Publications by authors named "Bave U"

Background: The optimal dose (number of pulses per session) of repetitive transcranial magnetic stimulation (rTMS), using the H-coil, in major depressive disorder (MDD) has not previously been reported.

Objective: To explore the relationship between rTMS dose and antidepressant effect, and collect data for the design of a definitive trial.

Methods: This was a double-blind, three-arm parallel-group, randomized [1:1:1], pilot trial conducted in Stockholm, Sweden (September 2014 to September 2016).

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Subjective memory deficits are common in depression and during series of treatment with electroconvulsive therapy (ECT). There is a need for feasible assessment of memory deficit. In the Swedish National Quality Register for ECT, patients' subjective memory function is rated by a clinician.

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Introduction: Electroconvulsive therapy (ECT) is used to treat postpartum depression and psychosis based on clinical experience and small observational studies.

Aims: The primary aim was to test the hypothesis that the response rate to ECT for depression and psychosis is higher during the postpartum period than outside this period. The secondary aim was to identify predictors of a response to ECT during the postpartum period.

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Background: The treatment of choice for cycloid psychosis has traditionally been electroconvulsive therapy (ECT), but there is a lack of studies on its effectiveness.

Aims: The primary aim of this register study was to determine the rates of remission and response after ECT for cycloid psychosis. The secondary aim was to examine possible predictors of outcome.

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Objectives: The aims of the present study were to describe the short-term rate of subjective memory worsening (SMW) and identify factors of importance for SMW in a large clinical sample treated for depression with electroconvulsive therapy (ECT).

Methods: This register-based study included 1212 patients from the Swedish National Quality Register for ECT. Subjective memory worsening was defined as a 2-point worsening on the memory item of the Comprehensive Psychopathological Rating Scale from before to within 1 week after treatment.

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Objectives: Scanning electron microscopy (SEM) is a powerful tool to identify pathogenic factors for which sensitive tests are lacking. The technique has been used to recognize structures in the cerebrospinal fluid (CSF) of patients with schizophrenia. The aim of this study was to use SEM to screen for potential particles in CSF in bipolar disorder.

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Objective: The etiopathogenesis of primary Sjögren's syndrome (SS) is largely unknown. In other autoimmune diseases, type I interferon (IFN) may play a pivotal role by triggering and sustaining the disease process. We therefore aimed to determine whether patients with primary SS had an activated type I IFN system.

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Interferon-beta (IFN-beta), an approved drug for multiple sclerosis (MS), acts on dendritic cells (DC) by suppressing IL-12p40 and increasing IL-10. This results in Th2-biased immune responses. The nature of IFN-beta-modulated DC remains elusive.

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Objective: To investigate the release of interferon-alpha (IFN alpha)-inducing material by necrotic or apoptotic cells, its properties, and the necessity of autoantibodies from systemic lupus erythematosus (SLE) patients for the interferogenic activity.

Methods: U937 monocytic leukemia cells or peripheral blood mononuclear cells (PBMCs) were rendered necrotic by freeze-thawing or apoptotic by treatment with ultraviolet light. Cell culture supernatants from these cells and IgG from SLE patients (SLE IgG) were added to cultures of normal PBMCs or purified plasmacytoid dendritic cells (PDCs).

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An ongoing production of IFN-alpha may be of etiopathogenic significance in systemic lupus erythematosus (SLE). It may be due to the natural IFN-producing cells (NIPC), also termed plasmacytoid dendritic cells (PDC), activated by immune complexes that contain nucleic acids derived from apoptotic cells. We here examined the role of FcgammaR in the IFN-alpha production in vitro by PBMC induced by the combination of apoptotic U937 cells and autoantibody-containing IgG from SLE patients (SLE-IgG).

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We recently demonstrated that IgG from patients with systemic lupus erythematosus (SLE) in combination with U937 cells made apoptotic by UV-irradiation, can induce interferon-alpha (IFN-alpha) production in normal peripheral blood mononuclear cells (PBMC). In the present study we show by flow cytometry that the actual IFN-alpha producing cells (IPC) among PBMC had the same phenotype (HLA-DR+, CD4+, CD11b-, CD11c-, CD14-, CD19-, CD32-, CD36+, CD40+, CD45RA+, CD68+, CD83+, CD86-, IL-3R+ and IL-10R-) and low frequency (approximately 2/10(4)PBMC) as the IPC activated by Herpes simplex virus type I. Consequently, these cells correspond to the natural IPC, also described as type 2 precursor dendritic cells.

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Patients with active systemic lupus erythematosus (SLE) have signs of an ongoing IFN-alpha production, that may be of pathogenic significance in the disease. We previously showed that SLE patients have an IFN-alpha-inducing factor in blood, probably consisting of complexes containing anti-DNA Abs and immunostimulatory DNA. The DNA component could be derived from apoptotic cells, because SLE patients have been reported to have both increased apoptosis and reduced clearance of apoptotic cell material.

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Defects in mitochondrial energy production have been implicated in several neurodegenerative disorders, such as Parkinson disease and amyotrophic lateral sclerosis. To study the contribution of mitochondrial defects to Alzheimer disease and schizophrenia, cytochrome-c oxidase (COX) activity and levels of the mtDNA4977 deletion in postmortem brain tissue specimens of patients were compared with those of asymptomatic age-matched controls. No difference in COX activity was observed between Alzheimer patients and controls in any of five brain regions investigated.

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Defects in cytochrome oxidase (CO; complex 4) have recently been demonstrated in blood platelets and in brain tissue from patients with Alzheimer's disease (AD) with possible etiological implications. Because of pathogenetic similarities with AD, we have measured the activities of several mitochondrially localised enzymes in the blood platelets of individuals afflicted with trisomy-21 (Down's syndrome). The activities of monoamine oxidase, cytochrome oxidase, isocitrate dehydrogenase, and glutamate dehydrogenase were assayed in washed platelets from sixty caucasian, male and female control individuals (ages 18-60) and ten, young Down's Syndrome patients (ages 9-21).

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