Medizinisches Callcenter im Nachtdienst, Teil 2: Die Wirkung auf die Befindlichkeit

Die Nächte stellen wohl die grösste Belastung der Ärzte2 im Notfalldienst dar, vor allem, nachdem wegen Überalterung Notfallkreise zusammengelegt werden mussten und damit der Druck auf den einzelnen Dienstarzt zugenommen hat. Die Dienstkreise Frauenfeld und Arbon–Romanshorn mit 30450 bzw. 37217 Einwohnern untersuchten, ob eine nächtliche Vortriagierung (22 bis 8 Uhr) der Anrufe durch ein medizinisches Callcenter die Dienstärzte entlasten könnte. Die Phase ohne Callcenter dauerte vom 1. 2. bis am 31. 5., jene mit vom 1. 6. bis 30. 9. 2007. 37 von 39 Ärzten nahmen an der Studie teil. Der Rücklauf der Fragebogen betrug 85 bis 92%. Die Ärzte äusserten eine verbesserte Schlaf- und Lebensqualität im Zusammenhang mit dem Notfalldienst und befürworteten den Callcentereinsatz tendenziell. Eine Beteiligung an den Kosten für das Callcenter lehnten sie jedoch allesamt ab. Die Anrufenden gaben sowohl den Dienstärzten als auch den Gesundheitsberatern des Callcenters gute Noten, beanstandeten aber den Tarif unserer 0900-Service-Nummern (CHF 1.93/min). Unsere Studie zeigt, dass eine Vortriagierung nächtlicher Anrufe im Notfalldienst von Patienten und Dienstärzten akzeptiert werden könnte

The primary headaches: genetics, epigenetics and a behavioural genetic model

The primary headaches, migraine with (MA) and without aura (MO) and cluster headache, all carry a substantial genetic liability. Familial hemiplegic migraine (FHM), an autosomal dominant mendelian disorder classified as a subtype of MA, is due to mutations in genes encoding neural channel subunits. MA/MO are considered multifactorial genetic disorders, and FHM has been proposed as a model for migraine aetiology. However, a review of the genetic studies suggests that the FHM genes are not involved in the typical migraines and that FHM should be considered as a syndromic migraine rather than a subtype of MA. Adopting the concept of syndromic migraine could be useful in understanding migraine pathogenesis. We hypothesise that epigenetic mechanisms play an important role in headache pathogenesis. A behavioural model is proposed, whereby the primary headaches are construed as behaviours, not symptoms, evolutionarily conserved for their adaptive value and engendered out of a genetic repertoire by a network of pattern generators present in the brain and signalling homeostatic imbalance. This behavioural model could be incorporated into migraine genetic research

Current and prospective pharmacological targets in relation to antimigraine action

Migraine is a recurrent incapacitating neurovascular disorder characterized by unilateral and throbbing headaches associated with photophobia, phonophobia, nausea, and vomiting. Current specific drugs used in the acute treatment of migraine interact with vascular receptors, a fact that has raised concerns about their cardiovascular safety. In the past, α-adrenoceptor agonists (ergotamine, dihydroergotamine, isometheptene) were used. The last two decades have witnessed the advent of 5-HT1B/1D receptor agonists (sumatriptan and second-generation triptans), which have a well-established efficacy in the acute treatment of migraine. Moreover, current prophylactic treatments of migraine include 5-HT2 receptor antagonists, Ca2+ channel blockers, and β-adrenoceptor antagonists. Despite the progress in migraine research and in view of its complex etiology, this disease still remains underdiagnosed, and available therapies are underused. In this review, we have discussed pharmacological targets in migraine, with special emphasis on compounds acting on 5-HT (5-HT1-7), adrenergic (α1, α2, and β), calcitonin gene-related peptide (CGRP 1 and CGRP2), adenosine (A1, A2, and A3), glutamate (NMDA, AMPA, kainate, and metabotropic), dopamine, endothelin, and female hormone (estrogen and progesterone) receptors. In addition, we have considered some other targets, including gamma-aminobutyric acid, angiotensin, bradykinin, histamine, and ionotropic receptors, in relation to antimigraine therapy. Finally, the cardiovascular safety of current and prospective antimigraine therapies is touched upon

Medizinisches Callcenter im Nachtdienst, Teil 1: Die Wirkung in Zahlen

Die Nächte stellen wohl die grösste Belastung für Ärzte1 im Notfalldienst dar, vor allem, nachdem wegen Überalterung Notfallkreise zusammengelegt werden mussten und damit der Druck auf den einzelnen Dienstarzt zugenommen hat. Die Dienstkreise Frauenfeld und Arbon–Romanshorn mit 30 450 bzw. 37217 Einwohnern untersuchten die Praktikabilität und den Nutzen einer nächtlichen Vortriagierung des Notfalldienstes durch ein medizinisches Callcenter zwischen 22 und 8 Uhr. Die Phase ohne Callcenter dauerte vom 1. 2. bis zum 31. 5. 2007, jene mit vom 1. 6. bis 30. 9. 2007. 35 von 39 Ärzten, 52 (39–65) Jahre alt, nahmen an der Studie teil. 85% aller Notfalldienste wurden erfasst. Pro Nacht und Dienstkreis wurden in der Vorphase 0,54 Telefonate und 0,73 Einsätze verzeichnet, während der Callcenter-Triagierung 0,37 bzw. 0,64. Ungefähr ein Drittel der nächtlichen Anrufe konnte durch das Callcenter abschliessend beraten werden. An den Notfallstationen unserer kantonalen Spitäler blieb der Anteil der Selbstzuweiser während der Studie konstant (31,0 vs. 31,6%); eine Abwanderung der Notfälle an die öffentlichen Spitäler oder saisonale Schwankungen konnten nicht festgestellt werden. Unsere Studie zeigt, dass eine Vortriagierung nächtlicher Anrufe im Notfalldienst machbar und sinnvoll ist

Conditionnement de déchets radioactifs par résines thermodurcissables

Les auteurs décrivent le principe du procédé de conditionnement des déchets de faible et moyenne activité par résines thermodurcissables. Ils analysent ensuite les deux phases essentielles de sa mise en œuvre : prétraitement et enrobage. Ils décrivent enfin, à titre d'exemple, l'installation (en exploitation au centre d'études nucléaires de Grenoble) où est appliqué ce procédé de conditionnement

Mechanisms of Abruption-Induced Premature Rupture of the Fetal Membranes: Thrombin-Enhanced Interleukin-8 Expression in Term Decidua.

Recent evidence has linked preterm premature rupture of the fetal membranes (PPROM) to placental abruption. Because neutrophils are a rich source of proteases that can degrade extracellular matrix in abruption-associated PPROM,we examined whether decidual neutrophil infiltration complicates abruption-associated PPROM. Accordingly, immunostaining for the neutrophil marker CD15 was performed in placentas obtained after overt abruption (decidual hemorrhage) with or without PPROM and in control placentas. Abruptions were associated with a marked decidual neutrophil infiltration that peaked after PPROM, whereas decidua from gestational age-matched controls were virtually devoid of neutrophils. Neutrophil infiltrates co-localized with fibrin deposition. Because abruptions elicit intense decidua- enhanced thrombin production, we examined the regulation of abruption-induced neutrophil infiltration. Expression of the primary neutrophil chemoattractant interleukin-8 (IL-8) was evaluated in leukocyte-free term decidual cells incubated with estradiol (E2; control) or with E2medroxyprogesterone acetate (to mimic pregnancy) thrombin. After 24 hours, enzyme-linked immunosorbent assay measurements indicated that thrombin (0.1 to 2.5 U/ml) elicited a dose-dependent elevation in secreted IL-8 (P < 0.05) with 2.5 U/ml of thrombin increasing IL-8 levels by >14-fold in E2 and E2 medroxyprogesterone incubations. Results were validated by Western blot and quantitative reverse transcriptase-polymerase chain reaction. In summary, thrombin-enhanced IL-8 expression in term decidual cells may explain how abruption-associated PPROM promotes decidual neutrophil infiltration

Mechanisms of leukocyte accumulation and activation in chorioamnionitis: interleukin 1 beta and tumor necrosis factor alpha enhance colony stimulating factor 2 expression in term decidua.

Chorioamnionitis is a major cause of prematurity as well as perinatal morbidity and mortality. The present study observed a marked increase in immunohistochemical staining for Colony Stimulating Factor 2 (CSF2; also known as granulocyte macrophage-colony stimulating factor), a potent neutrophil and macrophage chemoattractant and activator, in the decidua of patients with CAM compared with controls (n = 8; P = .001). To examine the regulation of this CSF2, cultured decidual cells primed with estradiol (E2) or E2 plus medroxyprogesterone acetate, were exposed to tumor necrosis factor-α or interleukin-1β and secreted CSF2 measured by ELISA. Levels of CSF2 in E2 plus MPA-treated cultures increased 18- and 245-fold following treatment with TNF or IL1B (n = 7, P < .05). Quantitative RT-PCR demonstrated parallel changes in mRNA levels. This study reveals that CSF2 is strongly expressed in decidua from patients with CAM and indicates TNF or IL1B as important regulators of CAM-related decidual leukocyte infiltration and activation

Differential Regulation of Colony Stimulating Factor 1 and Macrophage Migration Inhibitory Factor Expression by Inflammatory Cytokines in Term Decidua: Implications for Macrophage Trafficking at the Fetal-Maternal Interface

Macrophages are a major component of the leukocyte population of human pregnant endometrium. Although several crucial functions have been ascribed to these cells, the mechanisms underlying macrophage trafficking in the placental bed are poorly understood. The aim of this study was to evaluate the in vivo expression of two potentially antagonistic macrophage- targeting chemokines, colony stimulating factor 1 (CSF1, also known as M-CSF) and macrophage migration inhibitory factor (MIF), in term decidua, and to examine the effects of the inflammatory cytokines tumor necrosis factor (TNF, also known as TNF alpha) and interleukin 1beta (IL1B) on CSF1 and MIF expression in cultured decidual cells. The expression of CSF1 and MIF in term decidua was evaluated by immunohistochemistry. Cultured decidual cells were primed with estradiol (E2) or with E2 + medroxyprogesterone acetate (MPA), and then incubated with corresponding steroid(s) with or without TNF or IL1B. The levels of CSF1 and MIF protein and mRNA were assessed by ELISA and quantitative RT-PCR, respectively. Immunostaining for CSF1 and MIF was observed in term decidua. The levels of secreted CSF1 and MIF were similarly unchanged whether the decidual cells were incubated with E2 or with E2 + MPA. The CSF1 levels significantly increased in cultures exposed to E2 or E2 + MPA plus TNF or IL1B. In contrast, the MIF levels in TNF- and IL1B-treated cells were not changed significantly from the control cultures. The ELISA data were confirmed by quantitative RT-PCR analysis. These results indicate that CSF1 and MIF are involved in regulating macrophage trafficking at the fetal-maternal interface, and suggest a mechanism by which inflammatory cytokines influence pregnancy by regulating decidual macrophage infiltration