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“Cathecol-O-methyl transferase Val158Met genotype is not a risk factor for conversion disorder”, vol. 12, pp. 852-858, 2013.
, Albaugh MD, Harder VS, Althoff RR, Rettew DC, et al. (2010). COMT Val158Met genotype as a risk factor for problem behaviors in youth. J. Am. Acad. Child Adolesc. Psychiatry 49: 841-849.
http://dx.doi.org/10.1016/j.jaac.2010.05.015
PMid:20643317 PMCid:3141335
American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, DSM-IV-TP. 4th edn. Text Revision. American Psychiatric Association, Washington.
Binzer M, Andersen PM and Kullgren G (1997). Clinical characteristics of patients with motor disability due to conversion disorder: a prospective control group study. J. Neurol. Neurosurg. Psychiatry 63: 83-88.
http://dx.doi.org/10.1136/jnnp.63.1.83
PMid:9221972 PMCid:2169635
Caspi A, Langley K, Milne B, Moffitt TE, et al. (2008). A replicated molecular genetic basis for subtyping antisocial behavior in children with attention-deficit/hyperactivity disorder. Arch. Gen. Psychiatry 65: 203-210.
http://dx.doi.org/10.1001/archgenpsychiatry.2007.24
PMid:18250258
Chen J, Lipska BK, Halim N, Ma QD, et al. (2004). Functional analysis of genetic variation in catechol-O-methyltransferase (COMT): effects on mRNA, protein, and enzyme activity in postmortem human brain. Am. J. Hum. Genet. 75: 807- 821.
http://dx.doi.org/10.1086/425589
PMid:15457404 PMCid:1182110
Craddock N, Owen MJ and O'Donovan MC (2006). The catechol-O-methyl transferase (COMT) gene as a candidate for psychiatric phenotypes: evidence and lessons. Mol. Psychiatry 11: 446-458.
http://dx.doi.org/10.1038/sj.mp.4001808
PMid:16505837
DeYoung CG, Getchell M, Koposov RA, Yrigollen CM, et al. (2010). Variation in the catechol-O-methyltransferase Val 158 Met polymorphism associated with conduct disorder and ADHD symptoms, among adolescent male delinquents. Psychiatr. Genet. 20: 20-24.
http://dx.doi.org/10.1097/YPG.0b013e32833511e4
PMid:19997043 PMCid:2895253
Dula DJ and DeNaples L (1995). Emergency department presentation of patients with conversion disorder. Acad. Emerg. Med. 2: 120-123.
http://dx.doi.org/10.1111/j.1553-2712.1995.tb03174.x
PMid:7621217
Eisenberg J, Mei-Tal G, Steinberg A, Tartakovsky E, et al. (1999). Haplotype relative risk study of catechol-O-methyltransferase (COMT) and attention deficit hyperactivity disorder (ADHD): association of the high-enzyme activity Val allele with ADHD impulsive-hyperactive phenotype. Am. J. Med. Genet. 88: 497-502.
http://dx.doi.org/10.1002/(SICI)1096-8628(19991015)88:5<497::AID-AJMG12>3.0.CO;2-F
Glatt SJ, Faraone SV and Tsuang MT (2003). Association between a functional catechol O-methyltransferase gene polymorphism and schizophrenia: meta-analysis of case-control and family-based studies. Am. J. Psychiatry 160: 469-476.
http://dx.doi.org/10.1176/appi.ajp.160.3.469
PMid:12611827
Gogos JA, Morgan M, Luine V, Santha M, et al. (1998). Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior. Proc. Natl. Acad. Sci. U. S. A. 95: 9991-9996.
http://dx.doi.org/10.1073/pnas.95.17.9991
PMid:9707588 PMCid:21449
Gutierrez B, Bertranpetit J, Guillamat R, Valles V, et al. (1997). Association analysis of the catechol O-methyltransferase gene and bipolar affective disorder. Am. J. Psychiatry 154: 113-115.
PMid:8988970
Holmboe K, Nemoda Z, Fearon RM, Csibra G, et al. (2010). Polymorphisms in dopamine system genes are associated with individual differences in attention in infancy. Dev. Psychol. 46: 404-416.
http://dx.doi.org/10.1037/a0018180
PMid:20210499 PMCid:3276838
Kereszturi E, Tarnok Z, Bognar E, Lakatos K, et al. (2008). Catechol-O-methyltransferase Val158Met polymorphism is associated with methylphenidate response in ADHD children. Am. J. Med. Genet. B Neuropsychiatr. Genet. 147B: 1431-1435.
http://dx.doi.org/10.1002/ajmg.b.30704
PMid:18214865
Kunugi H, Vallada HP, Hoda F, Kirov G, et al. (1997). No evidence for an association of affective disorders with high- or low-activity allele of catechol-o-methyltransferase gene. Biol. Psychiatry 42: 282-285.
http://dx.doi.org/10.1016/S0006-3223(96)00366-6
Lachman HM, Papolos DF, Saito T, Yu YM, et al. (1996). Human catechol-O-methyltransferase pharmacogenetics: description of a functional polymorphism and its potential application to neuropsychiatric disorders. Pharmacogenetics 6: 243-250.
http://dx.doi.org/10.1097/00008571-199606000-00007
PMid:8807664
Lewis DA, Melchitzky DS, Sesack SR, Whitehead RE, et al. (2001). Dopamine transporter immunoreactivity in monkey cerebral cortex: regional, laminar, and ultrastructural localization. J. Comp. Neurol. 432: 119-136.
http://dx.doi.org/10.1002/cne.1092
PMid:11241381
Lotta T, Vidgren J, Tilgmann C, Ulmanen I, et al. (1995). Kinetics of human soluble and membrane-bound catechol O-methyltransferase: a revised mechanism and description of the thermolabile variant of the enzyme. Biochemistry 34: 4202-4210.
http://dx.doi.org/10.1021/bi00013a008
PMid:7703232
Monuteaux MC, Biederman J, Doyle AE, Mick E, et al. (2009). Genetic risk for conduct disorder symptom subtypes in an ADHD sample: specificity to aggressive symptoms. J. Am. Acad. Child Adolesc. Psychiatry 48: 757-764.
http://dx.doi.org/10.1097/CHI.0b013e3181a5661b
PMid:19465875
Palmason H, Moser D, Sigmund J, Vogler C, et al. (2010). Attention-deficit/hyperactivity disorder phenotype is influenced by a functional catechol-O-methyltransferase variant. J. Neural Transm. 117: 259-267.
http://dx.doi.org/10.1007/s00702-009-0338-2
PMid:19946713
Purcell TB (1991). The somatic patient. Emerg. Med. Clin. North Am. 9: 137-159.
PMid:2001663
Sadock BJ and Sadock VA (2000). Kaplan and Sadock's Comprehensive Textbook of Psychiatry. 7th edn. Lippincott Williams & Wilkins, Baltimore.
Sengupta S, Grizenko N, Schmitz N, Schwartz G, et al. (2008). COMT Val108/158Met polymorphism and the modulation of task-oriented behavior in children with ADHD. Neuropsychopharmacology 33: 3069-3077.
http://dx.doi.org/10.1038/npp.2008.85
PMid:18580877 PMCid:2885152
Shifman S, Bronstein M, Sternfeld M, Pisante A, et al. (2004). COMT: a common susceptibility gene in bipolar disorder and schizophrenia. Am. J. Med. Genet. B Neuropsychiatr. Genet. 128B: 61-64.
http://dx.doi.org/10.1002/ajmg.b.30032
PMid:15211633
Stonnington CM, Barry JJ and Fisher RS (2006). Conversion disorder. Am. J. Psychiatry 163: 1510-1517.
http://dx.doi.org/10.1176/appi.ajp.163.9.1510
PMid:16946174
Tunbridge EM, Bannerman DM, Sharp T and Harrison PJ (2004). Catechol-o-methyltransferase inhibition improves set-shifting performance and elevates stimulated dopamine release in the rat prefrontal cortex. J. Neurosci. 24: 5331- 5335.
http://dx.doi.org/10.1523/JNEUROSCI.1124-04.2004
PMid:15190105
Weinshilboum RM, Otterness DM and Szumlanski CL (1999). Methylation pharmacogenetics: catechol O-methyltransferase, thiopurine methyltransferase, and histamine N-methyltransferase. Annu. Rev. Pharmacol. Toxicol. 39: 19-52.
http://dx.doi.org/10.1146/annurev.pharmtox.39.1.19
PMid:10331075
Wirgenes KV, Djurovic S, Sundet K, Agartz I, et al. (2010). Catechol O-methyltransferase variants and cognitive performance in schizophrenia and bipolar disorder versus controls. Schizophr. Res. 122: 31-37.
http://dx.doi.org/10.1016/j.schres.2010.05.007
PMid:20605701
“Investigation of ABCB1 gene polymorphism with colchicine response in Behçet’s disease”, vol. 10, pp. 1-6, 2011.
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Babaoglu MO, Bayar B, Aynacioglu AS, Kerb R, et al. (2005). Association of the ABCB1 3435C>T polymorphism with antiemetic efficacy of 5-hydroxytryptamine type 3 antagonists. Clin. Pharmacol. Ther. 78: 619-626.
http://dx.doi.org/10.1016/j.clpt.2005.08.015
PMid:16338277
Behçet H (1937). Uber rezidivierende aphthöse, durch ein Virus verursachte Geschwure, am Mund, am Auge, und an den Genitalien. Dermatol. Wschr. 105: 1152-1157.
Ben-Chetrit E and Levy M (1998). Does the lack of the P-glycoprotein efflux pump in neutrophils explain the efficacy of colchicine in familial Mediterranean fever and other inflammatory diseases? Med. Hypotheses 51: 377-380.
http://dx.doi.org/10.1016/S0306-9877(98)90031-7
Ehrenfeld M, Levy M, Bar EM, Gallily R, et al. (1980). Effect of colchicine on polymorphonuclear leucocyte chemotaxis in human volunteers. Br. J. Clin. Pharmacol. 10: 297-300.
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Gershoni-Baruch R, Peretz Y, Merav L, Dagan E, et al. (2005). The Influence of Polymorphisms in MDR1 on Colchicine Unresponsiveness in Familial Mediterranean Fever. In: The Fourth International Congress on Systemic Autoinflammatory Diseases, November 6-10, Bethesda, 25.
Hoffmeyer S, Burk O, von Richter O, Arnold HP, et al. (2000). Functional polymorphisms of the human multidrug-resistance gene: multiple sequence variations and correlation of one allele with P-glycoprotein expression and activity in vivo. Proc. Natl. Acad. Sci. U. S. A. 97: 3473-3478.
http://dx.doi.org/10.1073/pnas.97.7.3473
PMid:10716719 PMCid:16264
Illmer T, Schuler US, Thiede C, Schwarz UI, et al. (2002). MDR1 gene polymorphisms affect therapy outcome in acute myeloid leukemia patients. Cancer Res. 62: 4955-4962.
PMid:12208746
International Study Group for Behçet's Disease Contributors (1991). Evaluation of Diagnostic ("Classification") Criteria in Behçet's Disease: Toward Internationally Agreed Criteria. In: Behçet's Disease: Basic and Clinical Aspects (O' Duffy and Kökmen B, eds.). Marcel Dekker, New York, 11-39.
Kim RB (2002). Drugs as P-glycoprotein substrates, inhibitors, and inducers. Drug Metab. Rev. 34: 47-54.
http://dx.doi.org/10.1081/DMR-120001389
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Marzolini C, Paus E, Buclin T and Kim RB (2004). Polymorphisms in human MDR1 (P-glycoprotein): recent advances and clinical relevance. Clin. Pharmacol. Ther. 75: 13-33.
http://dx.doi.org/10.1016/j.clpt.2003.09.012
PMid:14749689
Miao LY, Huang CR, Hou JQ and Qian MY (2008). Association study of ABCB1 and CYP3A5 gene polymorphisms with sirolimus trough concentration and dose requirements in Chinese renal transplant recipients. Biopharm. Drug Dispos. 29: 1-5.
http://dx.doi.org/10.1002/bdd.577
PMid:17941052
Rund D, Azar I and Shperling O (1999). A mutation in the promoter of the multidrug resistance gene (MDR1) in human hematological malignancies may contribute to the pathogenesis of resistant disease. Adv. Exp. Med. Biol. 457: 71-75.
http://dx.doi.org/10.1007/978-1-4615-4811-9_9
PMid:10500782
Tufan A, Babaoglu MO, Akdogan A, Yasar U, et al. (2007). Association of drug transporter gene ABCB1 (MDR1) 3435C to T polymorphism with colchicine response in familial Mediterranean fever. J. Rheumatol. 34: 1540-1544.
PMid:17610314
Yurdakul S, Mat C, Tuzun Y, Ozyazgan Y, et al. (2001). A double-blind trial of colchicine in Behcet's syndrome. Arthritis Rheum. 44: 2686-2692.
http://dx.doi.org/10.1002/1529-0131(200111)44:11<2686::AID-ART448>3.0.CO;2-H
Zhou SF (2008). Structure, function and regulation of P-glycoprotein and its clinical relevance in drug disposition. Xenobiotica 38: 802-832.
http://dx.doi.org/10.1080/00498250701867889
PMid:18668431
“Lack of association of ACE gene I/D polymorphism with obstructive sleep apnea syndrome in Turkish patients”, vol. 9, pp. 734-738, 2010.
, Agerholm-Larsen B, Nordestgaard BG and Tybjaerg-Hansen A (2000). ACE gene polymorphism in cardiovascular disease: meta-analyses of small and large studies in whites. Arterioscler. Thromb. Vasc. Biol. 20: 484-492.
http://dx.doi.org/10.1161/01.ATV.20.2.484
PMid:10669647
Ahmadi N, Shapiro GK, Chung SA and Shapiro CM (2009). Clinical diagnosis of sleep apnea based on single night of polysomnography vs. two nights of polysomnography. Sleep Breath. 13: 221-226.
http://dx.doi.org/10.1007/s11325-008-0234-2
PMid:19067010
Barceló A, Elorza MA, Barbé F, Santos C, et al. (2001). Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms. Eur. Respir. J. 17: 728-732.
http://dx.doi.org/10.1183/09031936.01.17407280
PMid:11401071
Bengtsson K, Orho-Melander M, Lindblad U, Melander O, et al. (1999). Polymorphism in the angiotensin converting enzyme but not in the angiotensinogen gene is associated with hypertension and type 2 diabetes: the Skaraborg Hypertension and Diabetes Project. J. Hypertens. 17: 1569-1575.
http://dx.doi.org/10.1097/00004872-199917110-00010
PMid:10608470
Butler R, Morris AD and Struthers AD (1997). Angiotensin-converting enzyme gene polymorphism and cardiovascular disease. Clin. Sci. 93: 391-400.
PMid:9486084
Candy GP, Skudicky D, Mueller UK, Woodiwiss AJ, et al. (1999). Association of left ventricular systolic performance and cavity size with angiotensin-converting enzyme genotype in idiopathic dilated cardiomyopathy. Am. J. Cardiol. 83: 740-744.
http://dx.doi.org/10.1016/S0002-9149(98)00981-3
Lee YJ and Tsai JC (2002). ACE gene insertion/deletion polymorphism associated with 1998 World Health Organization definition of metabolic syndrome in Chinese type 2 diabetic patients. Diabetes Care 25: 1002-1008.
http://dx.doi.org/10.2337/diacare.25.6.1002
PMid:12032106
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http://dx.doi.org/10.1161/01.CIR.97.18.1766
PMid:9603529
Patel SR, Larkin EK, Mignot E, Lin L, et al. (2007). The association of angiotensin converting enzyme (ACE) polymorphisms with sleep apnea and hypertension. Sleep 30: 531-533.
PMid:17520798
Piérola J, Barceló A, de la Pe-a M, Barbé F, et al. (2007). Beta3-adrenergic receptor Trp64Arg polymorphism and increased body mass index in sleep apnoea. Eur. Respir. J. 30: 743-747.
http://dx.doi.org/10.1183/09031936.00152006
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Sakai K, Takada T, Nakayama H, Kubota Y, et al. (2005). Serotonin-2A and 2C receptor gene polymorphisms in Japanese patients with obstructive sleep apnea. Intern. Med. 44: 928-933.
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Seckin D, Ilhan N, Ilhan N and Ozbay Y (2006). The relationship between ACE insertion/deletion polymorphism and coronary artery disease with or without myocardial infarction. Clin. Biochem. 39: 50-54.
http://dx.doi.org/10.1016/j.clinbiochem.2005.10.003
PMid:16303122
Ursavaş A and Ege E (2003). Obstructive sleep apnea and cardiovascular diseases. Anadolu. Kardiyol. Derg. 3: 150-155.
PMid:12826511
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http://dx.doi.org/10.1056/NEJMoa043104
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PMid:18330753
“Lack of association of genetic polymorphisms of angiotensin-converting enzyme gene I/D and glutathione-S-transferase enzyme T1 and M1 with retinopathy of prematures”, vol. 9, pp. 2131-2139, 2010.
, Abbas A, Delvinquiere K, Lechevrel M, Lebailly P, et al. (2004). GSTM1, GSTT1, GSTP1 and CYP1A1 genetic polymorphisms and susceptibility to esophageal cancer in a French population: different pattern of squamous cell carcinoma and adenocarcinoma. World J. Gastroenterol. 10: 3389-3393.
PMid:15526353
Balogh A, Derzbach L, Vannay A and Vásárhelyi B (2006). Lack of association between insulin-like growth factor I receptor G (+3174)A polymorphism and retinopathy of prematurity. Graefes Arch. Clin. Exp. Ophthalmol. 244: 1035-1038.
http://dx.doi.org/10.1007/s00417-005-0203-4
PMid:16362313
Bányász I, Bokodi G, Vannay A, Szebeni B, et al. (2006). Genetic polymorphisms of vascular endothelial growth factor and angiopoietin 2 in retinopathy of prematurity. Curr. Eye Res. 31: 685-690.
http://dx.doi.org/10.1080/02713680600801123
PMid:16877277
Barceló A, Elorza MA, Barbé F, Santos C, et al. (2001). Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms. Eur. Respir. J. 17: 728-732.
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PMid:11401071
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PMid:18546007
Lee YJ and Tsai JC (2002). ACE gene insertion/deletion polymorphism associated with 1998 World Health Organization definition of metabolic syndrome in Chinese type 2 diabetic patients. Diabetes Care 25: 1002-1008.
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PMid:18050122
Shastry BS (2009). Lack of association of VEGF (-2578 C→A) and ANG 2 (-35 G→C) gene polymorphisms with the progression of retinopathy of prematurity. Graefes Arch. Clin. Exp. Ophthalmol. 247: 859-860.
http://dx.doi.org/10.1007/s00417-008-0988-z
PMid:19018553
Shastry BS and Qu X (2007). Lack of association of the VEGF gene promoter (-634 G→C and -460 C→T) polymorphism and the risk of advanced retinopathy of prematurity. Graefes Arch. Clin. Exp. Ophthalmol. 245: 741-743.
http://dx.doi.org/10.1007/s00417-006-0480-6
PMid:17119993
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PMid:11335739
Uzunoğlu S, Acar H, Okudan N, Gökbel H, et al. (2006). Evaluation of the association between null genotypes of glutathione-S-transferases and Behcet's disease. Arch. Dermatol. Res. 297: 289-293.
http://dx.doi.org/10.1007/s00403-005-0617-1
PMid:16283344
Van der Hel OL, Peeters PH, Hein DW, Doll MA, et al. (2003). NAT2 slow acetylation and GSTM1 null genotypes may increase postmenopausal breast cancer risk in long-term smoking women. Pharmacogenetics 13: 399-407.
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