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Biomedical subjects

D Riemann

Publications and source records attributed to D Riemann.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Neurobiological findings in a patient with 48-hour rapid cycling bipolar affective disorder. A case report].

Forty-eight-hour rapid cycling is a rare subclass of affective disorders and entails a regular periodic change of moods. The following case study describes the symptoms, therapy, and outcome of a patient suffering from daily switching between mania and depression along with neurobiological findings correlated to the affective cycles. We found alternating reduction and prolongation of sleep duration during manic and depressive days as well as differences in the amount of REM sleep. Cortisol secretion was regularly increased during depressive days. Regarding thyroid-stimulating hormone (TSH) secretion, the circadian rhythm was absent on depressive days. However, the glucose metabolic rate as measured by positron emission tomography (PET) did not differ on manic and depressive days. The patient reached almost complete remission under treatment with lithium.

Bipolar Disorder↗
PubMed2001

A double-blind, randomized and placebo-controlled study on the polysomnographic withdrawal effects of zopiclone, zolpidem and triazolam in healthy subjects.

Rebound effects after withdrawal from hypnotics are believed to trigger their chronic use and to enhance the risk of tolerance and dependence. It was the purpose of this study to investigate the acute polysomnographic withdrawal effects after a 4 week treatment with standard doses of the non-benzodiazepine hypnotics zopiclone and zolpidem compared with triazolam and placebo. Healthy male subjects between 22 and 35 years of age participated in a parallel study design. They received either zopiclone 7.5 mg (n=11), zolpidem 10 mg (n=11), triazolam 0.25 mg (n=10) or placebo (n=7) over 4 weeks in randomized and double-blind order. Sleep EEG was registered during 2 nights before treatment under placebo, on days 1, 27 and 28 of treatment and on days 29,30,41 and 42 under placebo. Total sleep time and sleep efficiency were lower in the 1st night after discontinuation of triazolam (p < 0.05, t-test). After withdrawal from zopiclone or zolpidem slight but not significant rebound effects concerning sleep continuity were observed. Self-rating scales showed minimal rebound insomnia after discontinuation of all three hypnotics. In the placebo group no changes of sleep parameters were observed. Assuming that rebound insomnia is part of a withdrawal reaction, this study indicates that the risks of tolerance and dependency are low when administering zopiclone or zolpidem at the recommended doses.

Adult↗
PubMed2001

Long-term effectiveness of a short-term cognitive-behavioral group treatment for primary insomnia.

The long-term effectiveness of a short-term cognitive-behavioral therapy was evaluated. The structured group treatment consisted of six weekly sessions and included progressive muscle relaxation, cognitive relaxation, modified stimulus control with bedtime restriction, thought stopping and cognitive restructuring. Twenty patients with chronic primary insomnia took part in the study. All patients were referred by physicians for diagnosis and therapy of insomnia. During a waiting period of six weeks prior to treatment, patients did not experience any change of their sleep parameters. After therapy, patients improved their total sleep time and sleep efficiency and reduced their sleep latency and negative sleep-related cognitions. Furthermore, depression scores decreased. Most of the treatment effects were significant at the end of the treatment and remained stable over the long-term follow-up, which was evaluated after a mean of almost three years (35 +/- 6.7 months). The subjective estimated total sleep time improved from 298 +/- 109 min prior to therapy to 351 +/- 54 min at the end of treatment, to 376 +/- 75 min at the 3-month follow-up, to 379 +/- 58 min at the 12-month follow-up and to 381 +/- 92 min. at the long-term follow-up.

Adult↗
PubMed2001

IL-1 beta- and IL-4-induced down-regulation of autotaxin mRNA and PC-1 in fibroblast-like synoviocytes of patients with rheumatoid arthritis (RA).

Autotaxin (ATX) is a 125-kD ectonucleotide pyrophosphate/phosphodiesterase, which was initially isolated and cloned from human melanoma cells as a potent stimulator of tumour cell motility. ATX shows 44% identity to the plasma cell membrane marker PC-1. Recently, we described the decreased expression of ATX mRNA in cultured fibroblast-like synoviocytes (SFC) of patients with RA by interferon-gamma. In this study using a competitive reverse transcriptase-polymerase chain reaction, we show an increased ATX mRNA expression in SFC from patients with RA in comparison with synoviocytes from non-RA patients. The median ATX mRNA amount in SFC of RA patients (440 pg/microg total RNA) was five-fold higher than the expression in synoviocytes from non-RA patients (80 pg/microg total RNA) or foreskin fibroblasts (MRHF cells, 90 pg/microg total RNA). In contrast to the elevated ATX mRNA expression in SFC of patients with RA, we did not measure increased mRNA amounts of PC-1 in these cells. Both the ATX mRNA amount and the 5'-nucleotide phosphodiesterase (PDE) activity of SFC lysate were reduced after treatment of SFC with the cytokines IL-1beta or IL-4. IL-1beta and IL-4 induced a down-regulation of PC-1 mRNA and protein expression in SFC. In SFC treated with transforming growth factor-beta the expression of PC-1 mRNA and protein was increased, whereas no significant effect on ATX mRNA expression was detectable. Pharmacological drugs used in therapy for RA, such as dexamethasone, cyclosporin, methotrexate and indomethacin, did not show a statistically significant effect on either ATX mRNA or PC-1 mRNA expression. Only pentoxifylline suppressed ATX mRNA as well as PC-1 mRNA expression. In conclusion, we show a tight regulation of ATX and PC-1 gene expression by cytokines detectable in the inflamed tissue of RA. Further investigations will deal with the regulation of ATX protein expression as well as with the function of ATX in RA.

Anti-Inflammatory Agents↗
PubMed2001

Sodium block and depolarization diminish P2Z-dependent Ca2+ entry in human B lymphocytes.

Despite a high Ca2+ -permeability of the P2Z receptor in human B lymphocytes, extracellular ATP4- has only a minor effect on global [Ca2+]i. The aim of this study was to reveal the mechanisms responsible for this discrepancy. We investigated the relationship between ATP4- -application, Cai 2+ -response, membrane current and membrane potential in two human B cell lines and in human tonsillar B cells. This was achieved by a combination of FACS- and voltage clamp measurements and the usage of appropriate voltage- and Ca2 -sensitive fluorescent dyes. ATP4 -induced changes in whole-cell current and [Ca2]i were blocked by extracellular as well as intracellular Na+. Under current clamp conditions, ATP4- -induced Na+ -entry diminished the Ca2+ entry via reduction of the driving force. A substantial increase in [Ca2+]iinduced by ATP4- was only observed in Na+ -free solutions. The pathway of signal transduction activated by ATP4via P2Z receptor of human B lymphocytes under physiological conditions seems not to operate by an increase in the global intracellular Ca2+ -concentration, but rather by the depolarization of the cell membrane as a result of the Na+-influx.

Adenosine Triphosphate↗
PubMed2001

Differential effects of trimipramine and fluoxetine on sleep in geriatric depression.

The effects of trimipramine, a tricyclic antidepressant (TCA) with atypical pharmacological properties, and fluoxetine, a selective serotonine reuptake inhibitor (SSRI), were compared in an exploratory analysis using mood and polysomnographic parameters during a six-week double-blind trial in 19 depressed geriatric patients. In sleep EEG measures, trimipramine demonstrated clear-cut effects on sleep measures resulting in higher values for sleep efficiency, total sleep time, stage 2 sleep, and shorter wake time. Under fluoxetine treatment, the proportion of REM sleep was decreased and REM latency was lengthened, whereas no change in REM sleep parameters was observed in the trimipramine group. The present data suggest that early antidepressant effects of medication occur independently of drug-induced changes in objective measures of sleep, i.e. suppression of REM sleep.

Affect↗
PubMed2001

Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study.

BACKGROUND: Over recent years, the use of antidepressants for the symptomatic treatment of insomnia has grown substantially, but controlled studies are still lacking. Our study is the first investigation to prove objective efficacy and tolerability of low doses of a sedating antidepressant in a randomized, double-blind, and placebo-controlled manner in patients with primary insomnia. METHOD: Forty-seven drug-free patients meeting DSM-IV criteria for primary insomnia (mean +/- SD duration of complaints = 11.2+/-9.7 years) received either 25-50 mg of the tricyclic antidepressant doxepin or placebo for 4 weeks followed by 2 weeks of placebo withdrawal. Sleep was measured by polysomnography at baseline and the first night of application, at 4 weeks of treatment and the first to third night of withdrawal, and after 2 weeks of withdrawal. RESULTS: In the doxepin-treated patients who completed the study (N = 20, 47.6+/-11.3), medication significantly increased sleep efficiency after acute (night 1, p < or = .001) and subchronic (night 28, p < or = .05) intake compared with the patients who received placebo (N = 20, 47.4+/-16.8 years of age). Latency to sleep onset was not affected since the patients had normal baseline sleep latencies. Investigators found doxepin to cause significantly (p < or = .05) better global improvement at the first day of treatment. Patients rated sleep quality (p < or = .001) and working ability (p < or = .005) to be significantly improved by doxepin during the whole treatment period. Overall rebound in sleep parameters was not observed, but patients with severe rebound insomnia were significantly more frequent in the doxepin group (night 29, p < .01, night 30, p < or = .01; night 31, p < or = .05). No significant group differences in side effects were found, but 2 doxepin-treated patients dropped out of the study due to specific side effects (increased liver enzymes, leukopenia, and thrombopenia). CONCLUSION: The results support the effectiveness of low doses of doxepin to improve sleep and working ability in chronic primary insomniacs, although subjective effects were light to moderate, and in some patients, rebound insomnia and specific side effects have to be considered.

Antidepressive Agents, Tricyclic↗
PubMed2001

[NISAS-2000: The "Nationwide Insomnia Screening and Awareness Study". Prevalence and interventions in primary care].

AIM: To estimate the point prevalence of insomnia, recognition and prescription behavior in primary care. METHODS: Nationwide sample of 539 primary care settings along with their characterization (stage 1). Standardized assessment of all attenders (N = 19.155 patients) on the NISAS target day using a sleep questionnaire (PSQI) and additional questions to cover psychosocial and additional clinical variables. All patients were evaluated by the primary care doctors using a standardized clinical appraisal questionnaire, including a CGI-rating. RESULTS: Prevalence insomnia according to DSM-IV was 26.5%. Recognition of presence of any clinically significant sleep disorder was 72%, recognition of insomnia was poor 54.3%. 85.6% of insomnia patients were rated as chronic. Close to 50% of all insomnia cases did not receive a specific insomnia therapy. Herbals, followed by hypnotics and sedatives and antidepressants were the three most frequent treatments applied, psychotherapy was only seldomly indicated. DISCUSSION: NISAS provides for the first time nationally representative estimates of interventions for insomnia in primary care. The relatively low treatment rates and the high proportion of chronic patients receiving longterm prescription of benzodiazepines seem to be critical. Priorities for future agenda to improve this situation are discussed.

Adolescent↗
PubMed2001

[Generalized anxiety disorders (GAD)--a neglected illness? Background und aims of the GAD-P study].

In the past Generalized anxiety disorder (GAD)--previously classified as anxiety neurosis--was regarded as not being a separate diagnostic entity. On the basis of new explicit criteria for GAD in the 90ies, GAD-specific pharmacological (i.e. SNRI) and psychological treatments with improved efficacy have become available. The Generalized Anxiety and Depression in Primary care study (GAD-P) investigates the prevalence of GAD in primary care settings and evaluates the patterns of care provided. Aims, methods and findings of the GAD-P study are described in this supplement.

Anti-Anxiety Agents↗
PubMed2000

Increased lymphocytic aminopeptidase N/CD13 promoter activity after cell-cell contact.

Aminopeptidase N (APN)/CD13 is a transmembrane ectoenzyme expressed on a wide variety of cells. With respect to haematopoietic cells, APN/CD13 has been considered specific for the myeloid lineage, because granulocytes and monocytes/macrophages, but not lymphocytes of peripheral blood, show a surface expression of CD13 antigen. However, we could recently show that cell-cell contact of lymphocytes with endothelial cells, monocytes, and fibroblast-like synoviocytes (SFCs) results in an increase of steady-state APN/CD13 mRNA and a rapid expression of cell-surface protein on the lymphocytes. In this study using the Dual-Luciferase reporter assay, we demonstrate that interaction of the T-cell line Jurkat with SFCs results in a higher activity of the APN/CD13 myeloid promoter in T cells. An enhancer located between the myeloid and epithelial APN/CD13 promoter increases the response of the promoter to the cell-cell contact-induced expression of APN/CD13 in lymphocytes. Adhesion of lymphocytes to extracellular matrix did not result in increased promoter activity. The lymphocytic promoter response induced by direct cell-cell contact with SFCs is not affected by mutations of a proximal promoter element (nucleotides -48 to -35), which has a possible functional role in the basal APN/CD13 gene expression in lymphocytes. Upregulated peptidase-promoter activity via cell-cell contact shown in this study for the first time is discussed as a general mechanism in peptidase induction.

Base Sequence↗
PubMed2000

Aminopeptidase N/CD13 is directly linked to signal transduction pathways in monocytes.

In the present study, we characterized in monocytes the rise in [Ca(2+)](i) evoked by monoclonal antibodies (mAbs) to aminopeptidase N (APN)/CD13, showing a two-phase calcium increase with a small-belled [Ca(2+)](i) rise due to the release of calcium from intracellular stores and a more sustained plateau due to the influx of calcium from the extracellular environment. Tyrosine kinase inhibitors were able to inhibit the rise in [Ca(2+)](i) induced by ligation APN/CD13, as were inhibitors of the phosphatidylinositol 3-kinase. For the first time we can show that mAbs to APN/CD13 provoke phosphorylation of the mitogen-activated protein kinases ERK1/2, JNK, and p38. Furthermore, we show that mRNA of the chemotactic cytokine IL-8 is upregulated under the influence of APN/CD13 ligation. Although the in vivo ligand as well as possible cooperating membrane molecules remains to be identified, our results suggest that the membrane ectoenzyme APN/CD13 is a novel signal transduction molecule in monocytes.

Androstadienes↗
PubMed2000

Aminopeptidase N/CD13 is associated with raft membrane microdomains in monocytes.

Ectopeptidases play important roles in cell activation, proliferation, and communication. Human monocytic cells express considerable amounts of aminopeptidase N/CD13, a transmembrane protein previously proposed to play a role in the regulation of neuropeptides and chemotactic mediators as well as in adhesion and cell-cell interactions. Here, we report for the first time that aminopeptidase N/CD13 in monocytes is partially localized in detergent-insoluble membrane microdomains enriched in cholesterol, glycolipids, and glycosylphosphoinositol-anchored proteins, referred to as "rafts." Raft fractions of monocytes were characterized by the presence of GM1 ganglioside as raft marker molecule and by the high level of tyrosine-phosphorylated proteins. Furthermore, similar to polarized cells, rafts in monocytic cells lack Na(+), K(+)-ATPase. Cholesterol depletion of monocytes by methyl-beta-cyclodextrin greatly reduces raft localization of aminopeptidase N/CD13 without affecting ala-p-nitroanilide cleaving activity of cells.

CD13 Antigens↗
PubMed2000

Transforming growth factor-beta increases the expression of aminopeptidase N/CD13 mRNA and protein in monocytes and monocytic cell lines.

Aminopeptidase N (APN)/CD13 is a membrane-bound surface ectopeptidase with a ubiquitous distribution. In hematopoiesis, APN/CD13 is expressed on stem cells and during most developmental stages of myeloid cells. Because APN/CD13 has been implicated in the trimming on the cell surface of peptides that protrude out of MHC class II molecules, we wanted to study the regulation of this membrane peptidase in antigen presenting cells by TGF-beta. TGF-beta is a potent inducer of the maturation of monocyte precursors towards a macrophage phenotype. Using competitive RT-PCR and cytofluorimetric analyses, we quantified the modulation of the APN/CD13 mRNA as well as protein expression by TGF-beta 1 and -2 and found a stimulation of the APN/CD13 expression in a time- and dose-dependent manner in monocytic cells. In U937 cells, the time course showed a maximum for APN/CD13 mRNA at 24 hours incubation with TGF-beta. In experiments with actinomycin D- treated cells was found a stabilization of APN/CD13 mRNA by TGF-beta 1. Contrary to the IL-4-induced expression of APN/CD13 as well as of MHC class II in monocytic cells, we could show that TGF-beta is able to augment the APN/CD13 expression but decreases the MHC class II expression.

CD13 Antigens↗
PubMed2000

Comparison between eye movement latency and REM sleep parameters in major depression.

Alterations of sleep can be observed polysomnographically in approximately 90 percent of depressed patients. Most of the registered sleep abnormalities in depression also occur in other psychiatric disorders. Only some types of REM sleep alterations-- short REM latency, increase of REM density and shortening of mean latency of eye movements--were reported as more specific for affective disorders. In the present study polysomnograms of 21 medication free patients with major depressive disorder (assessed with a structured interview for DSM-III-R and Hamilton Scale) and 21 healthy controls were analysed. REM latency (LREM), REM density (RD), latencies of eye movements (LEM) and mean latency of eye movements (M-LEM) were calculated for both groups. Depressed patients (compared with healthy controls) showed increased RD (38.2% vs. 28.2%, p < 0.0001), shortened M-LEM (35.7 s vs. 48.3 s, p < 0.04) and shortening of LEM in the 1st (28.9 s vs. 48.9 s, p < 0.007) and 4th (27.0 s vs. 59.1 s, p < 0.043) REM sleep periods. LREM was not shortened significantly in depressives (78.5 min vs. 91.3 min, ns). In healthy subjects a negative correlation between M-LEM and RD was found (rho = -0.47, p < 0.03). Since in the current study depressed patients differed from healthy controls, especially concerning phasic activity during REM sleep, presented data support the essential role of REM density for the assessment of sleep in depression. As a quick and easy manner to compute measurement, M-LEM is suggested as additional parameter for the assessment of phasic activity during REM sleep.

Adult↗