[Why are so many children hospitalized with poisoning?].
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Child↗
Biomedical subjects
K Jensen
Publications and source records attributed to K Jensen.
Experiential factors in the expression of hypermotility produced by intradentate colchicine: lack of effect of GM1 ganglioside on colchicine-induced loss of granule cells and mossy fibers.
Adult male Fischer-344 rats were given bilateral injections of 2.5 micrograms colchicine or artificial cerebrospinal fluid into caudal and rostral sites of the dentate gyrus of the hippocampus. One group of rats received 21 consecutive daily injections of 20 mg/kg GM1 gangliosides, i.p., beginning the day prior to surgery. Another group received saline. Colchicine-induced hypermotility was not seen in animals repeatedly handled 21 d after surgery, in spite of significant decreases in granule cell number and decreases in the volume of hippocampal mossy fibers. Pretreatment with GM1 had no effect on behavior and it did not protect against the hippocampal damage produced by colchicine. Rats given colchicine, but not handled for 21 d, showed significant hypermotility, which was associated with decreases in hippocampal granule cells. These data underscore the importance of handling in postlesion functional recovery.
Animals↗
Cerebral blood flow and metabolism during controlled hypotension with sodium-nitroprusside and general anaesthesia for total hip replacement a.m. Charnley.
Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were studied during hypotension induced with sodium nitroprusside (SNP) in 10 patients undergoing total hip replacement a.m. Charnley. Cerebral blood flow was measured using an injection of xenon-133 into an arm vein. The decay curve was detected by five scintillation counters placed over each hemisphere and analysed with the Novo 10a cerebrograph. Blood samples were drawn from the radial artery and the jugular venous bulb to calculate the CMRO2. In the group as a whole, there were significant decreases in mean arterial pressure and in cerebrovascular resistance. There were no significant changes, in either CBF or CMRO2 in the group as a whole, but there were substantial individual differences. In conclusion, the use of SNP-induced hypotension for extracranial surgery should be used only in patients monitored closely.
Aged↗
Subcutaneous blood flow in the temporal region of migraine patients.
Subcutaneous blood flow in the temporal region (TSBF) was measured by the local 133 Xenon washout technique in 43 migraine patients; 19 were reexamined in the course of spontaneous attacks. During attacks, TSBF was normal compared to the headache-free state. In 13 unilateral attacks, the median ipsilateral to contralateral ratio of TSBF was 1:1.276, (NS). During 30 degrees passive head-up tilt, TSBF decreased by a median of 27% during headache-free intervals and by a median, 21% during migraine attacks. The difference between the 2 occasions was not significant. Head-up tilt resulted in a median 4.5% increase in mean arterial blood pressure (MAP) and a median 5.3% increase in heart rate (HR) during headache-free intervals and 3.4% and 3.2% respectively during migraine attacks. These results are evidence against a vasomotor disturbance of the extracranial tissues during attacks of migraine. The cardio-vascular response to the orthostatic stimulus indicates a normal function of this part of the autonomic nervous system during migraine attacks.
Adult↗
Plasma beta-endorphin during clinical and experimental ischaemic pain.
An improved radio-immunoassay using an antiserum directed towards the N-terminal part of the endogenous opioid peptide beta-endorphin 1-31 (beta-EP) was validated and applied to a study of beta-EP in plasma during ischaemic pain. Experimental ischaemic pain induced in seven healthy volunteers by the submaximal effort tourniquet test did not change plasma beta-EP or adrenocorticotrophin. Plasma beta-EP was determined in 21 patients with acute myocardial infarction (AMI) and in seven patients with unstable angina pectoris. Plasma beta-EP was 4.9 fmol/ml with 95% confidence limits, 3.2-7.8 fmol/ml in AMI patients at admittance, and 2.9 (2.0-3.4) fmol/ml one week later in stable and pain-free condition (p less than 0.05). The level in 49 healthy persons was 2.8 (2.4-2.9) fmol/ml. Elevated beta-EP levels were found in five AMI patients with cardiogenic shock and in four AMI patients dying within 24 h after admittance compared to the rest of AMI patients (p less than 0.02). beta-EP was not elevated during unstable angina pectoris, although pain scores were similar to AMI. The AMI group revealed a significant, although weak, positive correlation between plasma beta-EP and pain score (Spearman r = 0.49, p less than 0.05), while there was no correlation during unstable angina pectoris. beta-EP was not correlated to the amount of morphine required within the 48 h after admittance of AMI patients. We conclude that the increase of beta-EP in plasma during AMI may be due to stressful factors other than ischaemic pain and that it is questionable whether beta-EP in plasma is related to antinociception.
Adult↗
Inositol phospholipid and intracellular calcium metabolism in B lymphocytes stimulated with antigen.
Stimulation of B lymphocytes by anti mu antibody can activate the phosphatidylinositol pathway, but B cell activation by LPS does not involve this pathway. This study was done to determine if stimulation of B lymphocytes by their specific antigen involves this important activation pathway. We showed that levels of IP2 and IP3 increase while PIP and PIP2 decline when dinitrophenyl specific B lymphocytes are stimulated with the antigen DNP-Ficoll. Intracellular calcium concentration also increases with this stimulus. Thus, antigen stimulation of B lymphocytes is associated with activation of phosphatidylinositol pathway.
Antigens↗
[Paracetamol poisoning].
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Acetaminophen↗
Localization and effects of neuropeptide Y, vasoactive intestinal polypeptide, substance P, and calcitonin gene-related peptide in human temporal arteries.
Nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) were seen in the adventitia or at the adventitia-media border of the human temporal artery. Pharmacological experiments on isolated temporal artery segments revealed that NPY potentiated the vasoconstrictor responses to noradrenaline, but had no vasoconstrictor ability or only a small vasoconstrictor ability per se. VIP, peptide histidine methionine 27 (PHM-27), SP, neurokinin A (NKA), and CGRP potently relaxed vessels precontracted by prostaglandin F2 alpha, the relative potency being CGRP greater than SP greater than NKA = VIP = PHM-27. The amount of relaxation varied between 67 and 91% of the prostaglandin F2 alpha-induced contraction. The peptide effects were not antagonized by classic adrenergic or cholinergic blockers, suggesting interactions via separate receptor sites.
Calcitonin Gene-Related Peptide↗
Decrease in pulmonary diffusion capacity after maximal exercise.
Oppression of the chest, cough and orthopnea are well known to occur in some athletes after competitions, maybe reflecting an increase in lung water. In order to indicate if lung water increases after maximal exercise we measured pulmonary diffusion capacity before and 2.1 h after a short maximal arm exercise bout in 11 canoeists and showed a decrease of 6.7%. The result may be explained by a calculated 17% increase in alveolar interstitial volume.
Adolescent↗
Classic migraine. A prospective recording of symptoms.
Systematic prospective records of aura symptoms were obtained from 50 patients, who filled in report forms during the aura phase of two attacks. The pattern of the various aura symptoms was remarkably constant during two attacks. Visual aura was recorded by 94% of the patients, somato-sensory aura symptoms by 40%, motor disturbances by 18% and speech difficulties by 20%. Visual aura was unilateral in 55%, somato-sensory aura symptoms were unilateral in 80% and motor aura was unilateral in 100%. Surprisingly, headache was absent in 20% of the aura attacks. When unilateral headache and unilateral aura symptoms occurred in the same attack, headache was most often contralateral to the somato-sensory and motor aura symptoms. Our observations are in accordance with the hypothesis that the pathophysiological process responsible for the aura symptoms in classic migraine starts at the visual cortex.
Adolescent↗
Altered thalamocortical axon morphology following neonatal peripheral nerve damage: implications for the study of developmental neurotoxicity.
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Afferent Pathways↗
[Fatal cases of barbituric acid poisoning in drug addicts].
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Barbiturates↗
Volunteer bias in erotica research: effects of intrusiveness of measure and sexual background.
Volunteer characteristics and volunteer rates across several laboratory experiments of sexual arousal were compared. Conditions were created to assess which component of the experimental setting was responsible for low volunteer rates in experiments using genital measurement. Subjects were 324 male and 424 female undergraduate students who had volunteered for an experiment on sexuality and personality. After completing several measures of sexual experience and attitude, subjects received a written description of one of the following conditions and were asked if they wished to volunteer: sexual film, sexual film and subjective rating of arousal, sexual film and assessment through forehead temperature, sexual film and assessment with a device that was placed over the clothes and measured genital heat flow, sexual film and assessment with the heat flow device while partially undressed, or sexual film and assessment with the vaginal photoplethysmograph or penile strain gauge while partially undressed. Men were significantly more likely to volunteer than women, and volunteer rates for both men and women decreased significantly when and only when subjects were required to undress. Multivariate analyses of variance revealed that both male and female volunteers were more sexually experienced, reported more exposure to erotic materials, and worried less about their sexual performance than nonvolunteers. No differences in volunteer characteristics occurred across the increasingly intrusive conditions for women while a few differences occurred for men. The present findings suggest that researchers should be cautious about discussing the generality of findings of studies involving exposure to a sexually explicit film alone as well as of experiments that involve self-report or physiological measures of sexual arousal.
Attitude↗
Clinical trial of nimodipine for single attacks of classic migraine.
In a randomized, double-blind cross-over study, 43 patients with classic migraine received 40 mg Nimodipine and placebo as sublingual capsules. There was no significant effect on patients' preference, development of headache, need for escape medicine, duration of headache, severity of headache or headache index. Considerable methodological problems were encountered. Only 54% of the 79 patients selected for the trial could be evaluated. Suggestions for future trials are made.
Clinical Trials as Topic↗
Beta-endorphin and ACTH in plasma during attacks of common and classic migraine.
Plasma levels of beta-endorphin and ACTH were measured during and outside migraine attacks in 17 patients with common migraine and 11 patients with classic migraine. Specific radioimmunoassays for beta-endorphin and ACTH were used. The beta-endorphin assay did not cross-react with beta-lipotropin. In common migraine, median plasma beta-endorphin was 3.3 pmol/l (95% confidence limits: 2.5-4.0 pmol/l) during attacks and 2.9 (2.4-3.2) pmol/l in the headache-free period. In classic migraine, plasma beta-endorphin was 3.2 (1.4-4.3) pmol/l during attacks and 2.4 (1.1-3.6) pmol/l outside attacks. ACTH plasma levels were 15 (10.5-20) pmol/l during and 15.7 (13.4-17) pmol/l outside attacks in common migraine. In classic migraine, plasma ACTH was 16 (7-36) pmol/l and 12.3 (8-28) pmol/l respectively. No significant differences were found between attacks and headache-free periods in common or classic migraine. Accordingly, we could not add evidence to the theory of a dysfunction of the endogenous opioid system in migraine.
Adrenocorticotropic Hormone↗
Experimental toothclenching in common migraine.
The effect of 30 min voluntary toothclenching was studied in 48 patients with common migraine, randomized in two groups. Group 1 performed low-level tension at 5% and group 2, high-level tension at 30% of the individual maximum, as judged by surface EMG from the temporal muscle. Pericranial muscle tenderness was evaluated by manual palpation and a four-point verbal scale. Headache, nausea, and soreness of the chewing muscles were scored on visual analogue scales. Although surface EMG, soreness, blood pressure, heart rate and difficulty in completing the toothclenching session all showed that group 2 patients were subjected to significantly higher levels of muscle tension than group 1 patients, headache developed equally often in both groups (63%). Headache was even more pronounced in group 1 (n.s.). Five patients in group 1 and none in group 2 developed an attack of migraine during the following 24 h. Pericranial muscle tenderness was unaffected by the experimental procedure. There was no significant correlation between headache intensity and pericranial muscle tenderness. Muscle ischemia, muscle "fatigue", and strain on muscle insertions are thus unlikely to cause attacks of common migraine.
Adult↗
Temporal muscle blood flow in common migraine.
Temporal muscle blood flow (TMBF) was measured by the local 133-Xenon washout technique in 61 patients suffering from common migraine. Nineteen were re-examined in the course of spontaneous attacks. Muscle tension was quantified by surface EMG. During the attacks, median TMBF increased insignificantly, 33% on the ipsilateral and 24% on the contralateral side. During 15 unilateral attacks, the ipsilateral-contralateral ratio of TMBF was 1.02. Isometric and dynamic work tests showed intact metabolic regulation of TMBF. These results speak against a general vasomotor disturbance of the extracranial tissues during attacks of common migraine. There was also no indication that ischemia of the temporal muscle might explain the pain.
Adult↗