Photoemission spectroscopy of heterojunctions of hydrogenated amorphous silicon with silicon oxide and nitride.
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Biomedical subjects
Publications and source records attributed to W Eberhardt.
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Five case histories are presented of patients developing cholestatic hepatitis associated with the intake of the antibiotic combination agent amoxicillin and clavulanic acid (Augmentin). In two of these cases, signs of hepatic injury recurred after readministration of this combination but not after the intake of amoxicillin alone. In none of the patients was another cause for cholestatic hepatitis found and extrahepatic causes were excluded by ultrasonography, CT scanning, or ERCP. Most viral causes of hepatic injury were excluded in these patients. With the exception of one patient, who developed a transient rash, no immunoallergic signs were present. Biopsy in two patients showed extensive cholestasis without significant necrosis. Clavulanic acid seems to be responsible for this adverse effect.
Retinal glial (Müller) cells were grown from explants of early postnatal rabbit retinae. The resulting monolayers of flat cells were exposed to control media (containing 5.85 mM K+), and to media with enhanced K+ concentrations (10 and 20 mM) or arginine-vasopressin (AVP, 20 micrograms/ml) or epithelial growth factor (EGF, 10 ng/ml). Autoradiographically, protein synthesis was quantified as L-[3H]-lysine incorporation, and DNA synthesis as [3H]-thymidine incorporation. Furthermore, the activity of Na+,K(+)-ATPase was measured radiochemically. Short exposure to either moderately enhanced K+ concentrations (10 mM) or to AVP, stimulated L-[3H]-lysine incorporation into the cells. Long-lasting exposure to either high K+ concentrations (20 mM) or to EGF stimulated [3H]-uptake. The Na+,K(+)-ATPase activity of cell cultures increased with increasing K+ concentration of the media. It is suggested that release of K+ by active neuronal compartments stimulates local protein synthesis of glial cells, resulting in the formation of glial sheaths with active K+ uptake capacity. Strong K+ release may even induce glial proliferation.
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Müller (radial glial) cells were isolated from rabbit retinae by means of papaine and mechanical dissociation. Regional membrane properties of these cells were studied by intracellular microelectrode recordings of potential responses to local application of high K+ solutions. When different parts of the cell membrane were exposed to high K+, the amplitude of the depolarizing responses varied greatly, indicating a strong regional specialization of the membrane properties. Using morphometrical data of isolated rabbit Müller cells, and a simple circuit model, we calculated the endfoot membrane to constitute more than 80% of the total K+ conductance of the cell; the specific resistivity of the endfoot membrane was about 400 omega cm2, i.e., more than 40 times less than that of the membrane of the vitread process, which is immediately adjacent. This kind of regional membrane specialization seems to be optimized in respect to the Müller cells' ability to carry spatial buffering K+ currents.
Two hundred and thirty patients with histologically proven small cell lung cancer--133 patients with limited disease and 97 patients with extensive disease--were treated from 1979 to 1986 in 3 prospective clinical trials at a single institution. Univariate and multivariate statistical analyses (Cox-models) were used to determine whether pretherapeutic factors can be used to predict survival and long-term survival. Extent of disease, determined by pretherapeutic staging, turned out to be the most significant prognostic parameter. Survival beyond 2 years was almost exclusively confined to patients with limited disease. Further independent predictors of survival duration in patients with limited disease were serum levels of lactate dehydrogenase and urea. In extensive disease, however, performance status, levels of serum lactate dehydrogenase and the intensity of therapy turned out to be the best pretherapeutic prognostic factors.
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Rabbit retinal Müller (glial) cells were isolated by means of papain and mechanical dissociation. In a special perfusion chamber, the cells were penetrated with a recording microelectrode. Membrane potential changes were recorded in response to extracellular application of both high-K+ solutions and of ouabain, and that during perfusion with normal and Na+-free solutions, respectively. In other Müller cell preparations, Na+,K+-adenosine triphosphatase (ATPase) activity was measured using a radiochemical method, and its Na+ dependence was determined. All results strongly suggest that the Müller cell's Na+,K+ pump can be activated in the presence of extremely low amounts of Na+. This provides additional evidence for significant differences between the glial and the neuronal enzyme.
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In a previous study we found the morphometrical data of rabbit retinal Müller (radial glial) cells to vary greatly with their localization in various parts of the retina. The long cells of the central retina have thinner vitreal processes and smaller endfeet than the short cells of the retinal periphery. This configuration should impair the spatial buffering capacity of the central Müller cells for excess K+ ions. To test this hypothesis, we developed a simple modified model for the calculation of K+ clearance by spatial buffering, diffusion through the extracellular space, and co-operation of both processes. K+ clearance processes were demonstrated to depend greatly on the retinal geometry and Müller cell morphology in different parts of the retina. The efficiency of spatial buffering exhibited an obvious optimum for Müller cells of intermediate length, and decreased very steeply in longer cells. Some conclusions are drawn with respect to retinal physiology. In particular, it is suggested that very long and slender radial glia is unable to perform sufficient K+ clearance preventing long-lasting extracellular [K+] elevations after neuronal activity. Such [K+] elevations could depolarize these glial cells so as to enforce their mitotic division. This mechanism might lead to the perinatal transformation of embryonic radial glia into adult multipolar glia when neuronal activity commences in CNS tissues thicker than the maximal effective length of radial glial cells.
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Müller (glial) cells were isolated from rabbit retinae by papaine and mechanical dissociation. In a special perfusion chamber, the cells were penetrated with a recording electrode. When high-K+ solutions were applied into the environment of the cells by means of a second micropipette, the cell membrane depolarized strongly. During prolonged application of high-K+ solutions, however, there occurred a marked repolarization, and after cessation of high-K+ application, a strong hyperpolarization was observed. Both effects disappeared under the influence of ouabain, suggesting the accumulation of intracellular K+ by an active membrane pump. The data were used for calculation of the membrane's Na+:K+ permeability ratio, the intracellular K+ concentration, the pump rate and the mean pump site density. The calculated values are in good agreement with published data from mammalian astrocytes and are compared with those from amphibian Müller cells.
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Müller (glial) cells were isolated from rabbit retinae by papaine and mechanical dissociation. The cells were fixed on a gelatine-covered glass slide by means of concanavalin A, and the slide was mounted in a perfusion chamber under a light microscope with modified optics. Besides the recording microelectrode, two other micropipettes could be adjusted with their tips near the cell. These micropipettes were used for application of test solutions into the environment of the cells. On application of high K+ solutions, the cell depolarized strongly but during prolonged application there was a marked repolarization. After the end of high K+ application the cells showed a hyperpolarization which was enhanced in both amplitude and duration with prolongation of the K+ exposure. Both repolarization and afterhyperpolarization disappeared under ouabain. Ouabain application itself caused a small reversible depolarization. Na+ free solution caused hyperpolarization. The results suggest the existence of an active membrane pump mechanism in our cells. This pump seems to be electrogenic under our experimental conditions and seems to be activated even in the absence of sodium. The cell membrane is demonstrated to contain a significant Na+ conductance.