160 resultados para Praktika Klinikorako Gida (PKG)


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Ziel des Projekts "Lernen im Praktikum" (vgl. Hascher & Moser, 1999; Moser & Hascher, 2000) war, die Lernprozesse im Praktikum während der Ausbildung am Sekundarlehramt der Universität Bern differenzieren und erklären zu können. Ein zentrales, wenn auch nicht überraschendes Ergebnis dabei war, dass die Betreuung durch die Praktikumslehrer/innen für die Lernprozesse von Studierenden sehr wichtig ist. Im nachfolgenden Beitrag werden nun die Rollen der Praktikumslehr- Personen und ihre Unterstützungsformen näher beleuchtet. Dazu wird sowohl auf die quantitative als auch die qualitative Studie, sowohl auf die Sicht der Studierenden als auch auf die Perspektive der Praktikumsleiter/innen Bezug genommen. Ebenso werden schwierige Aspekte der Betreuung im Praktikum diskutiert.

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In various species, peripheral injury produces long-lasting sensitization of central and peripheral neurons representing the affected area. In Aplysia, memory-like traces (lasting days or weeks) of noxious peripheral stimulation include enhancement of central synaptic transmission and enhanced excitability of the central soma and peripheral branches of nociceptive sensory neurons. An important role for the cAMP-PKA-CREB pathway in consolidating long-term memory and inducing transcription-dependent synaptic potentiation has also been indicated by studies in rodents and Drosophila. ^ Much less attention has been paid to the cGMP-PKG pathway for transcription-dependent plasticity. Nevertheless, the cGMP-PKG pathway has been implicated in activity-dependent neural alterations lasting hours, and may trigger some forms of persistent pain. Recent evidence indicates PKG can regulate gene expression in the brain and several properties make it an attractive candidate for inducing long-term memories. ^ This dissertation reports that brief, noxious stimulation of a behaving, semi-intact preparation from mollusc, Aplysia californica, produces transcription-dependent, long-term hyperexcitability (LTH) of nociceptive sensory neurons that requires a nitric oxide (NO)-cGMP-protein kinase G (PKG) pathway and which lasts for at least 24 hours. Intracellular injection of cGMP is sufficient to induce LTH. Similarly, body wall injury induces LTH which can be blocked with specific inhibitors of the NO-cGMP-PKG pathway such as L-NMMA, ODQ, Rp-8-cGMPS, PKI-G and KT5823 by isolated perfusion of pleural ganglion sensory cells in or directly by intracellular injection. In contrast, specific inhibitors of the cAMP-PKA pathway (Rp-8-cAMPS, PKI-A and H-89) failed to block injury-induced LTH. Interestingly, co-injection of the cAMP-responsive element (CRE) blocked the induction of both cAMP and injury-induced LTH, but not cGMP-induced LTH. Furthermore, co-injection of cAMP and cGMP with the Ca2+ buffer BAPTA in reduced Ca2+ seawater blocked cAMP-, but not cGMP-induced LTH. These findings demonstrate that the NO-cGMP-PKG pathway and at least one other pathway (perhaps mediated by Ca2+), but not the cAMP-PKA pathway, are critical for inducing LTH during transient, noxious stimulation.^

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Includes bibliographical references.

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Riesheniia i opredieleniia S.-Peterburgskago Kommercheskago Suda i Pravitel'stvuiushchago Senata, 1882-1896 g.