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Biomedical subjects

R Ekman

Publications and source records attributed to R Ekman.

At least 91 records · Page 5Linked to original sources
PubMed1996

Disturbed motilin and cholecystokinin release in the irritable bowel syndrome.

BACKGROUND: The irritable bowel syndrome (IBS) is associated with motor abnormalities in the small intestine and colon. Neuropeptides may have an important role in initiating and regulating the intestinal motility. Motilin has been proposed to initiate the peristaltic reflex in the small intestine and cholecystokinin the gastrocolic reflex. METHODS: In 18 patients with IBS and 11 healthy control subjects plasma motilin and cholecystokinin (CCK) concentrations were measured after intraluminal stimulation of water and a fat-rich meal. RESULTS: The IBS patients had reduced motilin secretion after both water intake and the fat meal. In contrast, the fat meal elicited an exaggerated and prolonged CCK release in the IBS patients. CONCLUSIONS: Disturbed motilin and CCK release may partly be responsible for the intestinal dysmotility in the IBS patients.

Adult↗
PubMed1996

The concentrations of monoamine metabolites and neuropeptides in the cerebrospinal fluid of obese women with different body fat distribution.

DESIGN AND SUBJECTS: Several studies suggest neuroendocrine abnormalities in, particularly, abdominal, central obesity in humans, a condition with high morbidity and mortality. Therefore the concentrations of neuropeptides and catecholamines in cerebrospinal fluid (CSF) were analysed in 48 obese women, subdivided into groups with central, abdominal and gluteo-femoral distribution of body fat, utilising the waist-to-hip circumference ratio (WHR) for division. RESULTS: In comparisons with non-obese control women concentration of 5-hydroxyindol acetic acid (5-HIAA), methoxyhydroxyphenylglycol (MHPG), corticotropin releasing hormone (CRH), beta-endorphins (END) and neuropeptide Y (NPY) were lower, while homovanillic acid (HVA) was not different in obese women, HIAA, HVA and END correlated negatively with the WHR only in abdominally obese women, suggesting a threshold effect. HIAA vs HVA as well as CRF vs END correlated strongly in the total and both subgroups. An interrelationship between all these four substances was found in abdominal but not in gluteo-femoral obesity, suggesting a tighter functional coupling in the former group. Several correlations were found between CSF substance levels and appetite registrations, including END vs voracious eating, and for carbohydrate craving vs HIAA and vs HVA (negatively). This was also found only in abdominally obese women. CONCLUSION: Although the concentrations of monoamine metabolites and neuropeptides in the CSF sampled at the level of the lumber spine might not be representative for those at regulatory centers in the brain, the findings suggest that low 5-HIAA is characteristic of human obesity, and coupled to CRH as well as eating abnormalities, particularly in abdominal obesity. Since CRH is regulating the balance between the autonomic nervous systems, insulin secretion and thermogenesis in animals, corresponding anomalies in abdominal obesity in humans may have a central origin.

Adipose Tissue↗
PubMed1995

Cerebrospinal fluid neuropeptides in Alzheimer's disease and vascular dementia.

Cerebrospinal fluid (CSF) levels of several neuropeptides have been suggested as candidate markers in neurodegenerative disorders. We have examined the levels of corticotropin-releasing hormone (CRH), beta-endorphine (BEND), delta sleep-inducing peptide (DSIP), somatostatin (SRIF), and neuropeptide Y (NPY) in CSF samples obtained under highly standardized conditions from healthy aged controls and from patients suffering from Alzheimer's disease (AD) or vascular dementia (VAD). The influence of some potentially confounding factors was evaluated. CRH and BEND were markedly decreased in both AD and VAD patients, and BEND levels correlated negatively with degree of dementia within the patient population. SRIF was decreased in both AD and VAD patients. DSIP was slightly increased in AD, but not in VAD. NPY did not differ between groups. For none of the peptides did CSF concentrations correlate significantly with duration of illness, nor, with the exception of BEND, with its degree. Present data do not support the hypothesis that specific neuropeptide changes occur in different neurodegenerative disorders, but are in agreement with previous reports suggesting that neuropeptide systems are differentially affected by neurodegeneration.

Aged↗
PubMed1995

[Reduced concentration of beta-endorphin in cerebrospinal fluid and reduced pain tolerance in patients with functional dyspepsia].

It was investigated whether central pain mechanisms including the endogenous antinociceptive system were involved in functional dyspepsia defined as: abdominal pain without abnormal findings. Pain sensitivity was measured by an ischaemic pain test comparing 21 functional dyspepsia patients with two control groups: 1) 24 patients with organic abdominal pain, and 2) 13 healthy pain-free controls. The endogenous opioids beta-endorphin, met-enkephalin immunoreactivity, and dynorphin immunoreactivity were measured in cerebrospinal fluid (CSF) from nine patients with functional dyspepsia and pain-free controls undergoing minor surgery while under spinal analgesia. There was no significant difference between the groups in pain sensitivity, but subdivision of the functional dyspepsia group showed that individuals with pain and no symptoms of irritable bowel syndrome (IBS) were significantly more sensitive to ischaemic pain than functional dyspepsia patients with IBS. The CSF beta-endorphfin concentration was significantly decreased in the functional dyspepsia group as compared with the controls. There were no significant group differences regarding met-enkephalin immunoreactivity and dynorphin immunoreactivity. Because of post-lumbar-puncture headache, this part of the investigation was suspended after nine patients. Functional dyspepsia is probably a pain syndrome with decreased central antinociceptive activity.

Adolescent↗
PubMed1995

Noncompetitive enzyme immunoassay (hetero-two-site enzyme immunoassay) for gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) and measurement of immunoreactive gamma 2-MSH in plasma of healthy subjects.

A noncompetitive enzyme immunoassay (hetero-two-site enzyme immunoassay) for gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) was developed. gamma 2-MSH (1-12) was biotinylated, trapped onto an anti-gamma 2-MSH (1-12) IgG-coated polystyrene bead, eluted at pH 1 after washing to eliminate other biotinylated substances, and measured using two streptavidin-coated polystyrene beads and affinity-purified anti-gamma 2-MSH (1-12) Fab'-peroxidase conjugate. The detection limit of gamma 2-MSH (1-12) was 10-30 amol (16-48 fg)/assay and 130-400 fmol (210-630 pg)/L of plasma. There was little or only slight cross reaction with alpha-MSH, beta-MSH, and gamma 1-MSH. By this immunoassay, the concentration and molecular size of immunoreactive gamma 2-MSH in plasma of healthy subjects were examined, and the results were compared with those by competitive enzyme immunoassay. Immunoreactive gamma 2-MSH measured by competitive enzyme immunoassay was a mixture of substances with high molecular weights (100-500 kDa), and its concentration was calculated to be 50-60 pmol/L using gamma 2-MSH (1-12) as standard. Immunoreactive gamma 2-MSH detected by the noncompetitive enzyme immunoassay after removal of high molecular weight substances was not homogeneous and smaller than gamma 2-MSH (1-12), and its concentration was approximately 1 pmol/L. The exact nature of these immunoreactive gamma 2-MSHs remains to be elucidated. gamma 2-MSH (1-12) added to plasma was degraded rapidly, and the concentration of gamma 2-MSH (1-12) was very low, if any, in plasma of healthy subjects.

Adult↗
PubMed1995

Alterations in perivascular dilatory neuropeptides (CGRP, SP, VIP) in the external jugular vein and in the cerebrospinal fluid following subarachnoid haemorrhage in man.

A possible involvement of perivascular vasodilatory neuropeptides in subarachnoid haemorrhage (SAH) has been evaluated in man by measuring the levels of calcitonin gene related peptide (CGRP)-, substance P (SP)- and vasoactive intestinal peptide (VIP)-like immunoreactivity (LI) in the cranial venous outflow and in CSF in 34 patients admitted to the hospital after an acute SAH. After operation with aneurysm clipping and nimodipine treatment, blood samples were taken from the external jugular vein (EJV) or cerebrospinal fluid (CSF) and analysed for neuropeptide levels with specific radioimmuno assays (RIA) during the postoperative course. The degree of vasoconstriction in the patients was monitored with Doppler ultrasound recordings bilaterally from the middle cerebral (MCA) and internal carotid arteries (ICA) following the EJV blood sampling every second day. The mean value of all CGRP-LI measurements in EJV during the entire course of SAH (n = 20) revealed a significantly higher level as compared to controls. The highest CGRP-LI levels were found in patients with the highest velocity index values (vasospasm). The relationship Vmean MCA/Vmean ICA was used as an index of vasoconstriction. In patients with MCA aneurysms (n = 10), a significant correlation (r = 0.65, p < 0.05) was found between the vasospasm index and CGRP-LI levels. There were no changes observed in the SP- and VIP-LI levels. Alterations in cerebrovascular tone induced by changing arterial CO2 tension or lowering of blood pressure (ketanserin infusion test) did not alter the levels of the perivascular peptides in the EJV. In addition, CGRP-, SP-, VIP- and neuropeptide Y (NPY)-LI were analysed in CSF in the post-operative course after subarachnoid haemorrhage (SAH) in 14 patients. The CSF VIP-LI was lower in SAH than in control (p < 0.05). The CGRP-LI level was measurable in SAH CSF but not in CSF of controls. In individual patients with marked vasoconstriction increased levels of CGRP-LI (up to 14 pmol/L) and NPY-LI (up to 232 pmol/L) were observed. The results of this study are in support of our hypothesis that there is an involvement of the sensory peptide CGRP in a dynamic reflex aimed at counterbalancing vasoconstriction in SAH.

Adult↗
PubMed1995

ECT in Parkinson's disease. Changes in motor symptoms, monoamine metabolites and neuropeptides.

Electroconvulsive therapy (ECT) was given to 16 non-depressed, non-demented patients with advanced Parkinson's disease (PD). In all the patients an antiparkinsonian effect was seen, lasting for 18 months in one patient, 3-5 months in seven patients, and a few days to four weeks in eight patients. After ECT the levels of homovanillic acid and neuropeptide Y in cerebrospinal fluid (CSF) were significantly increased. The eight patients with long lasting motor improvement after ECT had significantly lower CSF-3-methoxy-4-hydroxyphenylglycol compared to the group with short lasting improvement. Five patients developed transitory mental confusion after ECT. In these patients, and in no others, a high albumin-ratio was found already before ECT was given - an indication of blood CSF barrier damage. Our results suggest that ECT is valuable in patients with drug refractory PD or PD with intolerance to antiparkinsonian drugs.

Aged↗
PubMed1995

Circulating neuropeptide Y in plasma from uremic patients consists of multiple peptide fragments.

Increased plasma levels of neuropeptide Y (NPY)-like immunoreactivity (p-NPY-LI) have been described in hemodialysis (HD) patients. In this investigation the effect of a standard HD on p-NPY-LI, analyzed by radioimmunoassay and reverse-phase high performance liquid chromatography (HPLC), was studied. During dialysis p-NPY-LI increased from 128 +/- 5 to 154 +/- 8 pmol/l (p < 0.01). The change in p-NPY-LI during the treatment correlated with the ultrafiltration volume (rs = +0.72, p < 0.05). The HPLC separation revealed a complex pattern of NPY-immunoreactive peptides. This was true of the plasma of the control subjects as well as of the uremic plasma. In the case of the controls and the HD patients prior to dialysis, the amount of NPY-LI was rather small. After the dialysis qualitative as well as quantitative changes of the chromatogram were found. Some of the peaks seemed to have a retention time similar to that of the known fragments of synthetic human NPY used as markers. In conclusion, an increase in p-NPY-LI occurred during the dialysis, probably due to fluid removal. The increased level of NPY-LI in uremic plasma represents a mixture of different NPY fragments.

Aged↗
PubMed1995

Chronic parenteral antidepressant treatment in rats: unaltered levels and processing of neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).

We have previously reported elevated brain tissue contents of neuropeptide Y-like immunoreactivity (NPY-LI) following 3 weeks of oral treatment with the antidepressants zimelidine and imipramine. Other studies have not reproduced this finding. To eliminate the possibility that this has been due to insufficient treatment duration, dosage, or differences in route of administration or assay specificity, we have administered the selective serotonin reuptake inhibitor citalopram and the preferential noradrenaline reuptake inhibitor desmethylimipramine parenterally for 6 weeks. NPY-LI was assayed using both the assay employed in the original study, and an assay based on a different antiserum which has been extensively examined for cross-reactivity. To exclude the possibility that differential processing rather than altered synthesis rate is responsible for apparent changes in NPY-LI, HPLC analysis of immunoreactive fragment profiles was used. No differences in NPY-LI levels were seen in the brain regions examined, and no differences in HPLC profiles of NPY-LI were present with either drug. We conclude that chronic parenteral administration of antidepressant drugs in naïve (non-depressed) animals does not affect the synthesis or processing of NPY. Another neuropeptide implicated in mechanisms of depression, corticotropin-releasing hormone (CRH) was also found to be unaffected by a similar analysis.

Analysis of Variance↗
PubMed1995

Increased cerebrospinal fluid Met-enkephalin immunoreactivity in patients with chronic tension-type headache.

Cerebrospinal fluid (CSF) concentration of Met-enkephalin immunoreactivity (Met-enkephalin-ir) was determined by radioimmunoassay in 47 patients with chronic tension-type headache and in 47 headache-free control subjects. Thirty-nine of the controls were patients receiving spinal analgesia before surgery for diseases not associated with pain; 8 were healthy paid volunteers. Patients reporting migraine more than 1 day per month were excluded. Pericranial tenderness, nociceptive flexion reflex and thermal pain thresholds were determined in the majority of the patients. The median level of CSF Met-enkephalin-ir was significantly higher (115 pmol/l) (quartiles (107-134) pmol/l) in the headache patients than in the controls (median 79 pmol/l) (quartiles (73-87) pmol/l) (Mann-Whitney, P < 0.001). No indication of sex-difference or correlation with age with respect to CSF Met-enkephalin-ir was found. No correlation was found between CSF Met-enkephalin-ir and either pericranial tenderness, nociceptive flexion-reflex threshold, or thermal pain threshold. There was no indication of correlation between consumption of mild analgesics and CSF Met-enkephalin-ir. The higher levels of CSF Met-enkephalin-ir in the headache patients may be indicate activation of the enkephalinergic antinociceptive system at the spinal/trigeminal level, whereas the beta-endorphinergic system appears normal. This enkephalinergic activation may be caused by increased activity in the primary nociceptive afferents, or may be compensatory to decreased activity in other endogenous antinociceptive systems than the opioid.

Adult↗
PubMed1995

The Lidköping Accident Prevention Programme--a community approach to preventing childhood injuries in Sweden.

OBJECTIVES: In Sweden about 100 children 0-14 years die from accidental injuries every year, roughly 40 girls and 60 boys. To reduce this burden the Safe Community concept was developed in Falköping, Sweden in 1975. Several years later a second programme was initiated in Lidköping. The objectives of this paper are to describe the programme in Lidköping and to relate it to changes in injury occurrence. SETTING: The Lidköping Accident Prevention Programme (LAPP) was compared with four bordering municipalities and to the whole of Skaraborg County. METHODS: The programme included five elements: surveillance, provision of information, training, supervision, and environmental improvements. Process evaluation was based mainly on notes and reports made by the health planners, combined with newspaper clippings and interviews with key people. Outcome evaluation was based on information from the hospital discharge registry. RESULTS: In Lidköping there was an on average annual decrease in injuries leading to hospital admissions from 1983 to 1991 of 2.4% for boys and 2.1% for girls compared with a smaller decline in one comparison area and an increase in the other. CONCLUSION: Because the yearly injury numbers are small there is a great variation from year to year. However, comparisons over the nine year study period with the four border municipalities and the whole of Skaraborg County strengthen the impression that the programme has had a positive effect. The findings support the proposition that the decrease in the incidence of childhood injuries after 1984 could be attributed to the intervention of the LAPP. Nevertheless, several difficulties in drawing firm conclusions from community based studies are acknowledged and discussed.

Accident Prevention↗
PubMed1994

Discovery of endogenous catecholamines in lymphocytes and evidence for catecholamine regulation of lymphocyte function via an autocrine loop.

Evidence has been obtained that catecholamines and their metabolites are present in single lymphocytes and extracts of T- and B-cell clones by use of capillary electrophoresis with electrochemical detection. Pharmacological inhibition of tyrosine hydroxylase reduces observed catecholamine levels, suggesting catecholamine synthesis by lymphocytes. Intracellular dopamine levels are shown to be increased by extra-cellular dopamine, suggesting a cellular-uptake mechanism. Furthermore, incubation with either dopamine or L-dihydroxyphenylalanine, a precursor of dopamine, results in a dose-dependent inhibition of lymphocyte proliferation and differentiation. Together, these results suggest the presence of an autocrine loop whereby lymphocytes down-regulate their own activity.

B-Lymphocytes↗
PubMed1994

Analysis of human cerebrospinal fluid by capillary electrophoresis with laser-induced fluorescence detection.

Capillary electrophoresis with laser-induced fluorescence detection is used to analyze 10 microL samples of human cerebrospinal fluid. Primary amine-containing compounds in untreated cerebrospinal fluid are labeled with 3-(4-carboxybenzoyl)-2-quinolinecarboxaldehyde prior to analysis, producing fluorescent isoindoles. Electropherograms containing approximately 50 peaks are obtained in less than 35 min from cerebrospinal fluid samples. Ten peaks in the electropherograms have been identified and quantitated: arginine, glutamine, threonine, valine, gamma-amino-n-butyric acid, serine, alanine, glycine, glutamic acid, and aspartic acid. Detection limits for these 10 amino acids range from 0.29 nM for gamma-amino-n-butyric acid to 100 nM for threonine, and separation efficiencies as high as 190,000 theoretical plates are obtained for these analytes. Electropherograms of cerebrospinal fluid samples from patients with Alzheimer's disease and from children with different neurological disorders are compared to those of healthy controls. Differences in individual amino acid levels are observed between the patient groups, and these differences appear to be disease and age related. These results indicate that analysis of cerebrospinal fluid by capillary electrophoresis will be useful as a selective, rapid, and sensitive tool for both diagnosis of central nervous system disorders and for study of the mechanisms of these disorders.

Adult↗
PubMed1994

Ontogeny of neuropeptides in the rat urinary bladder.

Urinary bladders of male rats at ages ranging from 1 day to 18 months were analysed for their neuropeptide content. NPY was detected at birth, VIP and CGRP at 1 week, and SP at 2 weeks. There was then a sharp increase in both the total amounts and concentrations of VIP, CGRP and SP until the rats had reached the age of 3-4 weeks. The total amount of NPY increased in two surges, between 2-3 weeks and between 4-5 weeks. The concentration of NPY showed a biphasic course, a decrease during the first two weeks and then an increase. In adults the total amounts of substance P and CGRP were higher than in younger animals, whereas that of VIP was lower. Following peaks at 3-8 weeks, the concentrations of VIP and substance P decreased with age, whereas that of CGRP remained unchanged. NPY was not followed beyond 8 weeks. The present findings offer a framework for future studies aimed at elucidating the functional role of neuropeptides in the regulation of micturition.

Aging↗
PubMed1994

Neuron specific enolase in cerebrospinal fluid: a biochemical marker for neuronal degeneration in dementia disorders?

Alzheimer's disease (AD) is the most common disease causing dementia. Today the clinical diagnosis of AD is made by way of exclusion, and no biochemical markers are available to assist the clinical diagnosis. We examined the potential of neuron-specific enolase (NSE) in cerebrospinal fluid (CSF) as a diagnostic marker for AD. NSE was determined with a monoclonal antibody two-site immunoradiometric assay (IRMA) in serum (S) and cerebrospinal fluid (CSF) samples from 45 patients with "probable Alzheimer's disease (AD)", 19 patients with vascular dementia (VAD) and 33 age-matched healthy individuals. There was no significant correlation between S-NSE and CSF-NSE, or between CSF/S albumin ratio and CSF-NSE, findings suggesting that the major portion of CSF-NSE is intrathecally produced and that analysis of CSF-NSE alone (without accompanying analysis of serum) is sufficient. CSF-NSE was significantly higher in the AD group (4.7 +/- 2.7 ng/mL; p < 0.0001) and in VAD group (4.5 +/- 2.5 ng/mL; p < 0.001) as compared with the control group (2.2 +/- 1.0 ng/mL), while it did not differ significantly between the AD and the VAD group. These findings suggest that CSF-NSE have a potential as a non-disease specific marker for the neuronal degeneration in dementia disorders.

Aged↗
PubMed1994

Effect of sulpiride or paroxetine on cerebrospinal fluid neuropeptide concentrations in patients with chronic tension-type headache.

In lumbar cerebrospinal fluid (CSF) obtained from patients with chronic tension-type headache (CTH), the concentrations of beta-endorphin, met-enkephalin, dynorphin, cholecystokinin (CCK), calcitonin gene-related peptide (CGRP), and somatostatin were measured before and after 8 weeks of treatment with sulpiride or paroxetine. We previously reported higher than normal met-enkephalin concentrations in CTH. The present study reveals normal basal concentrations of CCK, CGRP and somatostatin and slightly decreased dynorphin in the same patients. Treatment with sulpiride or paroxetine did not change the concentration of any of the neuropeptides measured. These data suggest central changes in opioid systems but not in other peptide systems (CCK, CGRP, somatostatin) involved in nociceptive processing at the level of the spinal cord dorsal horn/nucleus caudalis of the trigeminal nerve in CTH. Such central changes might be pathophysiologically important or merely secondary to other more important occurrences. The lack of changes in neuropeptide concentrations during drug treatment makes planning of studies involving CSF analysis easier, but also limits the probability of obtaining information on specific neuropeptide systems through CSF analysis.

Adult↗