FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1995761100> ?p ?o ?g. }

• W1995761100 endingPage "407" @default.
• W1995761100 startingPage "401" @default.
• W1995761100 abstract "Background Primary polydipsia is a common complication in patients with chronic psychoses, particularly schizophrenia. Disease pathogenesis is poorly understood, but one contributory factor is thought to be dopamine dysregulation caused by prolonged treatment with neuroleptics. Both angiotensin-converting enzyme (ACE) and orexin (hypocretin) signaling can modulate drinking behavior through interactions with the dopaminergic system. Methods We performed association studies on the insertion/deletion (I/D) sequence polymorphism of ACE and single nucleotide polymorphisms within the prepro-orexin (HCRT), orexin receptor 1 (HCRTR1), and orexin receptor 2 (HCRTR2) genes. Genotypes were determined by polymerase chain reaction amplification, followed by either electrophoretic separation or direct sequencing. Results The ACE I/D polymorphism showed no association with polydipsic schizophrenia. Screening of the orexin signaling system detected a 408 isoleucine to valine mutation in HCRTR1 that showed significant genotypic association with polydipsic–hyponatremic schizophrenia (p = .012). The accumulation of this mutation was most pronounced in polydipsic versus nonpolydipsic schizophrenia (p = .0002 and p = .008, for the respective genotypic and allelic associations). The calcium mobilization properties and the protein localization of mutant HCRTR1 seem to be unaltered. Conclusion Our preliminary data suggest that mutation carriers might have an increased susceptibility to polydipsia through an undetermined mechanism. Primary polydipsia is a common complication in patients with chronic psychoses, particularly schizophrenia. Disease pathogenesis is poorly understood, but one contributory factor is thought to be dopamine dysregulation caused by prolonged treatment with neuroleptics. Both angiotensin-converting enzyme (ACE) and orexin (hypocretin) signaling can modulate drinking behavior through interactions with the dopaminergic system. We performed association studies on the insertion/deletion (I/D) sequence polymorphism of ACE and single nucleotide polymorphisms within the prepro-orexin (HCRT), orexin receptor 1 (HCRTR1), and orexin receptor 2 (HCRTR2) genes. Genotypes were determined by polymerase chain reaction amplification, followed by either electrophoretic separation or direct sequencing. The ACE I/D polymorphism showed no association with polydipsic schizophrenia. Screening of the orexin signaling system detected a 408 isoleucine to valine mutation in HCRTR1 that showed significant genotypic association with polydipsic–hyponatremic schizophrenia (p = .012). The accumulation of this mutation was most pronounced in polydipsic versus nonpolydipsic schizophrenia (p = .0002 and p = .008, for the respective genotypic and allelic associations). The calcium mobilization properties and the protein localization of mutant HCRTR1 seem to be unaltered. Our preliminary data suggest that mutation carriers might have an increased susceptibility to polydipsia through an undetermined mechanism." @default.
• W1995761100 created "2016-06-24" @default.
• W1995761100 creator A5008400314 @default.
• W1995761100 creator A5008700394 @default.
• W1995761100 creator A5009666612 @default.
• W1995761100 creator A5012854197 @default.
• W1995761100 creator A5016054613 @default.
• W1995761100 creator A5050202886 @default.
• W1995761100 creator A5056887554 @default.
• W1995761100 creator A5061632695 @default.
• W1995761100 creator A5064366813 @default.
• W1995761100 creator A5072253152 @default.
• W1995761100 creator A5085932011 @default.
• W1995761100 creator A5089068964 @default.
• W1995761100 date "2005-09-01" @default.
• W1995761100 modified "2023-09-25" @default.
• W1995761100 title "Association of An Orexin 1 Receptor 408Val Variant with Polydipsia–Hyponatremia in Schizophrenic Subjects" @default.
• W1995761100 cites W1512329974 @default.
• W1995761100 cites W1519232679 @default.
• W1995761100 cites W1583745177 @default.
• W1995761100 cites W1964838514 @default.
• W1995761100 cites W1971388525 @default.
• W1995761100 cites W1982065572 @default.
• W1995761100 cites W1986593606 @default.
• W1995761100 cites W1993320404 @default.
• W1995761100 cites W1994915333 @default.
• W1995761100 cites W2009450158 @default.
• W1995761100 cites W2012124372 @default.
• W1995761100 cites W2013679503 @default.
• W1995761100 cites W2025641094 @default.
• W1995761100 cites W2027740042 @default.
• W1995761100 cites W2031294429 @default.
• W1995761100 cites W2031462960 @default.
• W1995761100 cites W2043875236 @default.
• W1995761100 cites W2045519574 @default.
• W1995761100 cites W2051408504 @default.
• W1995761100 cites W2061812026 @default.
• W1995761100 cites W2064416917 @default.
• W1995761100 cites W2076133202 @default.
• W1995761100 cites W2097532633 @default.
• W1995761100 cites W2105529259 @default.
• W1995761100 cites W2115437456 @default.
• W1995761100 cites W2123820078 @default.
• W1995761100 cites W2126718294 @default.
• W1995761100 cites W2136512028 @default.
• W1995761100 cites W2162530578 @default.
• W1995761100 cites W2168219052 @default.
• W1995761100 cites W2170390435 @default.
• W1995761100 cites W2440923228 @default.
• W1995761100 cites W4240700367 @default.
• W1995761100 doi "https://doi.org/10.1016/j.biopsych.2005.04.015" @default.
• W1995761100 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15978554" @default.
• W1995761100 hasPublicationYear "2005" @default.
• W1995761100 type Work @default.
• W1995761100 sameAs 1995761100 @default.
• W1995761100 citedByCount "38" @default.
• W1995761100 countsByYear W19957611002012 @default.
• W1995761100 countsByYear W19957611002013 @default.
• W1995761100 countsByYear W19957611002014 @default.
• W1995761100 countsByYear W19957611002015 @default.
• W1995761100 countsByYear W19957611002017 @default.
• W1995761100 countsByYear W19957611002018 @default.
• W1995761100 countsByYear W19957611002019 @default.
• W1995761100 countsByYear W19957611002020 @default.
• W1995761100 countsByYear W19957611002021 @default.
• W1995761100 countsByYear W19957611002022 @default.
• W1995761100 countsByYear W19957611002023 @default.
• W1995761100 crossrefType "journal-article" @default.
• W1995761100 hasAuthorship W1995761100A5008400314 @default.
• W1995761100 hasAuthorship W1995761100A5008700394 @default.
• W1995761100 hasAuthorship W1995761100A5009666612 @default.
• W1995761100 hasAuthorship W1995761100A5012854197 @default.
• W1995761100 hasAuthorship W1995761100A5016054613 @default.
• W1995761100 hasAuthorship W1995761100A5050202886 @default.
• W1995761100 hasAuthorship W1995761100A5056887554 @default.
• W1995761100 hasAuthorship W1995761100A5061632695 @default.
• W1995761100 hasAuthorship W1995761100A5064366813 @default.
• W1995761100 hasAuthorship W1995761100A5072253152 @default.
• W1995761100 hasAuthorship W1995761100A5085932011 @default.
• W1995761100 hasAuthorship W1995761100A5089068964 @default.
• W1995761100 hasConcept C118303440 @default.
• W1995761100 hasConcept C118552586 @default.
• W1995761100 hasConcept C126322002 @default.
• W1995761100 hasConcept C134018914 @default.
• W1995761100 hasConcept C137183658 @default.
• W1995761100 hasConcept C15744967 @default.
• W1995761100 hasConcept C170493617 @default.
• W1995761100 hasConcept C2776412080 @default.
• W1995761100 hasConcept C2779624480 @default.
• W1995761100 hasConcept C2779680196 @default.
• W1995761100 hasConcept C2780864610 @default.
• W1995761100 hasConcept C513476851 @default.
• W1995761100 hasConcept C555293320 @default.
• W1995761100 hasConcept C71924100 @default.
• W1995761100 hasConceptScore W1995761100C118303440 @default.
• W1995761100 hasConceptScore W1995761100C118552586 @default.
• W1995761100 hasConceptScore W1995761100C126322002 @default.
• W1995761100 hasConceptScore W1995761100C134018914 @default.

• next