Scope of practice of an Advanced Practice Nurse at the Swiss Epilepsy Centre

Epilepsy is, after stroke, the second most prevalent neurological disease. The disease has a manifold etiology and symptoms and hence treatment options. From the patients who seek treatment in epilepsy centres, some suffer from psychogenic, non-epileptic seizures. Patient with epileptic seizures have to integrate a medication regimen into their lives, accept symptoms and change their life style to seizure preventing habits. Patients with non-epileptic seizures need psychotherapeutic treatment. Care has to be offered over long periods of time and needs to be tailored to very diverse patients' and family situations. Nurses in this field need broad knowledge about the diseases and treatments as well as enhanced skills in counselling and caring for these patients. Therefore the Swiss Epilepsy Centre in Zurich hired an Advanced Practice Nurse (APN) to increase patients' satisfaction with care and enhance nurses' skills and knowledge. This article analyses the work content of the advanced practice nurse and describes first experiences one year after the implementation of an APN-role. The APN worked half of her time in direct patient and family care. The rest of her work load concerned practice development in coaching and educating the nursing staff, being involved in projects and collaborating with the head nurse on specific topics. In conclusion, implementation of an advanced practice nurse has been shown to be beneficial since patients' feedback were very positive and the increase in nurses' skills and competencies has been assessed as noticeable.     

Induction of cytokines in glial cells surrounding cortical β-amyloid plaques in transgenic Tg2576 mice with Alzheimer pathology

β-Amyloid plaque deposition observed in brains from Alzheimer patients, might function as immune stimulus for glial/macrophages activation, which is supported by observations of activated microglia expressing interleukin (IL)-1β and elevated IL-6 immunoreactivity in close proximity to amyloid plaques. To elucidate the mechanisms involved in β-amyloid-mediated inflammation, transgenic mice (Tg2576) expressing high levels of the Swedish double mutation of human amyloid precursor protein and progressively developing typical β-amyloid plaques in cortical brain regions including gliosis and astrocytosis, were examined for the expression pattern of a number of cytokines.Using ribonuclease protection assay, interleukin (IL)-1α,-β, IL-1 receptor antagonist, IL-6, IL-10, IL-12, IL-18, interferon-γ, and macrophage migration inhibitory factor (MIF) mRNA were not induced in a number of cortical areas of Tg2576 mice regardless of the postnatal ages studied ranging between 2 and 13 months. Using immunocytochemistry for IL-1α,β, IL-6, tumor necrosis factor (TNF)-α, and macrophage chemotactic protein (MCP)-1, only IL-1β was found to be induced in reactive astrocytes surrounding β-amyloid deposits detected in 14-month-old Tg2576 mice. Using non-radioactive in situ hybridization glial fibrillary acidic protein (GFAP) mRNA was detected to be expressed by reactive astrocytes in close proximity to β-amyloid plaques. The local immune response detected around cortical β-amyloid deposits in transgenic Tg2576 mouse brain is seemingly different to that observed in brains from Alzheimer patients but may represent an initial event of chronic neuroinflammation at later stages of the disease.     

Der Einfluss Von Strukturänderungen Auf Peroxydative Und Reduzierende Fermentreaktionen Bei Menschlichen Leukocyten

Zusammenfassung Das Freiwerden der Peroxydasereaktion menschlicher Leukocyten ist an eine Strukturschädigung gebunden, die der Hämolyse der Erythrocyten ähnlich ist. Die Strukturänderung schafft Vorbedingungen für ein Unwirksamwerden der Ascorbinsäure der Leukocyten. Das Triphenyltetrazoliumchlorid-reduzierende Fermentsystem stört die Peroxydasereaktion nicht.     

Varroatosis--a new mite pest of the honeybee in Europe

Notes on spreading, constitution, diagnosis, and control of Varroa jacobsonii OUDEMANS, 1904, the causal agent of a new mite pest in European honey bees.     

Stimulation of protein phosphatases as a mechanism of the muscarinic-receptor-mediated inhibition of cardiac L-type Ca2+ channels

Acetylcholine decreases currents through cardiac L-type Ca²⁺ channels after stimulation with agents which elevate levels of cyclic adenosine monophosphate, such as isoproterenol, but there is still a controversy over the mechnisms of this muscarinic effect. We tested the hypothesis of whether, after isoproterenol stimulation, protein phosphatases are activated by acetylcholine. Whole-cell currents were recorded from guinea-pig ventricular myocytes. The effect of 10^–5 M acetylcholine on currents induced by 10^–8 M isoproterenol was studied in the absence or presence of protein phosphatase inhibitors. Three agents reduced the acetylcholine response: okadaic acid (3 or 9 · 10^–6 M) and cantharidin (3 · 10^–6 M) added to the pipette solution, and bath-applied fluoride (3 mM). In contrast, pipette application of other phosphatase inhibitors, namely the inhibitor PPI₂ (1000 U/ml), ciclosporin (10^–5 M), or calyculin A (10^–6 M) did not significantly diminish the acetylcholine effect. Interestingly, there was no correlation between the effects of the compounds on basal Ca²⁺ current and their interference with the muscarinic response. An activation of type 2A phosphatases by acetylcholine would explain these findings. Indeed, okadaic acid is 3 orders of magnitude more potent in vitro in its inhibition of this isoform (purified from cardiac myocytes) than is calyculin A, while type-1 phosphatases are inhibited equally. The data support the attractive possibility that stimulation of protein phosphatases is part of the signal transduction cascade of Ca²⁺ channel inhibition by acetyl-choline.