Publications by authors named "R E Nacke"

The counter-electrode (CE) material in electrochemical metallization memory (ECM) cells plays a crucial role in the switching process by affecting the reactions at the CE/electrolyte interface. This is due to the different electrocatalytic activity of the CE material towards reduction-oxidation reactions, which determines the metal ion concentration in the electrolyte and ultimately impacts the switching kinetics. In this study, the focus is laid on Pt, TiN, and W, which are relevant in standard chip technology.

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Unlabelled: Metabolic disorders are frequently observed in pediatric patients with renal lithiasis.

Objectives: Study the metabolic and anatomical alterations and perform the chemical analysis of stones found in children with nephrolithiasis in our region.

Methods: A retrospective study on 158 children with evidence of recent renal stone formation was performed.

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Objective: To evaluate the ophthalmic community's current opinions of the management of bacterial keratitis and usage of the currently available ophthalmic antibiotics.

Methods: An anonymous questionnaire was mailed to ophthalmologists in California, Florida, Illinois, and Missouri. The results were tabulated and analyzed statistically.

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Background: This study assessed axial length measurements taken with MRI compared to A-scan ultrasonography for use in silicone-filled eyes with cataracts.

Methods: This study was a double-blinded prospective comparison study of axial length measurements made by MRI and A-scan ultrasonography. MRI scans of 20 patients undergoing MRI were reviewed to determine axial length.

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Neuronal programmed cell death, or apoptosis, occurs during development, following injury or in certain disease processes, and is regulated by members of the B-cell leukemia-2 (Bcl-2) protein family. These molecules include both positive and negative regulators of cell death and act by selective dimerization that results in permissive or inhibitory effects on a cascade of cellular events, including mitochondrial release of cytochrome c, stimulation of cysteine protease activity and subsequent cellular deterioration. Here, we have characterized the expression of the cell death agonist, Bad, in the postnatal rat retina and forebrain.

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