Wikipedia - Benutzerbeiträge [de]

Abū Ibrāhīm al-Hāschimī al-Quraschī

2019-11-01T05:57:45Z

Literaturegeek: Sorry but this is original research, the source does not call him a caliph. A caliphate requires large swathes of populated land e.g. multiple cities and towns under sharia law before a caliph can be elected. This is just false.

{{current person|date=November 2019}}
{{Infobox officeholder
| name = Abu Ibrahim al-Hashimi Al-Qurashi
| native_name = {{lang|ar|أبو إبراهيم الهاشمي القرشي}}
| image =
| caption = kos oma
| title =
| order = [[Caliphate|Caliph]] of the [[Islamic State of Iraq and the Levant|Islamic State]]
| term_start = 31 October 2019
| predecessor = [[Abu Bakr al-Baghdadi]]
| successor =
| allegiance ={{flag|Islamic State of Iraq and the Levant}}
| branch =
| serviceyears =
| blank1 = Religion
| data1 = [[Sunni Islam]]
}}
'''Abu Ibrahim al-Hashimi al-Qurashi''' ({{lang-ar|أبو إبراهيم الهاشمي القرشي}}<ref>{{Cite news|language=ar|url=https://www.bbc.com/arabic/middleeast-50251980|title=تنظيم الدولة الإسلامية يعلن عن خليفة للبغدادي|language=Arabic|date=2019-10-31|access-date=2019-10-31|language=en-GB}}</ref>) is the current leader of the [[Islamic State of Iraq and the Levant]]. His appointment was announced by ISIL media on 31 October 2019, less than a week after the death of [[Abu Bakr al-Baghdadi]].<ref name=":0" /> Al-Qurashi's name is believed to be a ''[[Nom-de-guerre|nom de guerre]]'', and his real identity is unknown.

==Background==
Little is known about al-Qurayshi, but his [[Nisba (onomastics)|nisbah]], al-Qurashi, suggests that he, like Baghdadi, claims a lineage to [[Muhammad]]'s tribe of [[Quraysh]], a position that offers legitimacy in some quarters.<ref name=":0">{{Cite news|url=https://www.theguardian.com/world/2019/oct/31/islamic-state-new-leader-abu-bakr-al-baghdadi-abu-ibrahim-al-hashimi-al-qurayshi|title=Islamic State names new leader after death of Abu Bakr al-Baghdadi|last=Chulov|first=Martin|date=2019-10-31|work=The Guardian|access-date=2019-10-31|language=en-GB|issn=0261-3077}}</ref> According to the group, he is a veteran in fighting against [[Western nations]],<ref name=":1">{{Cite web|url=https://www.bbc.co.uk/news/world-middle-east-50254785|title=Islamic State names its new leader as Abu Ibrahim al-Hashemi|website=www.bbc.com|access-date=2019-10-31}}</ref> being a religiously educated and experienced commander.<ref>{{Cite web|url=https://www.trouw.nl/gs-ba8b226e|title=IS heeft een nieuwe leider: Abu Ibrahim al-Hashemi al-Quraishi|last=Dahhan|first=Ghassan|date=2019-10-31|website=Trouw|language=nl|url-status=live|archive-url=|archive-date=|access-date=2019-10-31|quote=IS liet weinig los over de nieuwe leider, behalve dat hij zowel een religieus geleerde is als een ervaren commandant|trans-title=IS did not release much information about the new leader, except that he is both a religious scholar and an experienced commander.}}</ref>

Al-Qurashi's name is believed to be a ''[[Nom-de-guerre|nom de guerre]]'' and his real name is unknown.<ref name=":1" /> Observers of ISIL believe that al-Qurashi will become "the leader of a frayed organisation that has been reduced to scattered sleeper cells".<ref>{{Cite web|url=https://www.aljazeera.com/news/2019/10/isil-confirms-death-leader-al-baghdadi-names-chief-191031151709004.html|title=ISIL confirms death of leader al-Baghdadi, names new chief|website=www.aljazeera.com|access-date=2019-10-31}}</ref>

== References ==
{{reflist}}

{{Islamic State of Iraq and the Levant|state=collapsed}}

{{DEFAULTSORT:Qurayshi, Abu Ibrahim al Hashimi}}
[[Category:Year of birth missing (living people)]]
[[Category:Living people]]
[[Category:21st-century caliphs]]
[[Category:Islamic State of Iraq and the Levant members]]
[[Category:Leaders of Islamic terror groups]]

{{MEast-bio-stub}}

John Montagu, 11. Earl of Sandwich

2010-04-15T12:51:13Z

Literaturegeek: Adding a see also link.

'''John Edward Hollister Montagu, 11th Earl of Sandwich''' (born April 11, 1943) is a [[United Kingdom|British]] [[entrepreneur]], politician and [[nobility|nobleman]].

Montagu is the eldest son of [[Victor Montagu]], who disclaimed the earldom of Sandwich in 1964, and his first wife Maud Rosemary (née Peto). He succeeded his father in the earldom in 1995 and is one of the [[List of hereditary peers elected to sit in the House of Lords under the House of Lords Act 1999|ninety elected hereditary peers]] that remain in the [[House of Lords]] after the passing of the [[House of Lords Act 1999]]. He sits as a cross-bencher.

Taking advantage of the fame of one of his ancestors, [[John Montagu, 4th Earl of Sandwich]], who is the man known for popularizing the [[sandwich]] in [[Kingdom of Great Britain|Great Britain]] in the 18th century, he opened a sandwich shop, ''[[Earl of Sandwich (restaurant)|Earl of Sandwich]]'', at [[Downtown Disney (Florida)|Downtown Disney Marketplace]] in [[Walt Disney World Resort]]. The [[restaurant]] is a collaboration between him and [[Robert Earl (businessman)|Robert Earl]], founder of the [[Planet Hollywood]] chain.

Lord Sandwich married (Susan) Caroline, daughter of Reverend Perceval Hayman, on July 1, 1968, and they have three children.

*Luke Timothy Charles Montagu, Viscount Hinchingbrooke (born 5 December 1969). He married Julie Fisher from Chicago, IL on 11 June 2004. Their first son William James Hayman was born 2 November 2004<ref><Michael Rhodes>.
*They have another son Nestor John Sturges Montagu born 17 October 2006.
" Hon William James Hayman Montagu" birth announced on ''Peerage News'' group on Google Groups on 7 November 2005, based on birth notice in ''Daily Telegraph'' on 6 November 2004. Retrieved 10 August 2007. [http://groups.google.com/group/Peerage-News/browse_thread/thread/39b7f16ee28cdf8d/9ec62535681f8042]</ref>

*The Hon. Orlando William Montagu (born 16 January 1971). He married the model [[Laura Cavendish, Countess of Burlington|Laura Roundell]] in 1996, and they divorced in 2002, having had no children.<ref>Orlando's former wife is now wife of the aristocratic photographer [[William Cavendish, Earl of Burlington|Bill Burlington]], heir to the [[Duke of Devonshire]]. The engagement was announced on 23 December 2006 in The Times; the couple married quietly in 2007 according to Richard Kay of the ''Daily Mail''.</ref> In July 2004 Montagu married Lady Honor Wellesley, eldest daughter of the [[Arthur Wellesley, Marquess of Douro|Marquess of Douro]], heir to the [[Arthur Wellesley, 8th Duke of Wellington|8th Duke of Wellington]]<ref>Darryl Landy. Entry for "Hon. Orlando William Montagu" last edited on 10 July 2004. Retrieved on 10 August 2007 [http://www.thepeerage.com/p12423.htm#i124225]</ref>, with whom he has a son and a daughter
** Walter Frederick Montagu (b. 3 December 2005)<ref>Michael Rhodes. "Walter Frederick Montagu" birth announced on ''Peerage News'' group on Google Groups on 6 December 2005, based on birth notice in ''Daily Telegraph'' the same day. Retrieved 10 August 2007. [http://groups.google.com/group/Peerage-News/browse_thread/thread/46d7f07ab1047ca4/8935ce1357dd5c61]</ref>
**Nancy Jemima Montagu (b. January 2007)

*Lady Jemima Mary Montagu (born 14 October 1973)

==See also==
[[Earl of Sandwich]]

==External links==
*[http://www.disneycorner.com/modules.php?name=News&file=article&sid=61 The Earl of Sandwich] article on its opening at The Disney Corner
*[http://www.earlofsandwichusa.com Earl of Sandwich] link to the website for the restaurant Earl of Sandwich

==References==
*Kidd, Charles, Williamson, David (editors). ''Debrett's Peerage and Baronetage'' (1990 edition). New York: St Martin's Press, 1990.
*[http://www.thepeerage.com/ www.thepeerage.com], specifically [http://www.thepeerage.com/p2070.htm#i20700 entry for the 11th Earl of Sandwich]
{{Reflist}}
{{start box}}
{{s-reg|en}}
{{s-bef|before=[[Victor Montagu]]''' ''(disclaimed title 1964)''}}
{{s-ttl|title=[[Earl of Sandwich]]|years=1995—}}
{{s-inc|heir=[[Luke Montagu, Viscount Hinchingbrooke]]}}
{{end box}}
{{Earls}}

{{DEFAULTSORT:Sandwich, John Montagu, 11th Earl Of}}
[[Category:1943 births]]
[[Category:Living people]]
[[Category:Montagu family|John Montagu, 11th Earl of Sandwich]] 
[[Category:Earls in the Peerage of England]]
[[Category:British businesspeople]]

{{UK-noble-stub}}

[[pl:John Montagu, 11. hrabia Sandwich]]

Bromismus

2009-07-19T20:25:05Z

Literaturegeek: /* Treatment */

'''Bromism''' is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism was once a very common disorder being responsible for 5-10% of psychiatric hospital admissions. It is now an uncommon disorder due to bromide being withdrawn from clinical use in many countries and severely restricted in others. The mechanism of bromism is due to high levels of bromide chronically impairing the membrane of neurons which progressively impairs neuronal transmission which leads to toxicity. Bromide has a very long [[elimination half life]] of 9-12 days which can lead to excessive accumulation. Doses of 0.5-1 gram per day of bromide can lead to bromism. The therapeutic dose of bromide is about 3-5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. Whilst significant and sometimes serious disturbances of neurologic, psychiatric, gastrointestinal function as well as dermatological effects occur death is rare from bromism.<ref name=pdo2003>{{cite book |last1=Olson |first1=Kent R. |title=Poisoning & drug overdose |url=http://books.google.co.uk/books?id=vuec3nTovyUC |edition=4th |date=1st November 2003 |publisher=Appleton & Lange |isbn=978-0838581728 |pages=140-141 |chapter= |chapterurl= }}</ref> Bromide is still occasionally used however, for epilepsy in some countries. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==Diagnosis==
Bromism is diagnosed by checking the serum chloride level, as well as symptoms such as psychosis. Checking elctrolytes, glucose, BUN, creatinine. Bromide is also radiopaque, so an adominal x-ray may also help in the diagnosis.<ref name=pdo2003/>

===Presentation===
;Neurological and psychiatric
Neurological and psychiatric symptoms are [[protean]] and include the symptoms of [[restlessness]], [[irritability]], [[ataxia]], [[confusion]], [[hallucinations]], [[psychosis]], [[weakness]], [[stupor]] and in severe cases [[coma]].<ref name=pdo2003/>

;Gastrointestinal
Gastrointestinal effects include nausea and vomiting as acute adverse effects and [[anorexia]] and [[constipation]] with chronic use.<ref name=pdo2003/>

;Dermatological
Dermatological effects include [[acneiform]], [[pustular]] and [[erythematous]] rashes.<ref name=pdo2003/>

==Treatment==
There are no specific antidotes for bromide, although administering chloride and fluids can help the body to excrete bromide more quickly. Furosemide may help aid urinary excretion in individuals with renal impairment or where bromide toxicity is severe.<ref name=pdo2003/>

==References==
<references />

[[Category:Memory disorders]]
[[Category:Neurology]]
[[Category:Syndromes]]
[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-19T00:45:41Z

Literaturegeek:

'''Bromism''' is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism was once a very common disorder being responsible for 5-10% of psychiatric hospital admissions. It is now an uncommon disorder due to bromide being withdrawn from clinical use in many countries and severely restricted in others. The mechanism of bromism is due to high levels of bromide chronically impairing the membrane of neurons which progressively impairs neuronal transmission which leads to toxicity. Bromide has a very long [[elimination half life]] of 9-12 days which can lead to excessive accumulation. Doses of 0.5-1 gram per day of bromide can lead to bromism. The therapeutic dose of bromide is about 3-5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. Whilst significant and sometimes serious disturbances of neurologic, psychiatric, gastrointestinal function as well as dermatological effects occur death is rare from bromism.<ref name=pdo2003>{{cite book |last1=Olson |first1=Kent R. |title=Poisoning & drug overdose |url=http://books.google.co.uk/books?id=vuec3nTovyUC |edition=4th |date=1st November 2003 |publisher=Appleton & Lange |isbn=978-0838581728 |pages=140-141 |chapter= |chapterurl= }}</ref> Bromide is still occasionally used however, for epilepsy in some countries. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==Diagnosis==
Bromism is diagnosed by checking the serum chloride level, as well as symptoms such as psychosis. Checking elctrolytes, glucose, BUN, creatinine. Bromide is also radiopaque, so an adominal x-ray may also help in the diagnosis.<ref name=pdo2003/>

===Presentation===
;Neurological and psychiatric
Neurological and psychiatric symptoms are [[protean]] and include the symptoms of [[restlessness]], [[irritability]], [[ataxia]], [[confusion]], [[hallucinations]], [[psychosis]], [[weakness]], [[stupor]] and in severe cases [[coma]].<ref name=pdo2003/>

;Gastrointestinal
Gastrointestinal effects include nausea and vomiting as acute adverse effects and [[anorexia]] and [[constipation]] with chronic use.<ref name=pdo2003/>

;Dermatological
Dermatological effects include [[acneiform]], [[pustular]] and [[erythematous]] rashes.<ref name=pdo2003/>

==Treatment==
There are no specific antidotes for bromide, although administering chloride and fluids can help the body to excrete bromide more quickly. Furosemide may help aid urinary excretion. In individuals with renal impairment or where bromide toxicity is severe.<ref name=pdo2003/>

==References==
<references />

[[Category:Memory disorders]]
[[Category:Neurology]]
[[Category:Syndromes]]
[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-18T12:15:20Z

Literaturegeek:

Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism was once a very common disorder being responsible for 5-10% of psychiatric hospital admissions. It is now an uncommon disorder due to bromide being withdrawn from clinical use in many countries and severely restricted in others. The mechanism of bromism is due to high levels of bromide chronically impairing the membrane of neurons which progressively impairs neuronal transmission which leads to toxicity. Bromide has a very long [[elimination half life]] of 9-12 days which can lead to excessive accumulation. Doses of 0.5-1 gram per day of bromide can lead to bromism. The therapeutic dose of bromide is about 3-5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. Whilst significant and sometimes serious disturbances of neurologic, psychiatric, gastrointestinal function as well as dermatological effects occur death is rare from bromism.<ref name=pdo2003>{{cite book |last1=Olson |first1=Kent R. |title=Poisoning & drug overdose |url=http://books.google.co.uk/books?id=vuec3nTovyUC |edition=4th |date=1st November 2003 |publisher=Appleton & Lange |isbn=978-0838581728 |pages=140-141 |chapter= |chapterurl= }}</ref> Bromide is still occasionally used however, for epilepsy in some countries. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==Diagnosis==
Bromism is diagnosed by checking the serum chloride level, as well as symptoms such as psychosis. Checking elctrolytes, glucose, BUN, creatinine. Bromide is also radiopaque, so an adominal x-ray may also help in the diagnosis.<ref name=pdo2003/>

===Presentation===
;Neurological and psychiatric
Neurological and psychiatric symptoms are [[protean]] and include the symptoms of [[restlessness]], [[irritability]], [[ataxia]], [[confusion]], [[hallucinations]], [[psychosis]], [[weakness]], [[stupor]] and in severe cases [[coma]].<ref name=pdo2003/>

;Gastrointestinal
Gastrointestinal effects include nausea and vomiting as acute adverse effects and [[anorexia]] and [[constipation]] with chronic use.<ref name=pdo2003/>

;Dermatological
Dermatological effects include [[acneiform]], [[pustular]] and [[erythematous]] rashes.<ref name=pdo2003/>

==Treatment==
There are no specific antidotes for bromide, although administering chloride and fluids can help the body to excrete bromide more quickly. Furosemide may help aid urinary excretion. In individuals with renal impairment or where bromide toxicity is severe.<ref name=pdo2003/>

==References==
<references />

[[Category:Memory disorders]]
[[Category:Neurology]]
[[Category:Syndromes]]
[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-18T12:13:35Z

Literaturegeek: Added more data and removed tags.

Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism was once a very common disorder being responsible for 5-10% of psychiatric hospital admissions. It is now an uncommon disorder due to bromide being withdrawn from clinical use in many countries and severely restricted in others. The mechanism of bromism is due to high levels of bromide chronically impairing the membrane of neurons which progressively impairs neuronal transmission which leads to toxicity. Bromide has a very long [[elimination half life]] of 9-12 days which can lead to excessive accumulation. Doses of 0.5-1 gram per day of bromide can lead to bromism. The therapeutic dose of bromide is about 3-5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. Whilst significant and sometimes serious disturbances of neurologic, psychiatric, gastrointestinal function as well as dermatological effects occur death is rare from bromism.<ref name=pdo2003>{{cite book |last1=Olson |first1=Kent R. |title=Poisoning & drug overdose |url=http://books.google.co.uk/books?id=vuec3nTovyUC |edition=4th |date=1st November 2003 |publisher=Appleton & Lange |isbn=978-0838581728 |pages=140-141 |chapter= |chapterurl= }}</ref> Bromide is still occasionally used however, for epilepsy in some countries Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==Diagnosis==
Bromism is diagnosed by checking the serum chloride level, as well as symptoms such as psychosis. Checking elctrolytes, glucose, BUN, creatinine. Bromide is also radiopaque, so an adominal x-ray may also help in the diagnosis.<ref name=pdo2003/>

===Presentation===
;Neurological and psychiatric
Neurological and psychiatric symptoms are [[protean]] and include the symptoms of [[restlessness]], [[irritability]], [[ataxia]], [[confusion]], [[hallucinations]], [[psychosis]], [[weakness]], [[stupor]] and in severe cases [[coma]].<ref name=pdo2003/>

;Gastrointestinal
Gastrointestinal effects include nausea and vomiting as acute adverse effects and [[anorexia]] and [[constipation]] with chronic use.<ref name=pdo2003/>

;Dermatological
Dermatological effects include [[acneiform]], [[pustular]] and [[erythematous]] rashes.<ref name=pdo2003/>

==Treatment==
There are no specific antidotes for bromide, although administering chloride and fluids can help the body to excrete bromide more quickly. Furosemide may help aid urinary excretion. In individuals with renal impairment or where bromide toxicity is severe.<ref name=pdo2003/>

==References==
<references />

[[Category:Memory disorders]]
[[Category:Neurology]]
[[Category:Syndromes]]
[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-16T20:22:02Z

Literaturegeek:

{{expand|date=July 2009}}
{{expert-subject|Medicine|date=July 2009}}
Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==References==
<references />

[[Category:Memory disorders]]
[[Category:Neurology]]
[[Category:Syndromes]]
[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-16T20:16:34Z

Literaturegeek:

{{expand|date=July 2009}}
{{expert-subject|Medicine|date=July 2009}}
Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==References==
<references />

[[Category:Substance-related disorders]]
[[Category:Drug addiction]]

Bromismus

2009-07-16T05:25:15Z

Literaturegeek:

Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and [[delerium]].<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==References==
<references />

Bromismus

2009-07-16T05:24:09Z

Literaturegeek:

Bromism is the syndrome which results from the long-term use of the [[potassium bromide]] based sedatives. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and delerium.<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

==References==
<references />

Bromismus

2009-07-16T04:50:30Z

Literaturegeek: ←Created page with 'Bromism is the syndrome which results from the long-term use of the sedative-hypnotic bromides. Bromism is caused by a neurotoxic effect on the brain which results ...'

Bromism is the syndrome which results from the long-term use of the sedative-hypnotic bromides. Bromism is caused by a neurotoxic effect on the brain which results in [[somnolence]], [[psychosis]], [[seizures]] and delerium.<ref>{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=http://books.google.co.uk/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1585622764 |page=217 |chapter= |chapterurl= }}</ref>

Natriumthiopental

2009-01-20T21:43:55Z

Literaturegeek: /* Barbiturates */ correcting inaccurate info

{{dablink|[[Pentothal]] redirects here. For the fictional truth drug from the television series ''24'', see [[Hyoscine-pentothal]].}}
{{drugbox |
| IUPAC_name = [5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| image2 = Sodium-thiopental-3D-vdW-2.png
| width = 113
| CAS_number = 71-73-8
| ChemSpiderID = 2272257
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = APRD00660
| C = 11 | H = 17 | N = 2 | Na = 1 | O = 2 | S = 1
| molecular_weight = 264.321 g/mol
| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= |url= |accessdate=2008-07-18}}</ref>
| excretion =
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''trapanal''', is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. It is an intravenous ultra-short-acting barbiturate. Sodium thiopental is a depressant and is sometimes used during interrogations—not to cause pain (in fact, it may have just the opposite effect), but to weaken the resolve of the subject and make him or her more compliant to pressure.{{Fact|date=March 2008}} Thiopental is a ''core'' medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic health care system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel which decreases neuronal activity and the barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates which act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=ANESTHESIA AND ANALGESIA |accessdate=2007-08-05 |format= |work=}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and is most commonly used in the induction phase of [[general anaesthesia|general anesthesia]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.

A normal dose of thiopental (usually 4-6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Biological half-life#Zero-order elimination|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=}}</ref>

In [[veterinary medicine]], thiopental is also used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs, primarily the [[sight hounds]] can have prolonged recoveries from thiopental due to their lack of body fat and lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT) meaning infusions saturate peripheral compartments (Fat, muscle etc). When the infusion is stopped, the drug re-distributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of clearance becomes fixed which slows elimination from the body.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

:Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg pancuronium dibromide (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for [[pancuronium]] dibromide (Pavulon) are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg.<ref name=euthanasics />

===Lethal injection===
Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 35 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]] - Nebraska is the only retentionist state not to use the lethal injection, instead using the Electric Chair. A megadose is given which places the subject into a rapidly induced coma. Executions using the three drug combination are usually effective in approximately 10 minutes, but have been known to take several times this length. The use of thiopental alone is hypothesized to cause death in approximately 45 minutes.{{Fact|date=February 2008}}
The use of sodium thiopental has been the cause of current Supreme Court challenges to the lethal injection protocol, after a study in the medical journal the Lancet, where autopsy studies on executed inmates revealed that there was not a high enough concentration of thipoental in their blood to have caused unconciousness. The exclusion of physicians participating in executions is partly to blame for inept administration of the drugs.

===Truth serum===
Thiopental is still used in some places as a [[truth drug|truth serum]].<ref>[http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html Sydney Morning Herald], Truth serum used on 'serial child killers', January 12, 2007, Reuters.</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the "truth". However, the reliability of confessions made under thiopental is dubious; the drug tends to make subjects chatty and cooperative with interrogators, but a practiced liar or someone who has a false story firmly established would still be quite able to lie while under the influence of the drug.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with phobias,[http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580] and to "facilitate the recall of painful repressed memories."[http://www.time.com/time/magazine/article/0,9171,863001,00.html] One psychiatrist who worked with thiopental is Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.[http://www.maps.org/news-letters/v08n1/08118sne.html]

==Metabolism==
As with all lipid soluble anaesthetic drugs, the short duration of action of STP is almost entirely due to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]] and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor sensation, sometimes described as being similar to rotting onions. The hangover effects may last up to 36 hours.

Although [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Drug interaction==
Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>[http://www.anes.uab.edu/march.htm This Month in Anesthesia History: March]</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>Steinhaus, John E. [http://www.asahq.org/Newsletters/2001/09_01/steinhaus.htm The Investigator and His ‘Uncompromising Scientific Honesty’] American Society of Anesthesiologists. ''NEWSLETTER.'' September 2001, Volume 65, Number 9.</ref> Three months later,<ref>[http://www.aana.com/archives/imagine/1997/08imagine97.asp Imagining in Time—''From this point in time: Some memories of my part in the history of anesthesia—John S. Lundy, MD''] August 1997, AANA Archives-Library</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>[http://www.aana.com/archives/pdf/0008CHP7.pdf History of Anesthesia with Emphasis on the Nurse Specialist] ''Archives of the American Association of Nurse Anesthetists.'' 1953</ref>

It is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after its discovery, were due to excessive doses given to shocked trauma patients. Evidence has however become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless only 13 of 344 wounded admitted to the Tripler Army Hospital did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

In 1993, [[Anthrax (band)]] had a song off the album [[Sound of White Noise]] called C11H17N2O2SNA (Sodium Pentothal).

==Misc==
:''The fictional truth drug [[Hyoscine-pentothal]] does not describe real Pentothal accurately.''

==References==
{{Reflist|2}}

== External links ==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]
* [http://www.hospira.com/Files/PDF/Pentothal-PI.pdf Pentothal] Abbott Laboratories. 1993.

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}


[[Category:Anesthetics]]
[[Category:Barbiturates]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



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[[ur:تھایوپینٹال سوڈیئم]]

Parke-Davis

2008-08-12T15:22:18Z

Literaturegeek: /* Modern Events */

'''Parke-Davis''' is a [[subsidiary]] of the [[pharmaceutical company]] [[Pfizer Inc.|Pfizer]]. Although no longer an independent corporation, it was once America's oldest and largest drug maker,<ref>[http://www.pfizer.com/pfizer/history/2000.jsp Exploring Our History: 2000 - Pfizer acquires Warner-Lambert]. from Pfizer corporate website. Accessed May 19, 2006.</ref> and played an important role in medical history.

Parke-Davis originally was founded in [[Detroit, Michigan]] by Hervey Parke and George Davis in [[1886]]. It was once the world's largest [[pharmaceutical company]], and is credited with building the first modern pharmaceutical laboratory and developing the first systematic methods of performing [[clinical trials]] of new medications. Parke-Davis was acquired by [[Warner-Lambert]] in [[1970]], which in turn was bought by [[Pfizer Inc.|Pfizer]] in [[2000]].

One of Parke-Davis' early products was an [[amylase]] isolated from ''[[Aspergillus oryzae]]'' by Dr. [[Jokichi Takamine]].<ref>[http://www.deerland-enzymes.com/files/Dr_Jokichi%20Takamine_Bio.pdf Bennett, Joan and Yamomoto, Yutaka. Dr. Jokichi Takamine: Japanese father of American Biotechnology]. ''Deerland Enzymes''.</ref> The enzyme was originally intended for use in [[distilleries]], but was more successfully marketed as "Taka-diastase" for [[dyspepsia]]. They also developed Ketalar (ketamine hydrochloride), a general anesthetic and dissociative drug, in 1962.

Another of the company's products developed by Takamine was a pure form of adrenaline. The compound was patented in [[1900]] and trademarked as "Adrenalin". Because of the similarity of this name to "Adrenaline", the use of the alternative name "epinephrine" for generics was mandated in the United States and is used to this day. A lawsuit filed by H.K. Mulford challenged the patent on the grounds that it was a natural product and therefore unpatentable. The ruling in favor of Parke-Davis by judge [[Learned Hand]] is considered crucial to modern patent law.

Before the criminalization of cocaine, the drug was sold by Parke-Davis in various forms, including cigarettes, powder, and even a cocaine mixture that could be injected directly into the user’s veins with the included needle. The company promised that its cocaine products would “supply the place of food, make the coward brave, the silent eloquent and ... render the sufferer insensitive to pain.

[[Phencyclidine]] (PCP) was first patented in the 1950s by the Parke-Davis pharmaceutical company. PCP is listed as a Schedule II drug in the United States under the Convention on Psychotropic Substances.

Parke-Davis marketed the first widely available [[epilepsy]] treatment, [[Dilantin]], which was approved in [[1939]], although it discovered neither the compound nor the application on its own.<ref>[http://www.remarkablemedicine.com/Medicine/flaw2.html A Flaw in the System]. ''remarkablemedicine.com'' Accessed May 16, 2006.</ref>

The first bacterial [[vaccine]] was developed by Parke-Davis, and the company was thus known as a pioneer in the field of [[Vaccinology]]. It was also among the five firms contracted to manufacture the [[Jonas Salk|Salk]] [[polio vaccine|vaccine]] used to eradicate [[polio]]<ref> Bayly, M. Beddow. The Story of the Salk Anti-Poliomyelitis Vaccine. 1956.</ref> A combination of the [[DPT]] and polio vaccines, called [[Quadrigen]], was developed in [[1954]] and approved in [[1959]]. Quadrigen was later removed from the market in [[1968]] after a series of lawsuits pertaining to adverse effects in vaccinated children.

Other products popularized by the company included [[anti-infective]]s and brands of [[combined oral contraceptive pill]]s.

== Modern Events ==

In the case of ''Franklin v. Parke-Davis'' ([[2002]]) the company was accused of illegal [[marketing]] practices, including the promotion of [[Off-label use|off-label]] uses of its anticonvulsant medication [[Neurontin]].<ref>[http://bipolar.about.com/cs/neurontin/a/neurontin_suit.htm Suit: Neurontin Marketed Illegally for Bipolar Disorder]. ''About.com''. May 16, 2004.</ref> The drug had only been approved for use in patients with [[epilepsy]], but in [[2001]] over 80% of its $1.8 billion in sales were for indications unapproved by the [[FDA]]. In [[2004]], Pfizer "admitted that Parke-Davis aggressively marketed Neurontin by illicit means for unrelated conditions including bipolar disorder, pain, migraine headaches, and drug and [[alcohol withdrawal]]", and consented to $430 million dollars in penalties although it claimed the violations originated in [[1996]], well before Pfizer's acquisition of Warner-Lambert.<ref>[http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2004/05/14/BUGKK6L0LB1.DTL Huge penalty in drug fraud Pfizer settles felony case in Neurontin off-label promotion]. San Francisco Chronicle. Friday, May 14, 2004.</ref>

As announced on January 22, 2007, Pfizer closed its research facilities in Ann Arbor, MI.<ref>[http://www.forbes.com/2007/01/22/pfizer-changes-layoffs-biz-cz_mh_0122changes.html?partner=biotech_newsletter At Pfizer, Brutal Cuts And Big Changes]</ref>

== Trivia ==
{{Trivia|date=June 2008}}
Actor [[Calvert DeForest]], who appeared multiple times with [[David Letterman]], worked for the company for many years.

== References ==

<references />

==External links==
*[http://cocaine.org/parkedavis-works.htm A picture of a Parke Davis & Co. Cocaine injection kit from 1885](''discontinued'')
*[http://www.npr.org/templates/story/story.php?storyId=1145205 2002 NPR broadcast of the Neurontin lawsuit story] on the show [[All Things Considered]]

[[Category:Pharmaceutical companies of the United States]]
[[Category:Companies established in 1886]]