322 resultados para Wolfram


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Pliocene and Pleistocene sediments from Ocean Drilling Program Leg 151, Hole 911 A, drilled on the innermost Yermak Plateau (Eastern Arctic Ocean), were studied for their dinoflagellate cyst content. Three assemblage zones were tentatively defined, characterized by the predominance of few species. The composition of the assemblages changed markedly, even within single assemblage zones, during the last 2.6 to 2.8 m.y., reflecting the variable influence of warmer water from the Norwegian Sea, fluctuations in the influence of cold polar water masses, and the extent of sea-ice cover. Polar to subpolar surface water masses prevailed on the Yermak Plateau during the late Pliocene, when the eastern Arctic Ocean was probably isolated from the Norwegian-Greenland Sea. Intrusions of warmer water are recorded since the latest Pliocene, alternating with colder periods and a prolonged seasonal sea-ice cover. The composition of the dinoflagellate cyst assemblages has also changed considerably since the middle Pleistocene, reflecting the establishment of stronger fluctuations in surface water mass conditions than before at Yermak Plateau.

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Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed 'ventilator-induced diaphragmatic dysfunction' (VIDD) and should be distinguished from peripheral muscular weakness as observed in 'ICU-acquired weakness (ICU-AW)'. Interestingly, VIDD and ICU-AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross-sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.

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Bibliography: 2. Abth., 2. Bd., p. [vii]-viii, 3. Bd., p. [ix]-xii.

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Mode of access: Internet.

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V. 1=Parcival.

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Lieder.--Parzival.--Titurel.--Willehalm.

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Mode of access: Internet.

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Mode of access: Internet.

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Includes bibliographical references.

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"Anastatic reprint of the edition London 1894."

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Mode of access: Internet.