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Search: L773:0006 3223 OR L773:1873 2402

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1.
  • Skoglund, Charlotte, et al. (author)
  • Attention-deficit/hyperactivity disorder and risk for substance use disorders in relatives.
  • 2015
  • In: Biological Psychiatry. - Philadelphia, USA : Elsevier BV. - 0006-3223 .- 1873-2402. ; 77:10, s. 880-6
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Previous research indicates that attention-deficit/hyperactivity disorder (ADHD) is highly associated with substance use disorders (SUD). However, these studies have failed to clarify the nature of the overlap. The main aim of this study was to explore whether the overlap between ADHD and SUD could be explained by shared genetic and environmental factors or by harmful effects of ADHD medication.METHODS: We employed a matched cohort design across different levels of family relatedness recorded from 1973-2009. By linking longitudinal Swedish national registers, 62,015 ADHD probands and first-degree and second-degree relatives were identified and matched 1:10 with control subjects without ADHD and their corresponding relatives. Any record of SUD was defined by discharge diagnoses of the International Classification of Diseases or a purchase of any drug used in the treatment of SUD.RESULTS: First-degree relatives of ADHD probands were at elevated risk for SUD (odds ratios 2.2 and 1.8) compared with relatives of control subjects. The corresponding relative risk in second-degree relatives was substantially lower (odd ratios 1.4 and 1.4). The familial aggregation patterns remained similar for first-degree and second-degree relatives after excluding individuals with coexisting disorders such as schizophrenia, bipolar disorder, depression, and conduct disorder.CONCLUSIONS: Our findings suggest that the co-occurrence of ADHD and SUD is due to genetic factors shared between the two disorders, rather than to a general propensity for psychiatric disorders or harmful effects of ADHD medication.
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2.
  • Aardal-Eriksson, Elisabeth, et al. (author)
  • Salivary cortisol and serum prolactin in relation to stress rating scales in a group of rescue workers
  • 1999
  • In: Biological Psychiatry. - 0006-3223 .- 1873-2402. ; 46:6, s. 850-855
  • Journal article (peer-reviewed)abstract
    • Background: Rescue service personnel are often exposed to traumatic events as part of their occupation, and higher prevalence rates of psychiatric illness have been found among this group.Methods: In 65 rescue workers, salivary cortisol at 8 am and 10 pm and serum prolactin at 8 am were related to the psychiatric self-rating scale General Health Questionnaire (GHQ-28) measuring psychiatric health, and the Impact of Events Scale (IES) and Post Traumatic Symptom Scale (PTSS) measuring posttraumatic symptoms.Results: Seventeen percent of the study population scored above the GHQ-28 cut-off limit but none scored beyond the cut-off limit in the IES and PTSS questionnaires. Salivary cortisol concentration at 10 pm correlated with statistical significance to anxiety (p < .005) and depressive symptoms (p < .01) measured with GHQ-28, as well as to posttraumatic symptoms, with avoidance behavior measured with IES (p < .01) and PTSS (p < .005). Two of the rescue workers were followed over time with the same sampling procedure after a major rescue commission.Conclusions: The correlation between evening salivary cortisol and anxiety, depressiveness, and posttraumatic avoidance symptoms indicates that these parameters can be used in screening and follow-up after traumatic stress events.
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3.
  • Aardal-Eriksson, Elisabeth, et al. (author)
  • Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up
  • 2001
  • In: Biological Psychiatry. - 0006-3223 .- 1873-2402. ; 50:12, s. 986-993
  • Journal article (peer-reviewed)abstract
    • Background: Because traumatic events are unpredictable, there are few studies of psychobiological states immediately following such events. Our study aimed to determine the relation of salivary cortisol to psychologic distress immediately after a traumatic event and then during follow-up.Methods: Measurement of morning and evening salivary cortisol and ratings of psychologic distress (using the Impact of Events Scale [IES], the Post Traumatic Symptom Scale, and the General Health Questionnaire) were performed with 31 United Nations soldiers at three time points—5 days and 2 and 9 months—following a mine accident in Lebanon.Results: Five days after the accident, 15 subjects reported substantial posttraumatic distress according to the IES, as well as significantly lower morning and higher evening cortisol levels compared with the low-impact group. Within 9 months, the posttraumatic distress of the high-impact group was reduced, accompanied by an increase in morning and a decrease in evening cortisol levels. There were significant relationships between evening cortisol and all rating scales at the first and third time points.Conclusions: Subclinical posttraumatic stress following an adverse event can be measured biologically via salivary cortisol levels soon after the event.
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4.
  • Castensson, Anja, et al. (author)
  • Decrease of serotonin receptor 2C in schizophrenia brains identified by high-resolution mRNA expression analysis
  • 2003
  • In: Biological Psychiatry. - 0006-3223 .- 1873-2402. ; 54:11, s. 1212-1221
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: RNA expression profiling can provide hints for the selection of candidate susceptibility genes, for formulation of hypotheses about the development of a disease, and/or for selection of candidate gene targets for novel drug development. We measured messenger RNA expression levels of 16 candidate genes in brain samples from 55 schizophrenia patients and 55 controls. This is the largest sample so far used to identify genes differentially expressed in schizophrenia brains. METHODS: We used a sensitive real-time polymerase chain reaction methodology and a novel statistical approach, including the development of a linear model of analysis of covariance type. RESULTS: We found two genes differentially expressed: monoamine oxidase B was significantly increased in schizophrenia brain (p =.001), whereas one of the serotonin receptor genes, serotonin receptor 2C, was significantly decreased (p =.001). Other genes, previously proposed to be differentially expressed in schizophrenia brain, were invariant in our analysis. CONCLUSIONS:The differential expression of serotonin receptor 2C is particularly relevant for the development of new atypical antipsychotic drugs. The strategy presented here is useful to evaluate hypothesizes for the development of the disease proposed by other investigators.
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5.
  • Castensson, Anja, et al. (author)
  • Decrease of serotonin receptor 2C in schizophrenia brains identified by high-resolution mRNA expression analysis
  • 2003
  • In: Biological Psychiatry. - : Elsevier BV. - 0006-3223 .- 1873-2402. ; 54:11, s. 1212-1221
  • Journal article (peer-reviewed)abstract
    • Background: RNA expression profiling can provide hints for the selection of candidate susceptibility genes, for formulation of hypotheses about the development of a disease, and/or for selection of candidate gene targets for novel drug development. We measured messenger RNA expression levels of 16 candidate genes in brain samples from 55 schizophrenia patients and 55 controls. This is the largest sample so far used to identify genes differentially expressed in schizophrenia brains.Methods: We used a sensitive real-time polymerase chain reaction methodology and a novel statistical approach, including the development of a linear model of analysis of covariance type.Results: We found two genes differentially expressed: monoamine oxidase B was significantly increased in schizophrenia brain (p = .001), whereas one of the serotonin receptor genes, serotonin receptor 2C, was significantly decreased (p = .001). Other genes, previously proposed to be differentially expressed in schizophrenia brain, were invariant in our analysis.Conclusions: The differential expression of serotonin receptor 2C is particularly relevant for the development of new atypical antipsychotic drugs. The strategy presented here is useful to evaluate hypothesizes for the development of the disease proposed by other investigators.
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6.
  • Engström, Christer, et al. (author)
  • Relationship between prophylactic effect of lithium therapy and family history of affective disorders
  • 1997
  • In: Biological Psychiatry. - 0006-3223 .- 1873-2402. ; 42:6, s. 425-433
  • Journal article (peer-reviewed)abstract
    • Lithium therapy response and age of onset (AOO) were studied in 98 patients with bipolar affective disorder (BPAD) who were divided into subgroups depending on type of family history of affective disorders. The highest (33.0 years) and lowest (25.5 years) age of onset were found in nonfamilial patients and in familial patients with a first-degree relative of BPAD, respectively. Nonfamilial patients showed the best response to lithium. There were 0.9 episodes/year off lithium compared to 0.3 episodes/year on lithium (an 88% decrease). A poorer response (a 71% decrease; a reduction from 1.39 episodes per year off lithium to 0.65 on lithium) was found in familial patients with a first-degree relative of BPAD. Differences in serum lithium values between the groups could not explain the observed differences. Thus, familial patients showed a more severe manifestation of the disease with an earlier AOO and a lower prophylactic effect of lithium.
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7.
  • Gustafsson, Lennart (author)
  • Inadequate cortical feature maps : a neural circuit theory of autism
  • 1997
  • In: Biological Psychiatry. - 0006-3223 .- 1873-2402. ; 42:12, s. 1138-1147
  • Journal article (peer-reviewed)abstract
    • The autistic syndromes are caused by neurological dysfunctions. The capacity of autistic individuals to form representations of previous sensory impressions, useful for the processing of present information, is impaired. Self-organizing feature maps are mathematical models of cortical feature maps and may be used to simulate cortical processing. Dysfunctional self-organization, resulting in disability to extract features from stimuli, is proposed as a neural circuit theory of autism. The nature and a possible cause of dysfunction self-organization are examined. It is shown that impaired feature detection is valid for explaining the memory function in autism, the lack of drive for central coherence according to Frith's theory of autism, and a number of impairments from the diagnostic criteria. Unequal levels of impairment of different cortical feature maps can account for the typically uneven intelligence profile of autistic individuals. Excessive inhibitory lateral feedback synaptic connection strengths are presented as one factor impairing the development of feature maps. Strong or excessive inhibitory lateral feedback synaptic connection strengths also cause high sensory discrimination and abnormal sensory responses, both documented in autism. A neural circuit theory for autism has been presented. For a proof of this neural circuit theory neurological investigations are required.
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10.
  • Humble, Mats, 1952-, et al. (author)
  • Reactivity of serotonin in whole blood : relationship with drug response in obsessive-compulsive disorder
  • 2001
  • In: Biological Psychiatry. - New York, USA : Elsevier. - 0006-3223 .- 1873-2402. ; 49:4, s. 360-368
  • Journal article (peer-reviewed)abstract
    • Background: Obsessive-compulsive disorder responds almost only to potent serotonin reuptake inhibitors. Previous studies have suggested a relation between serotonergic function and clinical outcome in serotonin reuptake inhibitor treatment of obsessive-compulsive disorder.Methods: In a randomized, double-blind trial, comparing clomipramine, paroxetine, and a placebo in obsessive-compulsive disorder, serotonin levels in whole blood (WB-5-HT) were measured at baseline, after 1 week, and after 4 weeks of treatment and related to clinical outcome in 36 patients.Results: In patients treated with serotonin reuptake inhibitors there was a pronounced decrease of WB-5-HT, variable after 1 week and uniformly maximal after 4 weeks. The decrease of WB-5-HT after 1 week of serotonin reuptake inhibitor treatment correlated negatively with clinical outcome after 12 weeks (r = -.61, p =.0006); hence, patients with slower WB-5-HT reactivity eventually responded better to treatment. Baseline WB-5-HT, but not WB-5-HT reactivity, was related to season. Depression, autistic traits, and previous serotonin reuptake inhibitor treatment predicted nonresponse.Conclusions: A fast decrease of WB-5-HT was associated with poor clinical outcome. This may be related to faster serotonin efflux from platelets, which has previously been linked to autism. Further studies are necessary to identify the underlying mechanism and discern whether serotonin reuptake inhibitor-induced WB-5-HT decrease is clinically useful.
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