Barriers to nurse/nursing aide communication: the search for collegiality in a southeast Ohio nursing home.

Aim: The aims of this study were: (1) to identify barriers to nurse/nursing aide communication and to discuss and provide solutions to some of these problems through a focus group; and (2) to determine the effectiveness of this focus group on job satisfaction-related outcomes.

Background: Numerous studies have attributed problems with nurse staffing and turnover to faulty communication between nursing supervisors and nursing aides.

Methods: Registered nurses (RNs) (n = 2), licensed practical nurses (LPNs) (n = 10) and nursing aides (n = 19) were interviewed; narrative themes from the interviews were then used to guide focus group discussions.

Synaptic release of zinc from brain slices: factors governing release, imaging, and accurate calculation of concentration.

Cerebrocortical neurons that store and release zinc synaptically are widely recognized as critical in maintenance of cortical excitability and in certain forms of brain injury and disease. Through the last 20 years, this synaptic release has been observed directly or indirectly and reported in more than a score of publications from over a dozen laboratories in eight countries. However, the concentration of zinc released synaptically has not been established with final certainty.

A proton-dependent zinc uptake in PC12 cells.

Intracellular pH in pheochromocytoma (PC12) cells was manipulated by 'acid loading' the cells and the effect of such a change on radioactive zinc uptake was studied. It was found that zinc uptake was stimulated in cells loaded with protons without causing any measurable change in the intracellular pH. To confirm our assumption that the proton flux due to zinc entry is too small to be measured, we calculated the pH change that one would expect because of zinc influx.

Method for identifying neuronal cells suffering zinc toxicity by use of a novel fluorescent sensor.

During excitotoxic brain damage, injured neurons accumulate an anomalous, pathological burden of weakly bound, rapidly exchangeable Zn(2+) that diffusely fills the soma, nucleus and proximal dendrites. Mounting evidence indicates that this Zn(2+) is a major contributing factor in the subsequent demise of the damaged neurons. Thus, identifying, imaging, and characterizing zinc-filled cells have become essential steps in understanding excitotoxicity.

Clioquinol effects on tissue chelatable zinc in mice.

Recent evidence for the involvement of zinc in the formation of beta-amyloid plaques in the brain in Alzheimer's disease has led to the establishment of new therapeutic strategies for the degenerative disorder based on metal chelation. The present experiment was conducted on a membrane-permeable zinc chelator, clioquinol (CQ), that has shown potential in initial studies on a mouse model of Alzheimer's disease [1]. The degree of chelatable zinc in mice treated with CQ, delivered by two different routes, was measured using complementary protocols for identifying chelatable zinc: 6-methoxy-8-quinolyl- p-toluenesulfonamide (TSQ) histofluorescence, and selenite autometalography.

Depletion of intracellular zinc from neurons by use of an extracellular chelator in vivo and in vitro.

The membrane-impermeable chelator CaEDTA was introduced extracellularly among neurons in vivo and in vitro for the purpose of chelating extracellular Zn(2+). Unexpectedly, this treatment caused histochemically reactive Zn(2+) in intracellular compartments to drop rapidly. The same general result was seen with intravesicular Zn(2+), which fell after CaEDTA infusion into the lateral ventricle of the brain, with perikaryal Zn(2+) in Purkinje neurons (in vivo) and with cortical neurons (in vitro).