Interleukin-1 alpha, soluble interleukin-2 receptor, and IgG concentrations in cystic fibrosis treated with prednisolone

The cytokines interleukin-1 and interleukin-2 participate in the inflammatory response, and may contribute to hypergammaglobulinaemia G and the development of lung injury in cystic fibrosis. Anti-inflammatory treatment with corticosteroids may attenuate this response. The effect of a 12 week course of oral prednisolone on spirometry and serum concentrations of interleukin-1 alpha (IL-1 alpha), soluble interleukin-2 receptor (sIL-2R), and IgG was investigated in 24 children with cystic fibrosis. Prednisolone was administered, in a double blind and placebo controlled manner, at an initial dose of 2 mg/kg daily for 14 days and tapered to 1 mg/kg on alternate days for 10 weeks. The treated group (n = 12) experienced an increase in forced expiratory volume in one second and forced vital capacity at 14 days, however, these changes were smaller at 12 weeks. In the treated group, change in pulmonary function was associated with decreased serum IgG and cytokine concentrations. Prednisolone suppresses serum concentrations of these cytokines, which may participate in the inflammatory response, the excessive synthesis of IgG, and airflow obstruction observed in cystic fibrosis patients.     

Intimal hyperplasia as a cause of restenosis after percutaneous transluminal coronary angioplasty

We describe a patient who died 96 days after percutaneous transluminal coronary angioplasty was performed. The balloon-dilated segments of the left anterior descending artery and its first diagonal branch were found to be restenosed. Histologic examination of these arterial segments showed intimal hyperplasia without lipid deposition as the cause of restenosis, rather than common atherosclerotic plaque.     

Peripheral α2-adrenoceptor-mediated sympathoinhibitory effects of mivazerol

Summary— Mivazerol is a new compound that could potentially reduce perioperative cardiovascular morbidity and mortality in patients with or at risk of coronary disease and submitted to surgery. This action of mivazerol depends on a well documented centrally mediated reduction in sympathetic nerve activity, but a direct peripheral decrease in sympathetic neurotransmitter release induced by activation of prejunctional α₂-adrenoceptors located on sympathetic nerve endings could also contribute. To investigate this issue, the effects of mivazerol on the pressor, systemic and regional hemodynamic (pulsed Doppler technique) as well as on the cardiac responses to electrical stimulation of the spinal cord (SCS) were measured in pithed rats in the absence and in the presence of mivazerol. Mivazerol exerted strong sympathoinhibitory effects: SCS-induced increases in blood pressure, total peripheral resistance and heart rate were dose-dependently reduced by mivazerol, but among the regional vascular beds investigated, only the hindlimb vasoconstrictor responses were significantly drug-affected. All these sympathoinhibitory effects of mivazerol were abolished by prior yohimbine administration. Simultaneously, mivazerol did not induce any postjunctional adrenoceptor blockade as it did not affect noradrenaline cardiac and hemodynamic effects. On the contrary, through postjunctional α₂-adrenoceptor stimulation, mivazerol, in this pithed preparation, dose-dependently increased blood pressure, total peripheral and hindlimb vascular resistances, but heart rate was not affected. We conclude that, in the pithed rat, mivazerol exerts strong peripheral sympathoinhibitory effects. The mechanism involved is prejunctional α₂-adrenoceptor activation as i) mivazerol does not display any postsynaptic α-adrenoceptor blocking effect — it even behaves as a postsynaptic α₂-adrenoceptor agonist — and ii) yohimbine abolishes mivazerol's sympathoinhibitory effects. Thus, direct peripheral together with central mechanisms contribute to mivazerol's sympathoinhibitory effects and ultimately to its cardioprotective action.     

Scintigraphic diagnosis of tricuspid regurgitation

The authors describe a simple technique for diagnosis of tricuspid regurgitation. Red blood cells were labeled in vivo with 99mTc and 22 patients were studied with ECG-gated blood-pool imaging of the liver. A single region of interest was manually drawn around the liver and a time-activity curve obtained. The per cent change in liver counts during the cardiac cycle was found to be significantly higher in the 12 patients with tricuspid regurgitation (Group I) (mean, 4.04 +/- 1.6%; range, 1.3-21.4%) compared with the 10 controls (Group II) (mean, 0.35 +/- 0.16%; range, 0.013-1.3%) (p less than 0.05). Using a 1% change in liver counts as the criterion of a positive study, all 12 cases in Group I were diagnosed correctly, but there was one false positive in Group II; thus the sensitivity was 100% and the specificity 90%.     

Mechanisms of somatostatin-evoked responses in neurons of the rat lateral amygdala

The effects of somatostatin in the rat lateral amygdala (LA) in vitro were investigated through whole cell recording techniques. Somatostatin induced an inwardly rectifying K+ current in approximately 98% of LA projection neurons. Half-maximal effects were obtained by 189 nM somatostatin. The effects of somatostatin were insensitive to tetrodotoxin, reduced by Ba2+, occluded or abolished by the presence of nonhydrolysable GTP or GDP analogues, respectively, and blocked or mimicked by a somatostatin receptor type 2 antagonist (BIM-23627) or somatostatin receptor type 2 agonist (L-779,976), respectively, while somatostatin receptor type 1, 3 and 4 agonists were ineffective (L-797,591, L-796,778, L-803,087). Responses to somatostatin were associated with membrane hyperpolarization and decrease in input resistance, resulting in a dampening of cell excitability. It is suggested that these cellular mechanisms contribute to the role of somatostatin in decreasing anxiety behaviour as well as to anticonvulsant and antiepileptogenic actions of somatostatin or somatostatin agonists in the amygdala.     

The Preterm Prediction Study: association between maternal body mass index and spontaneous and indicated preterm birth

OBJECTIVE: The purpose of this study was to evaluate the relationship between prepregnancy maternal body mass index and spontaneous preterm birth and indicated preterm birth. STUDY DESIGN: This was a secondary analysis of the Maternal-Fetal Medicine Units Network, Preterm Prediction study. Patients were classified into categories that were based on their body mass index. Rates of indicated and spontaneous preterm birth were compared. RESULTS: Five hundred ninety-seven (20.5%) of 2910 women were obese. Obese women had fewer spontaneous preterm births at < 37 weeks of gestation (6.2% vs 11.2%; P < .001) and at < 34 weeks of gestation (1.5% vs 3.5%; P = .012). Women with a body mass index of < 19 kg/m2 had 16.6% spontaneous preterm birth, with a body mass index of 19 to 24.9 kg/m 2 had 11.3% spontaneous preterm birth, with a body mass index of 25 to 29.9 kg/m2 had 8.1% spontaneous preterm birth, with a body mass index of 30 to 34.9 kg/m2 had 7.1% spontaneous preterm birth, and with a body mass index of > or = 35 kg/m2 had 5.2% spontaneous preterm birth (P < .0001). Indicated delivery was responsible for an increasing proportion of preterm births with increasing body mass index (P = .001). Obese women had lower rates of cervical length < 25 mm (5% vs 8%; P = .012). Multivariable regression analysis confirmed a lower rate of spontaneous preterm birth in obese gravid women (odds ratio, 0.57; 95% CI, 0.39-0.83; P = .003). CONCLUSION: Obesity before pregnancy is associated with a lower rate of spontaneous preterm birth.