Hajak, Göran

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Kern, V."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Emrich, H. M."],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:20:37Z"],["dc.date.available","2018-11-07T11:20:37Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurotoxicity of first-generation antipsychotics: (FGAs) may be involved in lipid peroxidation, which is the pathogenesis of extrapyramidal symptoms, including tardive dyskinesia (TD). Blood samples at day 0, 7, and 21 drawn from patients taking antipsychotics were analyzed for malondialdehyde (MDA) in plasma, a marker of lipid peroxidation, by high-performance liquid chromatography. Of 115 patients enrolled, 92 patients completed the study. Most MDA levels were within normal ranges (<1.0 mu mol/liter). Malondialdehyde levels in patients receiving clozapine (p = 0.002), quetiapine (p = 0.003), amisulpride (p = 0.008), and risperidone (p = 0.008) were significantly lower than within the first generation antipsychotic group. The authors conclude that lipid peroxidation is significantly higher in treatment with FGAs."],["dc.identifier.doi","10.1176/appi.neuropsych.17.2.227"],["dc.identifier.isi","000229541000014"],["dc.identifier.pmid","15939978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Publishing, Inc"],["dc.publisher.place","Arlington"],["dc.relation.conference","Annual Meeting of the Nordic-Association-for-Psychiatric-Epidemiology"],["dc.relation.eventlocation","REYKJAVIK, ICELAND"],["dc.relation.issn","1545-7222"],["dc.relation.issn","0895-0172"],["dc.title","Oxidative stress during treatment with first- and second-generation antipsychotics"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","948"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Canadian Journal of Psychiatry"],["dc.bibliographiccitation.lastpage","952"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Tichauer, G. A."],["dc.contributor.author","Spath, C."],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T11:20:34Z"],["dc.date.available","2018-11-07T11:20:34Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: The association between separation anxiety in childhood and actual separation experiences during childhood has not yet been investigated in patients with panic disorder. Methods: In 115 patients with panic disorder with or without agoraphobia and in 124 control subjects without a history of psychiatric illness, we assessed separation anxiety during childhood, retrospectively, using DSM-IV and ICD-10 criteria and the Separation Anxiety Symptom Inventory (SASI). In addition, actual separation experiences from age 0 to 15 years were assessed, retrospectively. Results: A total of 22.6% of the patients and 4.8% of the Control subjects fulfilled both DSM-IV and ICD-10 criteria for childhood separation anxiety (chi(2) = 11.8; P < 0.0001). Further, 57.4% ofthepatients and 37.9% of the control subjects reported actual separation experiences during their childhood (chi(2) = 9. 09, P < 0.003). Separation anxiety and actual separation experiences, however, were independent of each other. Conclusion: These results suggest that separation anxiety during childhood is not a consequence of actual traumatic separation experiences in panic disorder patients."],["dc.identifier.isi","000173099800007"],["dc.identifier.pmid","11816316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Canadian Psychiatric Assoc"],["dc.relation.issn","0706-7437"],["dc.title","Separation anxiety and actual separation experiences during childhood in patients with panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","158"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Respiratory Journal"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Hagedohm, J."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Laier-Groeneveld, G."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:20:54Z"],["dc.date.available","2018-11-07T10:20:54Z"],["dc.date.issued","2002"],["dc.description.abstract","Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy. Therefore, in 10 patients with mild SAS (age 50.8+/-9.9 yrs, respiratory disturbance index (RDI) 18+/-3.6, lowest arterial oxygen saturation (min Sa,O-2) 80.5+/-4.06%) and nine patients with severe SAS (age 50.3+/-11.5 yes, RDI 75.4+/-21.7, min Sa,O-2 56.56+/-14.58%), serum concentrations of neuron-specific enolase (NSE), S-100beta protein, and beta-trace were measured just before and after sleep using commercially available assays. Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS. Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100beta, neuron-specific enolase and beta-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome."],["dc.identifier.doi","10.1183/09031936.02.00862001"],["dc.identifier.isi","000177188600026"],["dc.identifier.pmid","12166564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","European Respiratory Soc Journals Ltd"],["dc.relation.issn","0903-1936"],["dc.title","Biochemical markers of cerebrovascular injury in sleep apnoea syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0893-133X(02)00298-1"],["dc.bibliographiccitation.firstpage","270"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","278"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Koch, K."],["dc.contributor.author","Bartmann, U."],["dc.contributor.author","Kinkelbur, J."],["dc.contributor.author","Schweiger, U."],["dc.contributor.author","Hohagen, F."],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:17:13Z"],["dc.date.available","2018-11-07T10:17:13Z"],["dc.date.issued","2002"],["dc.description.abstract","Reduced 5-HT1A-receptor responsiveness has been reported in patients with panic disorder(PD) and/or agoraphobia 0 (PDA). Although many of these patients are regular smokers, it has not been examined whether psychological or neurobiological effects induced by the selective 5-HT1A-receptor agonist, ipsapirone, are affected by the smoking status of the patients. In order to clarify this question neuroendocrine challenges with oral doses of ipsapirone (0.3 mg/kg) and placebo were performed in 39 patients with PDA, and results were compared between patients who smoked (>10 cigarettes per day, n = 17) and patients who had been non-smokers for at least two years (n = 22). Patients who were smokers (but did not smoke during the challenge procedure) had significantly reduced baseline concentrations of cortisol and a significantly lower body temperature. In comparison to placebo, administration of ipsapirone was associated with significant increases of various psychological symptoms and plasma cortisol concentrations. The subgroup of PD patients who were smokers showed significantly higher cortisol responses to ipsapirone than non-smokers. In conclusion, smoking status has to be taken into account when assessing the responsiveness of 5-HT1A receptors in patients with psychiatric disorders. The prevention of smoking during challenge sessions might not be the ideal approach in heavy smokers, since sudden abstinence from smoking is likely to affect neurobiological and possibly psychological responses to ipsapirone."],["dc.identifier.doi","10.1016/S0893-133X(02)00298-1"],["dc.identifier.isi","000176402600014"],["dc.identifier.pmid","12093600"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41188"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0893-133X"],["dc.title","Smoking modulates neuroendocrine responses to ipsapirone in patients with panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","370"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","376"],["dc.bibliographiccitation.volume","208"],["dc.contributor.author","Wagner, Elias"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Kunze, Birgit"],["dc.contributor.author","Langguth, Berthold"],["dc.contributor.author","Landgrebe, Michael"],["dc.contributor.author","Eichhammer, Peter"],["dc.contributor.author","Frank, Elmar"],["dc.contributor.author","Cordes, Joachim"],["dc.contributor.author","Wölwer, Wolfgang"],["dc.contributor.author","Winterer, Georg"],["dc.contributor.author","Gaebel, Wolfgang"],["dc.contributor.author","Hajak, Göran"],["dc.contributor.author","Ohmann, Christian"],["dc.contributor.author","Verde, Pablo E."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Ahmed, Raees"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Siskind, Dan"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Hasan, Alkomiet"],["dc.date.accessioned","2020-12-10T15:21:10Z"],["dc.date.available","2020-12-10T15:21:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.schres.2019.01.021"],["dc.identifier.issn","0920-9964"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72938"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Efficacy of high-frequency repetitive transcranial magnetic stimulation in schizophrenia patients with treatment-resistant negative symptoms treated with clozapine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","160"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Somnologie"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Klotz, S."],["dc.contributor.author","Jordan, Wolfgang"],["dc.contributor.author","Cohrs, S."],["dc.contributor.author","Engelke, W."],["dc.contributor.author","Ludwig, A."],["dc.contributor.author","Hajak, G."],["dc.date.accessioned","2017-11-21T12:29:46Z"],["dc.date.available","2017-11-21T12:29:46Z"],["dc.date.issued","1997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10138"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.title","Erste Ergebnisse zum Training der suprahyoidalen Muskulatur bei Probanden und einem Patienten mit obstruktiver Schlafapnoe"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Sleep Research"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Kirov, Roumen"],["dc.contributor.author","Kinkelbur, J."],["dc.contributor.author","Heipke, S."],["dc.contributor.author","Kostanecka-Endress, T."],["dc.contributor.author","Westhoff, M."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Rothenberger, A."],["dc.date.accessioned","2018-11-07T10:50:47Z"],["dc.date.available","2018-11-07T10:50:47Z"],["dc.date.issued","2004"],["dc.description.abstract","The aim of the study was to characterize the sleep pattern in children with attention deficit/hyperactivity disorder (ADHD). By means of polysomnography (PSG), sleep patterns were studied in 17 unmedicated preadolescent boys rigorously diagnosed with ADHD and 17 control boys precisely matched for age and intelligence. Although ADHD children did not display a general sleep alteration, major PSG data showed a significant increase in the duration of the absolute rapid eye movement (REM) sleep and the number of sleep cycles in ADHD group when compared with controls. In addition, REM sleep latency tended to be shorter in ADHD children. These results suggest that in ADHD children, a forced REM sleep initiation may produce a higher incidence of sleep cycles and may also contribute to an increased duration of the absolute REM sleep. The overall pattern of the findings implies that a forced ultradian cycling appears characteristic for the sleep in ADHD children, which may be related to alterations of brain monoamines and cortical inhibitory control accompanying the ADHD psychopathology."],["dc.identifier.doi","10.1111/j.1365-2869.2004.00387.x"],["dc.identifier.isi","000189141800011"],["dc.identifier.pmid","14996040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48733"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0962-1105"],["dc.title","Is there a specific polysomnographic sleep pattern in children with attention deficit/hyperactivity disorder?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","867"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","SLEEP"],["dc.bibliographiccitation.lastpage","874"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Eggert, S."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Brunner, E."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:47:06Z"],["dc.date.available","2018-11-07T10:47:06Z"],["dc.date.issued","2004"],["dc.description.abstract","Study Objectives: The prostaglandin D system plays an important role in animal sleep. In humans, alterations in the prostaglandin D system have been found in diseases exhibiting sleep disturbances as a prominent symptom, such as trypanosoma infection, systemic mastocytosis, bacterial meningitis, major depression, or obstructive sleep apnea. Assessment of this system's activity in relation to human physiologic sleep was the target of the present study. Design: Serum concentrations of lipocalin-type prostaglandin D synthase (L-PGDS, former P-trace), and plasma levels of the pineal hormone melatonin were measured in 20 healthy humans (10 women, 10 men; aged: 23.3 +/- 2.39 years) at 4-hour intervals over a period of 5 days and nights, which included physiologic sleep, rapid eye movement sleep deprivation, and total sleep deprivation. In addition, the serum L-PGDS and plasma melatonin levels of 6 subjects were determined under conditions of bright white (10,000 lux) or dark red light (< 50 lux) in a crossover design during total sleep deprivation. Nocturnal blood sampling was performed by a through-the-wall tube system. L-PGDS was measured by an automated immunonephelometric assay, and melatonin was analyzed by direct radioimmunoassay. Results: Serum L-PGDS concentrations showed marked time-dependent changes with evening increases and the highest values at night (P < .0005). This nocturnal increase was suppressed during total sleep deprivation (P < .05), independent of external light conditions and melatonin secretion. Rapid eye movement sleep deprivation had no impact on circulating L-PGDS levels. Conclusions: The circadian L-PGDS pattern and its suppression by total sleep deprivation indicate an interaction of the prostaglandin D system and human sleep regulation. L-PGDS measurements may well provide new insights into physiologic and pathologic sleep regulation in humans."],["dc.identifier.isi","000223451400008"],["dc.identifier.pmid","15453544"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47897"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Academy Sleep Medicine"],["dc.relation.issn","0161-8105"],["dc.title","Prostaglandin D synthase (beta-trace) in healthy human sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","831"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","837"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T11:09:47Z"],["dc.date.available","2018-11-07T11:09:47Z"],["dc.date.issued","2000"],["dc.description.abstract","Background. Research on basal HPA axis activity in patients with panic disorder showed inconsistent results. Methods. Basal total plasma, plasma free and salivary cortisol levels were compared in patients with panic disorder (n = 47) and in healthy individuals (n = 23). Correlations between these fractions were calculated. Results. All three basal cortisol fractions were significantly elevated in patients compared to controls. There were significant correlations between all three cortisol fractions. Conclusions. Nonsignificant differences between cortisol levels of patients and healthy controls in previous studies may have been due to inclusion of less severely ill patients or to small sample sizes (96 words)."],["dc.identifier.doi","10.1007/s007020070062"],["dc.identifier.isi","000088415100008"],["dc.identifier.pmid","11005547"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Salivary, total plasma and plasma free cortisol in panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.lastpage","500"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Sojka, Felicita"],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruether, Eckart"],["dc.date.accessioned","2018-11-07T09:10:15Z"],["dc.date.available","2018-11-07T09:10:15Z"],["dc.date.issued","2006"],["dc.description.abstract","Background. - Earlier studies on the influence of pregnancy and postpartum period on the course of panic disorder have been inconsistent. The present study aims to quantify panic manifestations in these periods in large sample of women. Method. - Panic manifestations, including exacerbations and new manifestations of panic disorder, were assessed retrospectively in a sample of 128 women with panic disorder with or without agoraphobia, 93 of whom had had 195 pregnancies. Results. - Panic manifestations were fewer during pregnancy and more frequent in the postpartum period when compared with the control period. Women who had never been pregnant had significantly more panic manifestations than women with prior pregnancies. Breastfeeding and miscarriages did not have a significant effect. Women with postpartum panic reported more psychosocial stress events during this period. Conclusions. - Possible reasons for postpartum panic and the protective effects of pregnancy are discussed, including psychosocial or hormonal factors and other neurobiological changes. Postpartum panic coincides with a sudden drop of hormones after delivery. (c) 2006 Elsevier Masson SAS. All rights reserved."],["dc.identifier.doi","10.1016/j.eurpsy.2005.11.005"],["dc.identifier.isi","000241925900010"],["dc.identifier.pmid","16529913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier France-editions Scientifiques Medicales Elsevier"],["dc.relation.issn","0924-9338"],["dc.title","Panic disorder during pregnancy and postpartum period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]