA1. The counterfactual or unobserved risk RA0 corresponds to the risk which would have been observed if these same individuals had been unexposed (i.e. X = 0 for every unit of the population). The true effect of exposure therefore is: RA1 − RA0 (if one is interested in risk differences) or RA1/RA0 (if one is interested in relative risk). Since the counterfactual risk RA0 is unobservable we approximate it using a second population B and we actually measure the following relations: RA1 − RB0 or RA1/RB0. In this situation, confounding occurs when RA0 ≠ RB0.[47] (NB: Example assumes binary outcome and exposure variables.)

text: Some epidemiologists prefer to think of confounding separately from common categorizations of bias since, unlike selection and information bias, confounding stems from real causal effects.[44]

text: The profession[edit]

text: To date, few universities offer epidemiology as a course of study at the undergraduate level. One notable undergraduate program exists at Johns Hopkins University, where students who major in public health can take graduate level courses, including epidemiology, their senior year at the Bloomberg School of Public Health.[48]

text: Although epidemiologic research is conducted by individuals from diverse disciplines, including clinically trained professionals such as physicians, formal training is available through Masters or Doctoral programs including Master of Public Health (MPH), Master of Science of Epidemiology (MSc.), Doctor of Public Health (DrPH), Doctor of Pharmacy (PharmD), Doctor of Philosophy (PhD), Doctor of Science (ScD). Many other graduate programs, e.g., Doctor of Social Work (DSW), Doctor of Clinical Practice (DClinP), Doctor of Podiatric Medicine (DPM), Doctor of Veterinary Medicine (DVM), Doctor of Nursing Practice (DNP), Doctor of Physical Therapy (DPT), or for clinically trained physicians, Doctor of Medicine (MD) or Bachelor of Medicine and Surgery (MBBS or MBChB) and Doctor of Osteopathic Medicine (DO), include some training in epidemiologic research or related topics, but this training is generally substantially less than offered in training programs focused on epidemiology or public health. Reflecting the strong historical tie between epidemiology and medicine, formal training programs may be set in either schools of public health and medical schools.

text: As public health/health protection practitioners, epidemiologists work in a number of different settings. Some epidemiologists work 'in the field'; i.e., in the community, commonly in a public health/health protection service, and are often at the forefront of investigating and combating disease outbreaks. Others work for non-profit organizations, universities, hospitals and larger government entities such as state and local health departments, various Ministries of Health, Doctors without Borders, the Centers for Disease Control and Prevention (CDC), the Health Protection Agency, the World Health Organization (WHO), or the Public Health Agency of Canada. Epidemiologists can also work in for-profit organizations such as pharmaceutical and medical device companies in groups such as market research or clinical development.


document_title: Blood volume

question_text: what is the approximate volume of blood in your body

text: Blood volume

text: Humans[edit]

text: A typical adult has a blood volume of approximately 5 liters, with females generally having less blood volume than males.[1] Blood volume is regulated by the kidneys.

text: Blood volume (BV) can be calculated given the hematocrit (HC; the fraction of blood that is red blood cells) and plasma volume (PV), with the hematocrit being regulated via the blood oxygen content regulator:

text: Blood volume measurement may be used in people with congestive heart failure, chronic hypertension, renal failure and critical care.

text: The use of relative blood volume changes during dialysis is of questionable utility.[2]

text: Total Blood Volume can be measured manually via the Dual Isotope or Dual Tracer Technique, a classic technique, available since the 1950s.[3] This technique requires double labeling of the blood; that is 2 injections and 2 standards (51Cr-RBC for tagging red blood cells and I-HAS for tagging plasma volume)as well as withdrawing and re-infusing patients with their own blood for blood volume analysis results. This method may take up to 6 hours for accurate results.

text: Semi-automated system[edit]

text: Blood Volume may also be measured semi-automatically. The Daxor BVA-100 consists of an automated well counter interfaced with a computer.[4] It is able to report Total Blood Volume (TBV), Plasma Volume (PV) and Red Cell Volume (RCV) using the indicator dilution principle, microhematocrit centrifugation and the Ideal Height and Weight Method.[3] The indicator or tracer, is an I-131 albumin injection. An equal amount of the tracer is injected into a known and unknown volume. Clinically, the unknown volume is the patient’s blood volume, with the tracer having been injected into the patient’s blood stream and tagged to the blood plasma. Once the tracer is injected a technician takes five blood samples which undergo microhematocrit centrifugation to extrapolate true blood volume at time 0. The concentration of the I-131 in the blood is determined from the blood radioactivity against the standard, which has a known I-131 dilution in a known volume. The unknown volume is inversely proportional to the concentration of the indicator in the known volume; the larger the unknown volume, the lower the tracer concentration, thus the unknown volume can be calculated. The microhematocrit data along with the I-131 indicator data provide a normalized hematocrit number, more accurate than hematocrit or peripheral hematocrit measurements.[5] Measurements are taken 5 times in 6 minute intervals so that the BVA-100 can calculate the albumin transudation time to understand the flux of liquid through capillary membranes.

text: Other animals[edit]

text:
Animal
Blood volume
(ml/kg)[6]

Cat
55 (47-66)

Cow
55 (52-57)[7]

Dog
86 (79-90)

Ferret
75

Gerbil
67

Goat
70

Guinea pig
75 (67-92)

Hamster
78

Horse
76

Human
77

Monkey (rhesus)
54

Mouse
79 (78-80)

Pig
65

Rabbit
56 (44-70)

Rat
64 (50-70)

Sheep
60

Marmoset
60-70[8]

text: The table at right shows circulating blood volumes, given as volume per kilogram, for healthy adults and some animals.[6] However, it can be 15% less in obese and old animals.[6]


document_title: Occupation of the Ruhr

question_text: when did france and belgium invade the ruhr

text: Occupation of the Ruhr

text: Background[edit]

text: The Ruhr region had been occupied by Allied troops in the immediate aftermath of the First World War, during the Allied occupation of the Rhineland (1918–1919).  Under the terms of the Treaty of Versailles (1919), which formally ended the war, Germany accepted responsibility for the damages caused in the war and was obliged to pay war reparations to the various Allies, principally France. The total sum of reparations demanded from Germany—around 226 billion gold marks (US $878 billion in 2018)—was decided by an Inter-Allied Reparations Commission. In 1921, the amount was reduced to 132 billion (at that time, $31.4 billion (US $442 billion in 2018), or £6.6 billion (UK £284 billion in 2018)).[1]  Even with the reduction, the debt was huge.  As some of the payments were in raw materials, German factories were unable to function, and the German economy suffered, further damaging the country's ability to pay.[2]

text: By late 1922, the German defaults on payments had grown so regular that a crisis engulfed the Reparations Commission; the French and Belgian delegates urged occupying the Ruhr as a way of forcing Germany to pay more, while the British delegate urged a lowering of the payments.[3] As a consequence of a German default on timber deliveries in December 1922, the Reparations Commission declared Germany in default, which led to the Franco-Belgian occupation of the Ruhr in January 1923.[4] Particularly galling to the French was that the timber quota the Germans defaulted on was based on an assessment of their capacity the Germans made themselves and subsequently lowered.[5] The Allies believed that the government of Chancellor Wilhelm Cuno had defaulted on the timber deliveries deliberately as a way of testing the will of the Allies to enforce the treaty.[5] The entire conflict was further exacerbated by a German default on coal deliveries in early January 1923, which was the thirty-fourth coal default in the previous thirty-six months.[6] The French Premier Raymond Poincaré was deeply reluctant to order the Ruhr occupation and took this step only after the British had rejected his proposals for non-military sanctions against Germany.[7] Frustrated at Germany not paying reparations, Poincaré hoped for joint Anglo-French economic sanctions against Germany in 1922 and opposed military action. However, by December 1922 he was faced with Anglo-American-German opposition and saw coal for French steel production and payments in money as laid out in the Treaty of Versailles draining away.  Poincaré was exasperated with British opposition, and wrote to the French ambassador in London:

text: Judging others by themselves, the English, who are blinded by their loyalty, have always thought that the Germans did not abide by their pledges inscribed in the Versailles Treaty because they had not frankly agreed to them. ... We, on the contrary, believe that if Germany, far from making the slightest effort to carry out the treaty of peace, has always tried to escape her obligations, it is because until now she has not been convinced of her defeat. ... We are also certain that Germany, as a nation, resigns herself to keep her pledged word only under the impact of necessity.[8]

text: Occupation[edit]

text: Poincaré decided to occupy the Ruhr on 11 January 1923 to extract the reparations himself. The real issue during the Ruhrkampf (Ruhr struggle), as the Germans labelled the battle against the French occupation, was not the German defaults on coal and timber deliveries but the sanctity of the Versailles Treaty.[9] Poincaré often argued to the British that letting the Germans defy Versailles in regards to the reparations would create a precedent that would lead to the Germans dismantling the rest of the Versailles treaty.[10] Finally, Poincaré argued that once the chains that had bound Germany in Versailles were destroyed, it was inevitable that Germany would plunge the world into another world war.[10]

text: Initiated by French Prime Minister Raymond Poincaré, the invasion took place on 11 January 1923. General Alphonse Caron’s 32nd infantry corps under the supervision of General Jean-Marie Degoutte carried out the operation.[11] Some theories state that the French aimed to occupy the centre of German coal, iron, and steel production in the Ruhr area valley simply to get the money. Some others state that France did it to ensure that the reparations were paid in goods, because the Mark was practically worthless because of hyperinflation that already existed at the end of 1922. France had the iron ore and Germany had the coal. Each state wanted free access to the resource it was short of, as together these resources had far more value than separately. (Eventually this problem was resolved in the post-World War II European Coal and Steel community.)

text: Following France's decision to invade the Ruhr,[12] the Inter-Allied Mission for Control of Factories and Mines (MICUM)[13] was set up as a means of ensuring coal repayments from Germany.[14]

text: Passive resistance[edit]

text: The occupation was greeted by a campaign of passive resistance. Approximately 130 German civilians were killed by the French occupation army during the events,  including during civil disobedience protests, e.g. against dismissal of German officials.[15][16] Some theories assert that to pay for passive resistance in the Ruhr, the German government began the hyperinflation that destroyed the German economy in 1923.[9] Others state that the road to hyperinflation was well established before with the reparation payments that started on November 1921,[17] see 1920s German inflation. In the face of economic collapse, with high unemployment and hyperinflation, the strikes were eventually called off in September 1923 by the new Gustav Stresemann coalition government, which was followed by a state of emergency. Despite this, civil unrest grew into riots and coup attempts targeted at the government of the Weimar Republic, including the Beer Hall Putsch. The Rhenish Republic was proclaimed at Aachen (Aix-la-Chapelle) in October 1923.

text: Though the French did succeed in making their occupation of the Ruhr pay, the Germans through their passive resistance in the Ruhr and the hyperinflation that wrecked their economy, won the world's sympathy, and under heavy Anglo-American financial pressure (the simultaneous decline in the value of the franc made the French very open to pressure from Wall Street and the City), the French were forced to agree to the Dawes Plan of April 1924, which substantially lowered German reparations payments.[18] Under the Dawes Plan, Germany paid only 1 billion marks in 1924, and then increasing amounts for the next three years, until the total rose to 2.25 billion marks by 1927.

text: Sympathy for Germany[edit]

text: Internationally, the French invasion of Germany did much to boost sympathy for the German Republic although no action was taken in the League of Nations since it was technically legal under the Treaty of Versailles.[19] The French, with their own economic problems, eventually accepted the Dawes Plan and withdrew from the occupied areas in July and August 1925. The last French troops evacuated Düsseldorf and Duisburg along with the city's important harbour in Duisburg-Ruhrort, ending French occupation of the Ruhr region on 25 August 1925. According to Sally Marks, the occupation of the Ruhr "was profitable and caused neither the German hyperinflation, which began in 1922 and ballooned because of German responses to the Ruhr occupation, nor the franc's 1924 collapse, which arose from French financial practices and the evaporation of reparations".[20] Marks suggests the profits, after Ruhr-Rhineland occupation costs, were nearly 900 million gold marks.[21]

text: Poincaré[edit]

text: Despite his disagreements with Britain, Poincaré desired to preserve the Anglo-French entente and thus moderated his aims to a degree. His major goal was the winning of the extraction of reparations payments from Germany. His inflexible methods and authoritarian personality led to the failure of his diplomacy.[22]

text: British perspective[edit]

text: When on 12 July 1922, Germany demanded a moratorium on reparation payments, tension developed between the French government of Raymond Poincaré and the Coalition government of David Lloyd George. The British Labour Party demanded peace and denounced Lloyd George as a troublemaker. It saw Germany as the martyr of the postwar period and France as vengeful and the principal threat to peace in Europe. The tension between France and Britain peaked during a conference in Paris in early 1923, by which time the coalition led by Lloyd George had been replaced by the Conservatives. The Labour Party opposed the occupation of the Ruhr throughout 1923, which it rejected as French imperialism. The British Labour Party believed it had won when Poincaré accepted the Dawes Plan in 1924.[23]

text: Aftermath[edit]

text: Dawes Plan[edit]

text: To deal with the implementation of the Dawes Plan, a conference took place in London in July–August 1924.[24] The British Labour Prime Minister Ramsay MacDonald, who viewed reparations as impossible to pay, successfully pressured the French Premier Édouard Herriot into a whole series of concessions to Germany.[24] The British diplomat Sir Eric Phipps commented that “The London Conference was for the French 'man in the street' one long Calvary as he saw M. Herriot abandoning one by one the cherished possessions of French preponderance on the Reparations Commission, the right of sanctions in the event of German default, the economic occupation of the Ruhr, the French-Belgian railroad Régie, and finally, the military occupation of the Ruhr within a year”.[25] The Dawes Plan was significant in European history as it marked the first time that Germany had succeeded in defying Versailles, and revised an aspect of the treaty in its favour.

text: The Saar region remained under French control until 1935.

text: German politics[edit]

text: In German politics, the French occupation of the Rhineland accelerated the formation of right-wing parties. Disoriented by the defeat in the war, conservatives in 1922 founded a consortium of nationalist associations, the "Vereinigten Vaterländischen Verbände Deutschlands" (VVVD, United Patriotic Associations of Germany).  The goal was to forge a united front of the right. In the climate of national resistance against the French Ruhr invasion, the VVVD reached its peak strength. It advocated policies of uncompromising monarchism, corporatism and opposition to the Versailles settlement. However, it lacked internal unity and money and so it never managed to unite the right before it had faded away by the late 1920s, as the Nazis emerged.[26]


document_title: Figure skating at the 2018 Winter Olympics – Men's singles

question_text: who won the mens figure skating in 2018 olympics

text: Summary[edit]

text: With his victory at the 2018 Winter Olympics, Yuzuru Hanyu became the first male figure skater to win two consecutive gold medals after Dick Button, who did so in 1952. Fellow countryman Shoma Uno won the silver medal, and Spain's Javier Fernández won the bronze medal. Fernández won Spain's first figure skating medal and fourth medal at the Winter Olympics.

text: After the short program, Hanyu, Fernández, Uno, and Jin Boyang were first, second, third, and fourth respectively. Nathan Chen, originally one of the favorites for the podium, skated an uncharacteristically poor short program that placed him at 17th, but fought back to win the free skating with a score of 215.08--8.91 points above the second place free skating by Hanyu. He ended up fifth overall. In the free program, Jin Boyang overtook Chen by less than a point overall, and placed fourth.

text: In the victory ceremony, the medals were presented by Tsunekazu Takeda, member of the International Olympic Committee, accompanied by Alexander Lakernik, ISU Figure Skating Vice President.

text: Vincent Zhou landed the first quadruple lutz at the Olympics. Nathan Chen became the first to ever land six quads, five clean. He also landed the first quadruple flip at the Olympics. [5] With these jumps he holds the new record for highest free skating technical score.[6] For complete list of figure skating records, see list of highest scores in figure skating.

text: Qualification[edit]

text: A total of 30 skaters qualified to compete for the event, with each country allowed to only enter a maximum of three. 24 quotas were handed out during the 2017 World Figure Skating Championships and the remaining six were given out at the 2017 CS Nebelhorn Trophy. Each country decided the entry of its teams, and athletes winning the quota were not necessarily granted the right to compete.[7] All athletes competing must have met the minimum total elements score, which does not include component scores. For the short program this was 25.00 and the free skating 45.00.[8]

text: Schedule[edit]

text: All times are (UTC+9).

text:
Date
Time
Round

16 February
10:00[3]
Short program

17 February
10:00[3]
Free skating

text: Results[edit]

text: Short program[edit]

text: The short program was held on 16 February 2018.[3][9]

text:
Pl.
Name
Nation
TSS
TES
PCS
SS
TR
PE
CH
IN
Ded
StN

1
Yuzuru Hanyu
 Japan
111.68
63.18
48.50
9.71
9.43
9.86
9.75
9.75
0.00
25

2
Javier Fernández
 Spain
107.58
59.79
47.79
9.36
9.36
9.71
9.68
9.68
0.00
29

3
Shoma Uno
 Japan
104.17
58.13
46.04
9.29
9.00
9.25
9.29
9.21
0.00
28

4
Jin Boyang
 China
103.32
60.27
43.05
8.79
8.29
8.82
8.54
8.61
0.00
30

5
Dmitri Aliev
 Olympic Athletes from Russia
98.98
56.98
42.00
8.43
8.11
8.50
8.50
8.46
0.00
20

6
Patrick Chan
 Canada
90.01
45.08
45.93
9.36
9.07
9.00
9.29
9.21
–1.00
21

7
Adam Rippon
 United States
87.95
44.48
43.47
8.57
8.43
8.86
8.68
8.93
0.00
19

8
Mikhail Kolyada
 Olympic Athletes from Russia
86.69
43.84
43.85
8.96
8.54
8.64
8.82
8.89
–1.00
27

9
Michal Březina
 Czech Republic
85.15
44.34
40.81
8.25
7.89
8.25
8.21
8.21
0.00
13

10
Keegan Messing
 Canada
85.11
45.50
40.61
8.04
7.96
8.07
8.29
8.25
−1.00
12

11
Jorik Hendrickx
 Belgium
84.74
44.17
40.57
7.96
7.89
8.25
8.18
8.29
0.00
17

12
Vincent Zhou
 United States
84.53
48.50
36.03
7.39
6.96
7.11
7.32
7.25
0.00
3

13
Oleksii Bychenko
 Israel
84.13
43.63
40.50
7.93
7.71
8.36
8.18
8.32
0.00
23

14
Misha Ge
 Uzbekistan
83.90
41.75
42.15
8.18
8.18
8.54
8.46
8.79
0.00
16

15
Cha Jun-hwan
 South Korea
83.43
43.79
39.64
7.93
7.68
8.07
8.00
7.96
0.00
14

16
Brendan Kerry
 Australia
83.06
45.49
37.57
7.57
7.36
7.61
7.57
7.46
0.00
10

17
Nathan Chen
 United States
82.27
41.39
41.88
8.46
8.32
8.14
8.57
8.39
–1.00
26

18
Daniel Samohin
 Israel
80.69
43.29
38.40
7.79
7.29
7.79
7.71
7.82
–1.00
18

19
Yan Han
 China
80.63
40.99
40.64
8.46
8.07
7.86
8.18
8.07
−1.00
8

20
Keiji Tanaka
 Japan
80.05
40.30
40.75
8.36
7.86
8.07
8.21
8.25
–1.00
22

21
Deniss Vasiļjevs
 Latvia
79.52
39.34
41.18
8.25
8.00
8.18
8.39
8.36
–1.00
24

22
Moris Kvitelashvili
 Georgia
76.56
40.88
36.68
7.46
7.11
7.32
7.43
7.36
−1.00
11

23
Matteo Rizzo
 Italy
75.63
39.23
36.40
7.29
7.11
7.29
7.39
7.32
0.00
5

24
Paul Fentz
 Germany
74.73
37.71
37.02
7.46
7.25
7.46
7.46
7.39
0.00
15

Did not advance to free skating

25
Julian Yee
 Malaysia
73.58
38.37
35.21
7.07
6.82
7.11
7.14
7.07
0.00
9

26
Chafik Besseghier
 France
72.10
38.41
33.69
6.79
6.29
6.89
6.86
6.86
0.00
2

27
Denis Ten
 Kazakhstan
70.12
30.77
39.35
8.11
7.82
7.46
8.07
7.89
0.00
4

28
Michael Christian Martinez
 Philippines
55.56
26.04
29.52
5.96
5.64
5.96
6.00
5.96
0.00
6

29
Felipe Montoya
 Spain
52.41
22.59
30.82
6.25
6.07
6.00
6.25
6.25
−1.00
1

30
Yaroslav Paniot
 Ukraine
46.58
18.68
29.90
6.43
5.79
5.61
6.21
5.86
−2.00
7

text:
Notes:
WR - World record
TSS - Total Segment Score; TES - Technical Element Score; PCS - Program Component Score
SS - Skating Skills; TR - Transitions; PE - Performance/Execution
CH - Choreography; IN - Interpretation; Ded - Deduction; StN - Starting Number

text: Free skating[edit]

text: The free skating was held on 17 February 2018.[3][10]

text:
Pl.
Name
Nation
TSS
TES
PCS
SS
TR
PE
CH
IN
Ded
StN

1
Nathan Chen
 United States
215.08
127.64
87.44
8.82
8.32
9.04
8.79
8.75
0.00
9

2
Yuzuru Hanyu
 Japan
206.17
109.55
96.62
9.71
9.50
9.64
9.71
9.75
0.00
22

3
Shoma Uno
 Japan
202.73
111.01
92.72
9.36
9.07
9.25
9.32
9.36
–1.00
24

4
Javier Fernández
 Spain
197.66
101.52
96.14
9.46
9.43
9.64
9.79
9.75
0.00
23

5
Jin Boyang
 China
194.45
109.69
85.76
8.71
8.21
8.64
8.68
8.64
–1.00
20

6
Vincent Zhou
 United States
192.16
112.24
79.92
8.04
7.71
8.25
7.96
8.00
0.00
15

7
Mikhail Kolyada
 Olympic Athletes from Russia
177.56
91.62
87.94
9.00
8.64
8.68
8.86
8.72
–2.00
16

8
Patrick Chan
 Canada
173.42
81.56
91.86
9.32
9.14
8.66
9.29
9.32
0.00
21

9
Oleksii Bychenko
 Israel
172.88
89.08
83.80
8.39
8.04
8.61
8.43
8.43
0.00
7

10
Adam Rippon
 United States
171.41
84.47
86.94
8.75
8.54
8.68
8.71
8.79
0.00
18

11
Daniel Samohin
 Israel
170.75
89.03
81.72
8.32
7.75
8.32
8.18
8.29
0.00
8

12
Keegan Messing
 Canada
170.32
84.88
85.44
8.50
8.29
8.61
8.61
8.71
0.00
14

13
Dmitri Aliev
 Olympic Athletes from Russia
168.53
85.39
85.13
8.64
8.39
8.32
8.61
8.61
–2.00
19

14
Cha Jun-hwan
 South Korea
165.16
84.94
81.22
8.21
7.86
8.25
8.11
8.18
–1.00
13

15
Keiji Tanaka
 Japan
164.78
85.64
81.14
8.36
7.89
8.00
8.18
8.14
–2.00
5

16
Jorik Hendrickx
 Belgium
164.21
81.79
82.42
8.25
7.96
8.36
8.25
8.39
0.00
13

17
Misha Ge
 Uzbekistan
161.04
74.96
86.08
8.46
8.36
8.54
8.75
8.93
0.00
10

18
Michal Březina
 Czech Republic
160.92
76.58
84.34
8.57
8.21
8.39
8.57
8.43
0.00
17

19
Matteo Rizzo
 Italy
156.78
80.86
75.92
7.64
7.32
7.79
7.64
7.57
0.00
2

20
Deniss Vasiļjevs
 Latvia
155.06
76.42
80.64
8.14
7.86
7.96
8.18
8.18
–2.00
1

21
Brendan Kerry
 Australia
150.75
73.33
77.42
7.96
7.54
7.68
7.82
7.71
0.00
12

22
Paul Fentz
 Germany
139.82
66.98
72.84
7.50
7.14
7.14
7.39
7.25
0.00
3

23
Yan Han
 China
132.38
53.80
79.58
8.56
7.82
7.57
8.04
8.00
–1.00
4

24
Moris Kvitelashvili
 Georgia
128.01
63.35
70.66
7.34
6.86
6.68
7.32
7.04
–6.00
6

text:
Notes:
TSS - Total Segment Score; TES - Technical Element Score; PCS - Program Component Score
SS - Skating Skills; TR - Transitions; PE - Performance/Execution
CH - Choreography; IN - Interpretation; Ded - Deduction; StN - Starting Number

text: Overall[edit]

text: The skaters were ranked according to their overall score.[11]

text:
Rank
Name
Nation
TP
SP
FS

01 !
Yuzuru Hanyu
 Japan
317.85
111.68
1
206.17
2

02 !
Shoma Uno
 Japan
306.90
104.17
3
202.73
3

03 !
Javier Fernández
 Spain
305.24
107.58
2
197.66
4

4
Jin Boyang
 China
297.77
103.32
4
194.45
5

5
Nathan Chen
 United States
297.35
82.27
17
215.08
1

6
Vincent Zhou
 United States
276.69
84.53
12
192.16
6

7
Dmitri Aliev
 Olympic Athletes from Russia
267.51
98.98
5
168.53
13

8
Mikhail Kolyada
 Olympic Athletes from Russia
264.25
86.69
8
177.56
7

9
Patrick Chan
 Canada
263.43
90.01
6
173.42
8

10
Adam Rippon
 United States
259.36
87.95
7
171.41
10

11
Oleksii Bychenko
 Israel
257.01
84.13
13
172.88
9

12
Keegan Messing
 Canada
255.43
85.11
10
170.32
12

13
Daniel Samohin
 Israel
251.44
80.69
18
170.75
11

14
Jorik Hendrickx
 Belgium
248.95
84.74
11
164.21
16

15
Cha Jun-hwan
 South Korea
248.59
83.43
15
165.16
14

16
Michal Březina
 Czech Republic
246.07
85.15
9
160.92
18

17
Misha Ge
 Uzbekistan
244.94
83.90
14
161.04
17

18
Keiji Tanaka
 Japan
244.83
80.05
20
164.78
15

19
Deniss Vasiļjevs
 Latvia
234.58
79.52
21
155.06
20

20
Brendan Kerry
 Australia
233.81
83.06
16
150.75
21

21
Matteo Rizzo
 Italy
232.41
75.63
23
156.78
19

22
Paul Fentz
 Germany
214.55
74.73
24
139.82
22

23
Yan Han
 China
213.01
80.63
19
132.38
23

24
Moris Kvitelashvili
 Georgia
204.57
76.56
22
128.01
24

Did not advance to free skating

25
Julian Yee
 Malaysia

73.58
25

26
Chafik Besseghier
 France

72.10
26

27
Denis Ten
 Kazakhstan

70.12
27

28
Michael Christian Martinez
 Philippines

55.56
28

29
Felipe Montoya
 Spain

52.41
29

30
Yaroslav Paniot
 Ukraine

46.58
30

text: TP - Total points; SP - Short program; FS - Free skating