Epidemiology and Pathophysiology of Childhood Narcolepsy
It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produc...
Ausführliche Beschreibung
Autor*in: |
Dye, Thomas J. [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2018transfer abstract |
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Schlagwörter: |
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Umfang: |
5 |
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Übergeordnetes Werk: |
Enthalten in: Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation - Naef, Rahel ELSEVIER, 2021, Oxford [u.a.] |
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Übergeordnetes Werk: |
volume:25 ; year:2018 ; pages:14-18 ; extent:5 |
Links: |
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DOI / URN: |
10.1016/j.prrv.2016.12.005 |
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520 | |a It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. | ||
520 | |a It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. | ||
650 | 7 | |a Autoimmune mechanism |2 Elsevier | |
650 | 7 | |a Childhood narcolepsy |2 Elsevier | |
650 | 7 | |a H1N1 pandemic |2 Elsevier | |
650 | 7 | |a Streptococcal infection |2 Elsevier | |
650 | 7 | |a Narcolepsy |2 Elsevier | |
650 | 7 | |a Narcolepsy with cataplexy |2 Elsevier | |
650 | 7 | |a Narcolepsy epidemiology |2 Elsevier | |
650 | 7 | |a HLA |2 Elsevier | |
650 | 7 | |a H1N1 vaccination |2 Elsevier | |
650 | 7 | |a Narcolepsy genetics |2 Elsevier | |
650 | 7 | |a Narcolepsy pathogenesis |2 Elsevier | |
700 | 1 | |a Gurbani, Neepa |4 oth | |
700 | 1 | |a Simakajornboon, Narong |4 oth | |
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10.1016/j.prrv.2016.12.005 doi GBV00000000000158A.pica (DE-627)ELV041802179 (ELSEVIER)S1526-0542(16)30134-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.63 bkl 44.69 bkl Dye, Thomas J. verfasserin aut Epidemiology and Pathophysiology of Childhood Narcolepsy 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. Autoimmune mechanism Elsevier Childhood narcolepsy Elsevier H1N1 pandemic Elsevier Streptococcal infection Elsevier Narcolepsy Elsevier Narcolepsy with cataplexy Elsevier Narcolepsy epidemiology Elsevier HLA Elsevier H1N1 vaccination Elsevier Narcolepsy genetics Elsevier Narcolepsy pathogenesis Elsevier Gurbani, Neepa oth Simakajornboon, Narong oth Enthalten in Elsevier Naef, Rahel ELSEVIER Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation 2021 Oxford [u.a.] (DE-627)ELV006845770 volume:25 year:2018 pages:14-18 extent:5 https://doi.org/10.1016/j.prrv.2016.12.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.63 Krankenpflege VZ 44.69 Intensivmedizin VZ AR 25 2018 14-18 5 045F 610 |
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10.1016/j.prrv.2016.12.005 doi GBV00000000000158A.pica (DE-627)ELV041802179 (ELSEVIER)S1526-0542(16)30134-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.63 bkl 44.69 bkl Dye, Thomas J. verfasserin aut Epidemiology and Pathophysiology of Childhood Narcolepsy 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. Autoimmune mechanism Elsevier Childhood narcolepsy Elsevier H1N1 pandemic Elsevier Streptococcal infection Elsevier Narcolepsy Elsevier Narcolepsy with cataplexy Elsevier Narcolepsy epidemiology Elsevier HLA Elsevier H1N1 vaccination Elsevier Narcolepsy genetics Elsevier Narcolepsy pathogenesis Elsevier Gurbani, Neepa oth Simakajornboon, Narong oth Enthalten in Elsevier Naef, Rahel ELSEVIER Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation 2021 Oxford [u.a.] (DE-627)ELV006845770 volume:25 year:2018 pages:14-18 extent:5 https://doi.org/10.1016/j.prrv.2016.12.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.63 Krankenpflege VZ 44.69 Intensivmedizin VZ AR 25 2018 14-18 5 045F 610 |
allfields_unstemmed |
10.1016/j.prrv.2016.12.005 doi GBV00000000000158A.pica (DE-627)ELV041802179 (ELSEVIER)S1526-0542(16)30134-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.63 bkl 44.69 bkl Dye, Thomas J. verfasserin aut Epidemiology and Pathophysiology of Childhood Narcolepsy 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. Autoimmune mechanism Elsevier Childhood narcolepsy Elsevier H1N1 pandemic Elsevier Streptococcal infection Elsevier Narcolepsy Elsevier Narcolepsy with cataplexy Elsevier Narcolepsy epidemiology Elsevier HLA Elsevier H1N1 vaccination Elsevier Narcolepsy genetics Elsevier Narcolepsy pathogenesis Elsevier Gurbani, Neepa oth Simakajornboon, Narong oth Enthalten in Elsevier Naef, Rahel ELSEVIER Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation 2021 Oxford [u.a.] (DE-627)ELV006845770 volume:25 year:2018 pages:14-18 extent:5 https://doi.org/10.1016/j.prrv.2016.12.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.63 Krankenpflege VZ 44.69 Intensivmedizin VZ AR 25 2018 14-18 5 045F 610 |
allfieldsGer |
10.1016/j.prrv.2016.12.005 doi GBV00000000000158A.pica (DE-627)ELV041802179 (ELSEVIER)S1526-0542(16)30134-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.63 bkl 44.69 bkl Dye, Thomas J. verfasserin aut Epidemiology and Pathophysiology of Childhood Narcolepsy 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. Autoimmune mechanism Elsevier Childhood narcolepsy Elsevier H1N1 pandemic Elsevier Streptococcal infection Elsevier Narcolepsy Elsevier Narcolepsy with cataplexy Elsevier Narcolepsy epidemiology Elsevier HLA Elsevier H1N1 vaccination Elsevier Narcolepsy genetics Elsevier Narcolepsy pathogenesis Elsevier Gurbani, Neepa oth Simakajornboon, Narong oth Enthalten in Elsevier Naef, Rahel ELSEVIER Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation 2021 Oxford [u.a.] (DE-627)ELV006845770 volume:25 year:2018 pages:14-18 extent:5 https://doi.org/10.1016/j.prrv.2016.12.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.63 Krankenpflege VZ 44.69 Intensivmedizin VZ AR 25 2018 14-18 5 045F 610 |
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10.1016/j.prrv.2016.12.005 doi GBV00000000000158A.pica (DE-627)ELV041802179 (ELSEVIER)S1526-0542(16)30134-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.63 bkl 44.69 bkl Dye, Thomas J. verfasserin aut Epidemiology and Pathophysiology of Childhood Narcolepsy 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. Autoimmune mechanism Elsevier Childhood narcolepsy Elsevier H1N1 pandemic Elsevier Streptococcal infection Elsevier Narcolepsy Elsevier Narcolepsy with cataplexy Elsevier Narcolepsy epidemiology Elsevier HLA Elsevier H1N1 vaccination Elsevier Narcolepsy genetics Elsevier Narcolepsy pathogenesis Elsevier Gurbani, Neepa oth Simakajornboon, Narong oth Enthalten in Elsevier Naef, Rahel ELSEVIER Impact of a nurse-led family support intervention on family members' satisfaction with intensive care and psychological wellbeing: A mixed-methods evaluation 2021 Oxford [u.a.] (DE-627)ELV006845770 volume:25 year:2018 pages:14-18 extent:5 https://doi.org/10.1016/j.prrv.2016.12.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.63 Krankenpflege VZ 44.69 Intensivmedizin VZ AR 25 2018 14-18 5 045F 610 |
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It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. |
abstractGer |
It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. |
abstract_unstemmed |
It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States. |
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Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. The data from the Pediatric Working Group of the Sleep Research Network have shown similar increases of early onset narcolepsy in the United States.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">It is now recognized that there are two types of narcolepsy. Narcolepsy type I or Narcolepsy with cataplexy is caused by the loss of hypocretin or orexin neurons. Narcolepsy type II or narcolepsy without cataplexy has normal hypocretin and the etiology is unknown. Hypocretin is a neuropeptide produced by neurons in the lateral hypothalamus. Both genetic and environmental factors play a crucial role in the pathogenesis of narcolepsy. Most patients with narcolepsy type I and half of patients with narcolepsy type II carry HLA-DQB1*0602. HLA-DQB1*0602 forms a heterodimer with HLA-DQA1*0102 and may act as an antigen presenter to the T cell receptors, resulting in narcolepsy susceptibility. In addition, narcolepsy has been shown to be linked to polymorphisms in other non-HLA genes that may affect immune regulatory function, leading to speculation that autoimmune processes may play a crucial role in the loss of hypocretin neurons. Infections have been proposed as a potential trigger for the autoimmune-mediated mechanism. Several recent studies have shown increased cases of narcolepsy, especially in children and adolescents in relation with H1N1 influenza. The increased cases in Europe seems to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. 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