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Biomedical subjects

L Lauritzen

Publications and source records attributed to L Lauritzen.

At least 19 recordsLinked to original sources
PubMed2004

British Columbia Provincial Eating Disorders Program: an organizational description.

The British Columbia Provincial Eating Disorders Program (BCEDP) is a small government funded body that communicates eating disorder treatment needs to the government, helps communication between primary, secondary, and tertiary care givers, gives treatment advice and teaching to primary and secondary care givers, and assists the Provincial Eating Disorders Resource Centre in decision making and communication with government. The program deals with anorexia nervosa and bulimia nervosa, but not obesity, for budgetary reasons.

Adolescent↗
PubMed2001

Prophylactic effect of citalopram in unipolar, recurrent depression: placebo-controlled study of maintenance therapy.

BACKGROUND: Major depression is highly recurrent. Antidepressant maintenance treatment has proven efficacy against recurrent depression. AIMS: Comparison of prophylactic efficacy of citalopram versus placebo in unipolar, recurrent depression. METHODS: Patients 18-65 years of age with recurrent unipolar major depression (DSM-IV), a Montgomery-Asberg Depression Rating Scale score of > or =22 and two or more previous depressive episodes, one within the past 5 years, were treated openly with citalopram (20-60 mg) for 6-9 weeks and, if responding, continued for 16 weeks before being randomised to double-blind maintenance treatment with citalopram or placebo for 48-77 weeks. RESULTS: A total of 427 patients entered acute treatment and 269 were randomised to double-blind treatment. Time to recurrence was longer in patients taking citalopram than in patients taking placebo (P:<0.001). Prophylactic treatment was well tolerated. CONCLUSIONS: Citalopram (20, 40 and 60 mg) is effective in the prevention of depressive recurrences. Patients at risk should continue maintenance treatment at the dose necessary to resolve symptoms in the acute treatment phase.

Adolescent↗
PubMed1999

The subcellular localization of phospholipase D activities in rat Leydig cells.

Rat Leydig cells contain a phospholipase D (PLD), which can be activated by vasopressin and phorbol ester. In order to clarify which Leydig cell organelles that express PLD activity, the subcellular localization of two differently regulated PLD activities was investigated by subcellular fractionation on a 40% (v/v) self-generating Percoll gradient. PLD activities in broken cells were estimated using radiolabeled didecanoylphosphatidylcholine as a substrate. Initial experiments revealed the presence of an oleate Mg2+ -activated PLD and a phosphatidylinositol 4,5-bisphosphate-activated PLD (PIP2-PLD) in the microsomal fraction of Leydig cells. The latter activity could be further stimulated by recombinant nonmyristoylated ADP ribosylating factor 1 (ARF1) plus GTPgammaS. The peak of oleate Mg2+ -PLD activity colocalized with the plasma membrane marker, whereas the highest specific activity of the PIP2-PLD activity was found in fractions with a slightly lower density than those containing the plasma membrane and trans-Golgi marker enzymes. In order to localize phorbol ester-stimulated PLD activity in intact Leydig cells, the cells were prelabeled with [14C]-palmitate and then stimulated for 15 min with 100 nM 4-beta-phorbol-12-myristate-13-acetate (PMA) in the presence of ethanol or butanol. The PLD product [14C]-phosphatidylethanol, expressed as the percentage of total labeled phospholipids in the fraction, was slightly increased in all Percoll fractions and showed a prominent peak in the fractions containing plasma membrane, trans-Golgi, and fractions of slightly lower density. The PMA-induced formation of [14C]-phosphatidylbutanol could be inhibited dose-dependently with brefeldin A suggesting that the activation of PLD by the phorbol ester was mediated by ARF.

ADP-Ribosylation Factor 1↗
PubMed1998

Formation of N-acyl-phosphatidylethanolamines and N-acetylethanolamines: proposed role in neurotoxicity.

The formation of N-acyl-phosphatidylethanolamine (NAPE) and N-acylethanolamine (NAE), including anandamide, in mammals in relation to neurotoxicity is discussed. Data on the characterization of the NAPE-forming N-acyltransferase, the NAPE-hydrolyzing phospholipase D, and the NAE-hydrolyzing amidase are reviewed. We suggest that NAPE and NAE, including anandamide, are formed in neurons in response to the high intracellular calcium concentrations that occur in injured neurons, e.g. due to glutamate excitotoxicity. NAPE may have functions of its own besides being a precursor for NAE. The formation of both of these lipids may serve as a cytoprotective response, whether mediated by physical interactions with membranes or enzymes, or mediated by activation of cannabinoid receptors. This suggestion implies that NAPE and NAE may have pathophysiological roles in the brain. Whether these lipids also have physiological roles is uncertain.

Amidohydrolases↗
PubMed1997

Cell swelling activates phospholipase A2 in Ehrlich ascites tumor cells.

Ehrlich ascites tumor cells, loaded with 3H-labeled arachidonic acid and 14C-labeled stearic acid for two hours, were washed and transferred to either isotonic or hypotonic media containing BSA to scavenge the labeled fatty acids released from the cells. During the first two minutes of hypo-osmotic exposure the rate of 3H-labeled arachidonic acid release is 3.3 times higher than that observed at normal osmolality. Cell swelling also causes an increase in the production of 14C-stearic acid-labeled lysophosphatidylcholine. This indicates that a phospholipase A2 is activated by cell swelling in the Ehrlich cells. Within the same time frame there is no swelling-induced increase in 14C-labeled stearic acid release nor in the synthesis of phosphatidyl 14C-butanol in the presence of 14C-butanol. Furthermore, U7312, an inhibitor of phospholipase C, does not affect the swelling induced release of 14C-labeled arachidonic acid. Taken together these results exclude involvement of phospholipase A1, C and D in the swelling-induced liberation of arachidonic acid. The swelling-induced release of 3H-labeled arachidonic acid from Ehrlich cells as well as the volume regulatory response are inhibited after preincubation with GDP beta S or with AACOCF3, an inhibitor of the 85 kDa, cytosolic phospholipase A2. Based on these results we propose that cell swelling activates a phospholipase A2--perhaps the cytosolic 85 kDa type--by a partly G-protein coupled process, and that this activation is essential for the subsequent volume regulatory response.

Arachidonic Acid↗
PubMed1997

Characterization of glutamate-induced formation of N-acylphosphatidylethanolamine and N-acylethanolamine in cultured neocortical neurons.

Glutamate-induced formation of N-acylethanolamine (NAE) and N-acylphosphatidylethanolamine (NAPE) was studied in primary cultures of mouse neocortical neurons prelabeled with [14C] ethanolamine. The formation of these two lipids was dependent on the maturity of the cell culture; i.e., no glutamate-induced formation was seen in 2-day-old cultures, whereas glutamate induced a pronounced formation in 6-day-old cultures. The calcium ionophore A23187 (2 microM) stimulated, within 2 h, formation of NAPE in 2-day-old cultures (fourfold) as well as in 6-day-old cultures (eightfold). Glutamate exerted its effect via NMDA receptors as seen by the inhibitory action of the NMDA-selective receptor antagonists D-(-)-2-amino-5-phosphonovalerate and N-(1-(2-thienyl)cyclohexyl)piperidine and the lack of effect of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate-receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In 6-day-old cultures, exposure to NMDA (100 microM for 24 h) induced a linear increase in the formation of NAPE and NAE as well as a 40-50% neuronal death, as measured by a decrease in cellular formazan formation [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay]. The increase in NAPE and NAE could be detected earlier than the neuronal death. Neither cyclic AMP, cyclic GMP, nitric oxide, protein kinase C, nor peroxidation appears to be involved in the formation of NAPE and NAE, as assessed by the use of different pharmacological agents. Exposure to 5 mM NaN3 for 8 h resulted in a >80% decrease in the cellular MTT staining and a pronounced linear increase in the formation of NAE and NAPE (reaching 25-30% of total labeling). [14C]Anandamide was also formed in [14C]arachidonic acid-labeled neurons exposed to NaN3. No NAPE formation was detected in A23187-stimulated mouse astrocytes, rat Leydig cells and cardiomyocytes, and several other cells. These results suggest that the glutamate-induced formation of NAPE and NAE was mediated by the NMDA receptor and the formation of these lipids may be associated with neuronal death.

2-Amino-5-phosphonovalerate↗
PubMed1996

Screening and treating depressed patients. A comparison of two controlled citalopram trials across treatment settings: hospitalized patients vs. patients treated by their family doctors. Danish University Antidepressant Group.

This study is a comparison across treatment settings of two previously published trials, namely the Danish University Antidepressant Group (DUAG) study on citalopram vs. clomipramine in hospitalized patients with major depression, and the Nordic citalopram vs. imipramine study of depressed patients treated by their family doctors. The Hamilton Depression Scale (HAM-D) had the same level of inter-rater reliability and construct validity in the two settings. Using a HAM-D score of 7 or less as the criterion for full two remission, clomipramine was superior to imipramine and citalopram. Using a reduction of the baseline HAM-D score by 50% or more as a response criterion, there were no differences between the three antidepressants after 5 or 6 weeks of treatment. Citalopram showed superior tolerability to the tricyclic antidepressants.

Citalopram↗
PubMed1996

Relapse prevention by means of paroxetine in ECT-treated patients with major depression: a comparison with imipramine and placebo in medium-term continuation therapy.

In-patients with severe major depression were treated in the acute phase with electroconvulsive therapy (ECT) in combination with antidepressants. The drug treatment consisted of two randomized trials which were both extended into the post-ECT continuation phase. Patients with electrocardiological impairment were randomized to either 30 mg paroxetine daily or placebo under blind conditions. Patients without electrocardiological impairment were randomized to either 30 mg paroxetine daily or 150 mg imipramine daily. There was a high level of agreement between the Hamilton Depression Scale and the Melancholia Scale, demonstrating that the patients treated with ECT plus imipramine in the acute phase showed greater symptom reduction than those treated with ECT plus paroxetine. However, in the post-ECT phase paroxetine was superior to both imipramine and placebo in preventing relapse. Thus in the post-ECT phase 65% of the placebo-treated patients relapsed, compared to 30% of the imipramine-treated patients and 10% of the paroxetine-treated patients. The psychometric analysis of the Melancholia Scale in the continuation or post-ECT phase showed that relapsing patients displayed a pattern with lack of interests, impaired concentration, depressed mood and anxiety among the less severe symptoms (first-compartment symptoms). In other words, these symptoms represent the gate to full-blown depression (second-compartment symptoms). Serotonin-selective antidepressants such as paroxetine appear to be more effective in controlling the first-compartment symptoms.

Adult↗
PubMed1995

Differential phospholipid-labeling suggests two subtypes of phospholipase D in rat Leydig cells.

The aim of the present study was to compare the transphosphatidylation activity of phospholipase D (PLD) under different substrate labeling conditions, in order to investigate whether PLD in rat Leydig cells exhibited any substrate preferences for the alkyl- or acyl-form of phosphatidylcholine (PtdCho). The [3H]phosphatidylethanol formation in response to 4 beta-phorbol 12-myristate 13-acetate (PMA), sphingosine, or Ca(++)-ionophore A23187, was lower when Leydig cells were labeled with 1-O-[3H]alkyl lysoPtdCho compared with the responses when [3H]myristic acid was employed. In contrast, the results for the receptor agonists (vasopressin, bradykinin, and lysophosphatidic acid), using the two labels, showed more consistency. Thus, the PLD-activity induced by PMA, sphingosine, or A23187 has a more selective substrate range (i.e. mainly acyl-linked PtdCho) than the PLD-activity stimulated via a receptor. Our data suggests the existence of PLD isozymes that differ with respect to substrate specificity and activation mechanisms.

Animals↗
PubMed1995

Glutamate stimulates the formation of N-acylphosphatidylethanolamine and N-acylethanolamine in cortical neurons in culture.

The formation of anandamide (N-arachidonoylethanolamine), N-acylethanolamine, and N-acylphosphatidylethanolamine was studied in primary cultures of rat cortical neurons. The cells were incubated for 22 h with [14C]ethanolamine, [U-14C]arachidonic acid, [3H]arachidonic acid, [32P]phosphate, [14C]stearic acid, or [3H]myristic acid. The lipids from the cells and media were separated by thin layer chromatography. [14C]Ethanolamine labelling revealed two compounds (I and II), which on different thin layer chromatography systems migrated as N-acylethanolamine (0.06-0.55% of total radioactivity) and N-acylphosphatidylethanolamine (0.66-6.49% of total radioactivity), respectively. Compound II was also labelled with [32P]phosphate, and radioactive fatty acids. Treatment of compound II with phospholipase D (Streptomyces chromofuscus) resulted in two compounds, one comigrating as phosphatidic acid and the other as N-acylethanolamine. Compound I could be labelled with [14C]stearic acid and [3H]myristic acid, but not with [3H]- or [14C]arachidonic acid. Exogenous [3H]anandamide was metabolised with a t1/2 of 2.6 h. The labelling of the two compounds identified as N-acylethanolamine and N-acylphosphatidylethanolamine were more pronounced the older the culture. The neurotoxic amino acid, glutamate, stimulated within 2 h dose-dependently (ED50 = 40 microM) the formation of both compounds. It is suggested that N-acylethanolamine and N-acylphosphatidylethanolamine are formed in relation to the cytotoxicity induced by glutamate, and that these compounds may be markers of neurotoxicity. We could not detect any formation of anandamide using radioactive arachidonic acid.

Animals↗
PubMed1995

A definite and a semidefinite questionnaire version of the Hamilton/melancholia (HDS/MES) scale.

A definite (anchored) and a semidefinite (semi-anchored) questionnaire version of the Hamilton Depression Rating Scale (HDS) and the Bech-Rafaelsen Melancholia Scale (MES) were compared with the HDS/MES by observer-rating and self-rating of 24 patients fulfilling the DSM-3R criteria for major depressive disorder. Both types of questionnaire showed substantial agreement with the observer scale from which they were derived. The sum scores were for the definite questionnaires and the corresponding observer scales closely similar whereas the sum scores of the semidefinite questionnaires were significantly higher than the sum scores of the corresponding observer scales. These results indicate that patients' 'halo' effect may be avoided by using definite scaling criteria for self-rating. Thus, of the two versions of questionnaires the definite versions are recommended.

Adult↗
PubMed1995

Risk factors for post-stroke depression.

An unselected cohort of 285 stroke patients, median age 69 years, were studied for correlation between potential risk factors and the 1-year incidence of post-stroke depression (PSD). The following factors correlated significantly with PSD: a history of previous stroke, a history of previous depression, female gender, living alone and social distress prestroke. Further, social inactivity, decrease in social activity, pathological crying and intellectual impairment at 1 month but not functional outcome correlated to PSD. A multivariate regression analysis showed that intellectual impairment explained 42% of variance of mood score. Major depression was unrelated to lesion location. We conclude that etiology to PSD is a complex mixture of prestroke personal and social factors, and stroke induced social, emotional and intellectual handicap.

Activities of Daily Living↗
PubMed1994

Post-stroke depression: combined treatment with imipramine or desipramine and mianserin. A controlled clinical study.

In a 6-week study the efficacy of combined treatment of imipramine plus mianserin was compared to combined treatment of desipramine plus mianserin in patients with post-stroke depression. Patients were required to have a minimum baseline total score of 15 on the 17-item Hamilton Depression Scale (HAMD). The Melancholia Scale (MES) was also used to measure severity of depressive states to show that somatic symptoms had little influence on the evaluation of depression. Out of 120 stroke patients screened, 20 patients fulfilled the inclusion criteria. The doses of the drugs were flexible, using side-effects as a guide during treatment. Both intention to treat analysis and efficacy data (excluding patients who had dropped out during the first 2 weeks of treatment) showed that imipramine (mean dose 75 mg daily) plus mianserin (mean dose 25 mg daily) was superior to desipramine (mean dose 66 mg daily) plus mianserin (27 mg daily). The MES was found to be more sensitive than the HAMD for measuring change in depressive states during treatment. The assessment of side-effects using the UKU scale showed good tolerance in general. The only difference between the two treatment groups was seen in micturition disturbances, where the imipramine treated patients had most complaints after 14 days of treatment, but the symptoms disappeared despite continuous treatment.

Aged↗
PubMed1994

Agents that increase phosphatidic acid inhibit the LH-induced testosterone production.

The results of the present study point to phosphatidic acid (PtdOH) as a possible intracellular messenger, which might be involved in local modulation of testicular testosterone production in vivo. Propranolol (27-266 microM) induced an increased level of [3H]PtdOH in isolated rat Leydig cells, prelabeled with [3H]myristate, and at the same time a strong dose-dependent inhibition of the acute testosterone production stimulated by luteinizing hormone (LH). The inhibition was not bypassed by the addition of dibutyryl-cAMP but was overcome, when 22(R)-hydroxycholesterol was added as a direct substrate for cytochrome P-450 side chain cleavage enzyme. Thus, the inhibition appears to be exerted at a point distal to cAMP-generation but before the first enzyme in the testosterone synthetic pathway. Treatment with other agents (4 beta-phorbol 12-myristate 13-acetate (PMA), A23187, and sphingosine) giving rise to increases in the PtdOH-level resulted in the inhibition of the LH-induced testosterone formation as well, thus indicating a connection between the two effects. Furthermore, we were able to demonstrate a highly significant correlation between the PtdOH-increase and the inhibition of the LH-stimulated testosterone production. This may suggest a causal relationship between these two parameters.

Animals↗
PubMed1994

Incidence of post-stroke depression during the first year in a large unselected stroke population determined using a valid standardized rating scale.

This study describes the development of post-stroke depression (PSD) prospectively during the first year post-stroke in 285 unselected stroke patients. An appropriate unselected population-based control group without cerebral pathology is included for comparison. Psychiatric assessment with the Hamilton Depression Rating Scale (HDRS) was undertaken unmodified. PSD was defined as HDRS > or = 13. The one-year incidence of PSD among the 209 survivors able to communicate reliably at 1 month was 41%. Most cases develop within the first months following stroke (79%), the frequency of new cases of PSD at one year being 5%, a level comparable to that in the control group. Depressed and nondepressed stroke patients consistently scored 4 points greater on total HDRS than in the corresponding controls.

Adult↗