Skip header and navigation

3 records – page 1 of 1.

5-HT2C receptor and MAO-A interaction analysis: no association with suicidal behaviour in bipolar patients.

https://arctichealth.org/en/permalink/ahliterature157011
Source
Eur Arch Psychiatry Clin Neurosci. 2008 Oct;258(7):428-33
Publication Type
Article
Date
Oct-2008
Author
Vincenzo De Luca
Subi Tharmaligam
John Strauss
James L Kennedy
Author Affiliation
Dept. of Psychiatry, University of Toronto, 250 College Street, R-30, Toronto (ON), Canada M5T 1R8. vincenzo_deluca@camh.net
Source
Eur Arch Psychiatry Clin Neurosci. 2008 Oct;258(7):428-33
Date
Oct-2008
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Bipolar Disorder - genetics - psychology
Canada
Family Health
Female
Gene Frequency
Genes, X-Linked
Genetic Predisposition to Disease
Genotype
Haplotypes
Humans
Male
Middle Aged
Monoamine Oxidase - genetics
Nuclear Family
Polymorphism, Single Nucleotide
Receptor, Serotonin, 5-HT2C - genetics
Suicide, Attempted - psychology
Young Adult
Abstract
The serotonin 2C (HTR2C) receptor has been implicated in suicide-related behaviours, however there are not many studies to date about HTR2C and suicidality. We studied HTR2C haplotypes in suicide attempters, where our sample composed of 306 families with at least one member affected by bipolar disorder. HTR2C (Cys23Ser and a common STR in the promoter) variants were analyzed with respect to attempter status and the severity of suicidal behaviour. The X-linked haplotype analysis in relation to suicide attempt did not reveal any significant association. Furthermore, we performed a particular gene-gene interaction for the X-linked serotonergic genes (HTR2C and MAOA), and found no association among this intergenic haplotype combination and suicidal behaviour in bipolar disorder.
PubMed ID
18504633 View in PubMed
Less detail

Genome-wide association study of bipolar disorder in Canadian and UK populations corroborates disease loci including SYNE1 and CSMD1.

https://arctichealth.org/en/permalink/ahliterature105424
Source
BMC Med Genet. 2014;15:2
Publication Type
Article
Date
2014
Author
Wei Xu
Sarah Cohen-Woods
Qian Chen
Abdul Noor
Jo Knight
Georgina Hosang
Sagar V Parikh
Vincenzo De Luca
Federica Tozzi
Pierandrea Muglia
Julia Forte
Andrew McQuillin
Pingzhao Hu
Hugh M D Gurling
James L Kennedy
Peter McGuffin
Anne Farmer
John Strauss
John B Vincent
Author Affiliation
Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health (CAMH), R-32, 250 College Street, Toronto, ON M5T 1R8, Canada. john.vincent@camh.ca.
Source
BMC Med Genet. 2014;15:2
Date
2014
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - genetics
Canada
Cohort Studies
Genetic Loci - genetics
Genome-Wide Association Study
Genotype
Great Britain
Humans
Membrane Proteins - genetics
Nerve Tissue Proteins - genetics
Nuclear Proteins - genetics
Pedigree
Reproducibility of Results
Young Adult
Abstract
Recently, genome-wide association studies (GWAS) for cases versus controls using single nucleotide polymorphism microarray data have shown promising findings for complex neuropsychiatric disorders, including bipolar disorder (BD).
Here we describe a comprehensive genome-wide study of bipolar disorder (BD), cross-referencing analysis from a family-based study of 229 small families with association analysis from over 950 cases and 950 ethnicity-matched controls from the UK and Canada. Further, loci identified in these analyses were supported by pathways identified through pathway analysis on the samples.
Although no genome-wide significant markers were identified, the combined GWAS findings have pointed to several genes of interest that support GWAS findings for BD from other groups or consortia, such as at SYNE1 on 6q25, PPP2R2C on 4p16.1, ZNF659 on 3p24.3, CNTNAP5 (2q14.3), and CDH13 (16q23.3). This apparent corroboration across multiple sites gives much confidence to the likelihood of genetic involvement in BD at these loci. In particular, our two-stage strategy found association in both our combined case/control analysis and the family-based analysis on 1q21.2 (closest gene: sphingosine-1-phosphate receptor 1 gene, S1PR1) and on 1q24.1 near the gene TMCO1, and at CSMD1 on 8p23.2, supporting several previous GWAS reports for BD and for schizophrenia. Pathway analysis suggests association of pathways involved in calcium signalling, neuropathic pain signalling, CREB signalling in neurons, glutamate receptor signalling and axonal guidance signalling.
The findings presented here show support for a number of genes previously implicated genes in the etiology of BD, including CSMD1 and SYNE1, as well as evidence for previously unreported genes such as the brain-expressed genes ADCY2, NCALD, WDR60, SCN7A and SPAG16.
Notes
Cites: PLoS Genet. 2006 Dec;2(12):e19017194218
Cites: Proc Natl Acad Sci U S A. 2009 May 5;106(18):7501-619416921
Cites: Mol Psychiatry. 2009 Apr;14(4):351-319308021
Cites: Mol Psychiatry. 2013 Jan;18(1):11-222182936
Cites: Mol Cell Biol. 2009 Jul;29(13):3633-4319398580
Cites: Nature. 2009 Aug 6;460(7256):748-5219571811
Cites: Nature. 2009 Oct 15;461(7266):992-619794415
Cites: Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):86-9619350560
Cites: Nat Genet. 2010 Feb;42(2):128-3120081856
Cites: Neuropsychopharmacology. 2001 Oct;25(4):608-1311557174
Cites: Stat Med. 2002 Jan 15;21(1):35-5011782049
Cites: Mol Psychiatry. 2002;7(4):424-711986988
Cites: J Psychiatr Res. 2003 Jul-Aug;37(4):297-30312765852
Cites: Genet Epidemiol. 2003 Dec;25(4):327-3814639702
Cites: Arch Gen Psychiatry. 1982 Aug;39(8):879-837103676
Cites: Br J Psychiatry. 1989 Sep;155:294-3042692760
Cites: Arch Gen Psychiatry. 1990 Jun;47(6):589-932190539
Cites: JAMA. 1990 Nov 21;264(19):2511-82232018
Cites: Arch Gen Psychiatry. 1991 Aug;48(8):764-701883262
Cites: Am J Hum Genet. 1993 Mar;52(3):506-168447318
Cites: Br J Psychiatry. 1994 Aug;165(2):2727832868
Cites: Psychiatr Genet. 1994 Winter;4(4):195-2007712114
Cites: Am J Med Genet. 1995 Apr 24;60(2):94-1027485258
Cites: Br J Psychiatry. 1997 Sep;171:209-199337969
Cites: Psychiatr Genet. 1998 Autumn;8(3):131-409800214
Cites: Arch Gen Psychiatry. 1999 Jun;56(6):554-510359471
Cites: J Med Genet. 1999 Aug;36(8):585-9410465107
Cites: Neuroreport. 1999 Jun 3;10(8):1747-5010501568
Cites: Neuron. 2004 Nov 18;44(4):677-9015541315
Cites: Ann Hum Genet. 2005 May;69(Pt 3):329-3515845037
Cites: Eur Neuropsychopharmacol. 2005 Aug;15(4):425-3415935623
Cites: Am J Manag Care. 2005 Jun;11(3 Suppl):S80-416097718
Cites: J Immunol. 2006 Apr 1;176(7):4419-3016547280
Cites: Nat Rev Genet. 2006 May;7(5):385-9416619052
Cites: Eur J Hum Genet. 2006 Jun;14(6):660-816721402
Cites: Biol Psychiatry. 2006 Jul 15;60(2):123-3116843095
Cites: Br J Psychiatry. 2006 Oct;189:317-2317012654
Cites: Pharmacogenomics J. 2007 Apr;7(2):123-3216733521
Cites: Psychiatr Genet. 2007 Jun;17(3):129-3317417055
Cites: Nat Genet. 2007 Nov;39(11):1329-3717952073
Cites: Neuron. 2007 Nov 21;56(4):621-3918031681
Cites: Mol Psychiatry. 2008 Feb;13(2):197-20717486107
Cites: Schizophr Res. 2008 Apr;101(1-3):36-4918394866
Cites: Mol Psychiatry. 2008 Jun;13(6):558-6918317468
Cites: BMC Psychiatry. 2008;8:8718992145
Cites: Nat Genet. 2008 Sep;40(9):1053-518677311
Cites: Nat Genet. 2008 Sep;40(9):1056-818711365
Cites: Am J Hum Genet. 2009 Feb;84(2):210-2319200528
Cites: Mol Psychiatry. 2010 Mar;15(3):319-2518794890
Cites: Biol Psychiatry. 2010 Aug 15;68(4):320-820346443
Cites: Bipolar Disord. 2010 Aug;12(5):579-8120712760
Cites: J Affect Disord. 2010 Oct;126(1-2):312-620451256
Cites: Eur J Med Genet. 2010 Sep-Oct;53(5):239-4320601260
Cites: Psychiatry Res. 2011 Jan 30;185(1-2):27-3220580841
Cites: Mol Psychiatry. 2011 Jan;16(1):2-420351715
Cites: Mol Psychiatry. 2011 Mar;16(3):240-220351716
Cites: Mol Psychiatry. 2011 Apr;16(4):452-6120308991
Cites: Biol Psychiatry. 2011 Jul 1;70(1):35-4221439553
Cites: Neurosci Biobehav Rev. 2012 Jan;36(1):556-7121946175
Cites: Hum Genet. 2012 Jul;131(7):1047-5622160351
Cites: PLoS One. 2012;7(7):e4009822768332
Cites: J Affect Disord. 2013 Jan 10;144(1-2):16-2722749156
Cites: Am J Hum Genet. 2007 Sep;81(3):559-7517701901
PubMed ID
24387768 View in PubMed
Less detail

Speech recognition software and electronic psychiatric progress notes: physicians' ratings and preferences.

https://arctichealth.org/en/permalink/ahliterature141262
Source
BMC Med Inform Decis Mak. 2010;10:44
Publication Type
Article
Date
2010
Author
Yaron D Derman
Tamara Arenovich
John Strauss
Author Affiliation
Information Management Group, Centre for Addiction and Mental Health, 1001 Queen St, West, Toronto, Ontario, M6J 1H4, Canada.
Source
BMC Med Inform Decis Mak. 2010;10:44
Date
2010
Language
English
Publication Type
Article
Keywords
Adult
Attitude of Health Personnel
Canada
Community Mental Health Services
Critical Pathways
Documentation - methods - standards
Electronic Health Records
Female
Humans
Male
Mandatory Programs
Psychiatry
Psychotherapeutic Processes
Quality of Health Care
Speech Recognition Software
Technology Assessment, Biomedical
Abstract
The context of the current study was mandatory adoption of electronic clinical documentation within a large mental health care organization. Psychiatric electronic documentation has unique needs by the nature of dense narrative content. Our goal was to determine if speech recognition (SR) would ease the creation of electronic progress note (ePN) documents by physicians at our institution.
Twelve physicians had access to SR software on their computers for a period of four weeks to create ePN.
We examined SR software in relation to its perceived usability, data entry time savings, impact on the quality of care and quality of documentation, and the impact on clinical and administrative workflow, as compared to existing methods for data entry.
A series of Wilcoxon signed rank tests were used to compare pre- and post-SR measures. A qualitative study design was used.
Six of twelve participants completing the study favoured the use of SR (five with SR alone plus one with SR via hand-held digital recorder) for creating electronic progress notes over their existing mode of data entry. There was no clear perceived benefit from SR in terms of data entry time savings, quality of care, quality of documentation, or impact on clinical and administrative workflow.
Although our findings are mixed, SR may be a technology with some promise for mental health documentation. Future investigations of this nature should use more participants, a broader range of document types, and compare front- and back-end SR methods.
Notes
Cites: J Am Med Inform Assoc. 2000 Sep-Oct;7(5):462-810984465
Cites: Am J Emerg Med. 2001 Jul;19(4):295-811447517
Cites: J Am Coll Radiol. 2008 Dec;5(12):1196-919027683
Cites: Mod Pathol. 2002 May;15(5):565-7112011262
Cites: J Digit Imaging. 2002 Mar;15(1):43-5312134214
Cites: J Am Med Inform Assoc. 2003 Jan-Feb;10(1):85-9312509359
Cites: Pediatrics. 2004 Sep;114(3):e290-315342888
Cites: Radiology. 1981 Mar;138(3):585-87465833
Cites: Radiology. 1987 Aug;164(2):569-733602404
Cites: Radiology. 1988 Jun;167(3):853-53363152
Cites: J Am Med Inform Assoc. 1995 Jan-Feb;2(1):46-577895136
Cites: J Am Med Inform Assoc. 1997 Nov-Dec;4(6):436-419391931
Cites: MedGenMed. 2004;6(3):5415520678
Cites: J Digit Imaging. 2008 Dec;21(4):384-917554582
Cites: J Digit Imaging. 2008 Dec;21(4):378-8218437491
Cites: J Am Med Inform Assoc. 2001 Jan-Feb;8(1):101-211141516
PubMed ID
20738875 View in PubMed
Less detail