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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 71 (1993), S. 208-213 
    ISSN: 1432-1440
    Keywords: Allergy ; Whooping cough ; Pertussis toxin ; IgE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate whether pertussis induces the development of allergy, a prospective study was performed in 25 children aged 0.8–12.2 years. The patients underwent allergy diagnostics during pertussis infection and at a follow-up visit 8–14 months later. Diagnostic criteria included the medical history of the patients and their families, a modified skin prick test, measurement of serum IgE and radio-allergosorbent test screening for specific sensitizations. At the time of pertussis, serum IgE concentration in the study group was 62+ 30 kU/ml. At the follow-up visit, there was a significant increase in serum IgE to 137 ± 51 kU/ml, which was also significantly higher than IgE in an age-matched control group. Children at a significantly higher risk for developing IgE increase or new allergic sensitizations were those with a family history of allergy or potentially allergic disease in their personal history. Our results indicate that pertussis may induce IgE production in affected children.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1076
    Keywords: Human basophils ; Histamine release ; Pertussis toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of childhood pertussis infection and of purified pertussis toxin on histamine relase from human basophil leucocytes was investigated. Three different stimuli, the peptide N-formyl-Met-Phe (NFMP), anti-IgE, and the calciuminnophore A23187 were used to challenge the cells. When NFMP was the stimulus, histamine release in the control group (age 0.5–17 years) increased in an age-dependent fashion, whereas anti-IgE and A23187 stimulated release did not vary with age. During the convulsive state of pertussis infection there was a significant reduction of histamine release in response to 10 μM NFMP (from 9.5±1.4 [n=21] to 6.7±1.5 [n=19],P〈0.05) and in response to 800 and 80 U/ml anti-IgE (from 28.5±5 [n=19] to 16.3±5 [n=13],P〈0.05, and from 6.9±1.7 [n=16] to 2±0.8 [n=13],P〈0.01), whereas histamine release stimulated by A23187 was unchanged compared to release in control children. In vitro pretreatment of basophils from healthy children and adults with pertussis toxin also inhibited histamine release. When NFMP was the stimulus, release was completely blocked by pertussis toxin with an IC50 of about 11 ng/ml whereas anti-IgE stimulated release was only inhibited by 20%–30% and release induced by A23187 was reduced to 40%–50% by toxin treatment. In conclusion we have demonstrated a functional impairment of histamine release during the convulsive state of pertussis and that this inhibition is likely to be mediated by pertussis toxin.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1076
    Keywords: β-adrenoceptors ; Down-regulation ; Catecholamines ; Congenital heart disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Twenty-six infants and children with congenital heart disease (CHD) undergoing cardiac surgery were investigated for alterations in myocardial β-adrenoceptor density. The patients were divided into three groups according to type and severity of CHD: group I consisted of 6 patients with acyanotic shunt lesions of moderate severity; group II comprised 13 children with severe acyanotic shunt and valve lesions and group III included 7 children with cyanotic CHD. The myocardial β-adrenoceptor density was determined using (−)3-[125I] Iodocyanopindolol ([125I]ICYP) and was reduced by approximately 50% in severe acyanotic CHD (33.6 fmol/mg protein) and cyanotic CHD (35.3 fmol/mg protein) in comparison with the group with less severe acyanotic shunt defects (64.4 fmol/mg protein). The affinity dissociation constant (K d, ICYP) did not differ statistically between the groups. The proportion of β1- and β1-subpopulation was evaluated by ICI 118,551-[125I]ICYP competition studies. In group II (61.5%) and group III (69.1%) significant lower portions of β1-adrenoceptors were found compared with group I (78.2%). This shift of subpopulations was due to a decreased β1-receptor density while β2-receptor density was unchanged in all groups. While the plasma noradrenaline levels of group I were similar to those of a control group of 13 healthy children, respective values of group II and III were significantly elevated. A significant negative correlation was found between plasma noradrenaline levels and myocardial β-adrenoceptor density. It is concluded that exposure of these receptors to increased circulating catecholamines, due to an enhanced sympathetic tone, leads to a reduction of their density. Noradrenaline, a preferential agonist of β1-adrenoceptors, is most probably responsible for the shift of the β-adrenoceptor subpopulations from the β1- to β2-subtype, depending on severity and type of cardiac disease.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1076
    Keywords: Allergic asthma ; Children ; Phospholipids ; Fatty acids ; Glucocorticoids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fatty acid (FA) composition of plasma phospholipids and phospholipids extracted from peripheral mononuclear white blood cells (MNC) was investigated in 11 allergic asthmatic children (age 8.9±4.6 years), in 10 age-matched non-allergic healthy controls and in 14 allergic and non-allergic children with an acute attack of asthma, who had received prednisolone medication for 2–4 days. In allergic asthmatics eicosapentaenoic acid (20∶5n−3) was significantly elevated in both plasma and MNC. The relative amount of 20∶5n−3 in MNC as well as in plasma correlated positively with increasing levels of total serum IgE (P〈0.02). The pattern of the other FAs in plasma and of MNC phospholipids did not differ between allergic asthmatic and non-allergic control children. In children with an acute attack of asthma, who had been treated with glucocorticoids (2 mg prednisolone/kg body weight for 2–4 days), distinct changes of relative FA composition of phospholipids were restricted to plasma, where some very long chain FA (22∶4n−6, 22∶5n−6) were elevated. No significant changes in FA from MNC phospholipids could be observed after glucocorticoid treatment. These findings may indicate a possible role of 20∶5n−3, the precursor of “group 3” eicosanoids, in allergic asthmatic children.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1076
    Keywords: Asthmatic children ; β-Adrenoceptors ; β-Sympathomimetic drugs ; Lung function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical observations have shown that some asthma patients develop tachyphylaxis to β-sympathomimetic drugs. As down-regulation of the number of β-adrenoceptors in different human tissues after exposure to catecholamines and β-adrenergic drugs is well known, we investigated whether a interrelation exists between β-adrenoceptor down-regulation and clinically detectable β-adrenergic subsensitivity during β-sympathomimetic treatment. The following results were obtained: 1. β2-Sympathomimetic inhalation treatment with salbutamol in therapeutic doses led to a significant downregulation of β2-adrenoceptors and consecutive cyclic adenosine monophosphate response to isoprenaline. This effect was already detectable after short-term treatment of 3–7 days in 9 asthmatic children. 2. In the long-term study over 6 months, salbutamol inhalation in 12 asthmatic children led to a significant down-regulation of β-adrenoceptor binding sites on mononuclear blood cells (MNC) from 1539±91 to 1115±99 after 14 days, remaining in this range thereafter. 3. The mean airway resistance (Raw) of these 12 patients decreased significantly within 14 days from 8.1±0.8 to 5.7±0.5 cm H2O/l/s to remain stable throughout the 6 months of salbutamol treatment. The differences in Raw before and immediately after inhalation of 0.2 mg salbutamol (2 puffs) were unchanged during the study period. It is concluded, that long-term inhalative treatment with salbutamol over a period of 6 months does not result in refractoriness to β-adrenergic drugs in the airways of asthmatic children, even though a significant down-regulation of β2-receptors on peripheral MNC occurs.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Keywords: Β-Adrenoceptors ; Mononuclear leukocytes ; Right atrium ; Down-regulation ; Catecholamines ; Congenital heart disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sympathetic regulation of myocardial performance has been shown to be altered in congestive heart failure. Right atrial tissue of children with severe acyanotic and cyanotic congenital heart disease (CHD) showed a significantly lowerΒ-receptor density than that of children with less severe defects. Since mononuclear leukocytes (MNL) contain a homogeneous population ofΒ 2-adrenoceptors which have similar properties to those of cardiacΒ 2-adrenoceptors, they are frequently used for studying theΒ-adrenergic system. In a group of 37 children with CHD of different types and severity who underwent cardiac surgery, we compared the MNLΒ-adrenoceptor density to the type and severity of CHD and looked for a possible relationship to plasma catecholamine levels and to the right atrialΒ-adrenoceptor density. Membranes of MNL and myocardial cells were radiolabeled with (−)3-[125I]Iodocyanopindolol ([125I]ICYP). A significantly higherΒ-adrenoceptor density on MNL was found in patients with moderate acyanotic CHD (group I) than in those with severe acyanotic (group II) and cyanotic CHD (group III). Patients of group I showed approximatively 50% higher myocardialΒ-receptor density than those of groups II and III. ICI 118.551-[125I]ICYP competition studies revealed that in groups II and III significantly lower proportions and densities ofΒ 1-receptors were found compared to group I. Noradrenaline (NA) plasma levels in group II and group III were significantly higher than those in group I. The adrenaline plasma levels were found to be very high in all children with CHD. A significant negative correlation between NA levels and myocardial total andΒ 1-adrenoceptor density, but no correlation between plasma catecholamines and MNLΒ-adrenoceptor density, was calculated. We conclude that modulation of MNLΒ-adrenoceptors is not simply controlled by circulating catecholamine levels. CardiacΒ 2-adrenoceptor density remained unaltered, but theΒ 1-density was significantly lowered.Β 2-adrenoceptors on MNL showed a slight but significant decrease. However, cardiacΒ 2-adrenoceptor density cannot be predicted by measuring theΒ-adrenoceptor density on MNL.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 69 (1991), S. 1038-1038 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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