The process of translating research findings into nursing practice

Action research studies are described which involved nurse teachers, ward sisters and nurse managers in the processes of: nursing practice problem identification and the search for relevant research literature; the evaluation and synthesis of the collected literature; the identification of the need to change practice and the translation of the research synthesis into practice if warranted. The processes engaged in by the groups in each of the three phases in relation to the management of mouth care and preoperative fasting are analysed. The findings suggest that the demands of these processes are beyond the capacity of any one individual nurse and require systematic organizational approaches such as that proposed by quality assurance programmes. The need is emphasized for as much status and resources to be expended on the utilization of existing information as is given to the generation of new knowledge.     

The expression of N-methyl-D-aspartate-receptor-mediated component during epileptiform synaptic activity in hippocampus.

1 The possible involvement of N-methyl-D-aspartate (NMDA)-receptors in epileptiform synaptic activity in the kainic acid (KA) lesioned hippocampus was investigated. In this chronic model of epilepsy there is a loss of both the early and the late components of synaptic inhibition as well as changes in the membrane properties of the surviving CA1 pyramidal cells. 2 The action of the specific NMDA-receptor antagonist D-2-amino-5-phosphonovalerate (D-APV) was tested on evoked bursts of action potentials recorded intracellularly from cells of lesioned hippocampi. The effects of D-APV on control synaptic responses from the contralateral, unlesioned hippocampi were also recorded. 3 In the presence of Mg2+ (1 mM), D-APV (20 microM) had a profound effect on the evoked epileptiform activity. Both the number of action potentials in the burst, as well as the area under the excitatory postsynaptic potential (e.p.s.p.) was considerably reduced. Furthermore this D-APV-sensitive component of the epileptiform burst had a very early onset, coincident with the first action potential in the burst. 4 D-APV (20 microM) was ineffective in blocking the e.p.s.p. evoked by Schaffer collateral afferents onto CA1 cells in slices of hippocampus contralateral to the KA lesion. 5 D-APV had no effect on the passive membrane properties of either population of cells. Hyperpolarizing potentials such as the inhibitory postsynaptic potentials (i.p.s.ps) or the afterhyperpolarization following a current-induced burst of action potentials were also unaffected. 6 It appears that an NMDA-receptor component is expressed during synaptically evoked epileptiform activity in this chronic model of epilepsy.     

Changes to synaptic ultrastructure in field CA1 of the rat hippocampus following intracerebroventricular injection of kainic acid

To assess the nature and extent of ultrastructural damage due to low unilateral intracerebroventricular doses of kainic acid, treated rats were killed at survival times from 8 h to 14 weeks. Degenerative changes in field CA1 of the hippocampus included dark profiles (often presynaptic), lucent areas enveloping axonic or dendritic elements, damaged myelin sheaths, and enlarged glial profiles. The effect of kainic acid ipsilaterally was maximal at three days but also apparent up to 14 weeks. Contralateral CA1 showed similar though less extensive abnormalities.

These observations suggest that, despite rapid synaptic replacement (Nadler et al., Brain Res.191, 387–403, 1980), long-term electrophysiological abnormalities (Cornish and Wheal, Neuroscience 28, 563–571, 1989) may stem not only from inappropriate reactive synaptogenesis but also from a continuing state of neuronal degeneration.     

Interventions for replacing missing teeth: treatment of perimplantitis

Background : One of the key factors for the long‐term success of oral implants is the maintenance of healthy tissues around them. Bacterial plaque accumulation induces inflammatory changes in the soft tissues surrounding oral implants and it may lead to their progressive destruction (perimplantitis) and ultimately to implant failure. Different treatment strategies for perimplantitis have been suggested, however it is unclear which are the most effective. Objectives : To identify the most effective interventions for treating perimplantitis around osseointegrated dental implants. Search strategy : We searched the Cochrane Oral Health Group's Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE. Handsearching included several dental journals. We checked the bibliographies of the identified randomized controlled trials (RCTs) and relevant review articles for studies outside the handsearched journals. We wrote to authors of all identified RCTs, to more than 55 oral implant manufacturers and an Internet discussion group to find unpublished or ongoing RCTs. No language restrictions were applied. The last electronic search was conducted on 15 March 2006. Selection criteria : All RCTs of oral implants comparing agents or interventions for treating perimplantitis around dental implants. Data collection and analysis : Screening of eligible studies, assessment of the methodological quality of the trials and data extraction were conducted in duplicate and independently by two review authors. We contacted the authors for missing information. Results were expressed as random‐effects models using weighted mean differences for continuous outcomes and risk ratios for dichotomous outcomes with 95% confidence intervals (CI). Heterogeneity was to be investigated including both clinical and methodological factors. Main results : Seven eligible trials were identified, but two were excluded. The following procedures were tested: (1) use of local antibiotics versus ultrasonic debridement; (2) benefits of adjunctive local antibiotics to debridement; (3) different techniques of subgingival debridement; (4) laser versus manual debridement and chlorhexidine irrigation/gel; (5) systemic antibiotics plus resective surgery plus two different local antibiotics with and without implant surface smoothening. Follow up ranged from 3 months to 2 years. No meta‐analysis was conducted due to different interventions tested and outcomes used. No side effects occurred in any of the trials. The only significant statistically differences were observed in a 4‐month follow‐up RCT evaluating the use of adjunctive local antibiotics to manual debridement in patients having lost at least 50% of the supporting bone around the implants. There were improved probing attachment levels (PAL) mean differences of 0.61mm (95% CI 0.40 to 0.82), and reduced probing pockets depths (PPD) mean differences of 0.59mm (95% CI 0.39 to 0.79) in those patients receiving adjunctive local antibiotics. This trial was judged to be at high risk of bias. Authors' conclusions : There is no reliable evidence suggesting which could be the most effective interventions for treating perimplantitis. This is not to say that currently used interventions are not effective. However, the use of local antibiotics in addition to manual subgingival debridement was associated with a 0.6mm additional improvement for PAL and PPD over a 4‐month period in patients associated with severe forms of perimplantitis. In three trials, the control therapy which basically consisted of a simple subgingival mechanical debridement seemed to be sufficient to achieve results similar to the more complex and expensive therapies. Smoothening of rough implant surfaces was not associated with statistically significant improvements of the clinical outcomes. However, sample sizes were small, therefore these conclusions have to be considered with great caution. More well‐designed RCTs are needed. Plain language summary : As with natural teeth, dental implants can be lost due to gum disease (perimplantitis). This review looked at which are the most effective treatments to arrest perimplantitis Five studies were included in the review and evaluated five different treatment modalities. In one small study of short duration (4 months) it was shown that the use of locally applied antibiotics in addition to the deep manual cleaning of the diseased implants decreased the depth of the pockets around the implants of an additional 0.6mm in patients affected by severe forms of perimplantitis. In conclusion, at present, there is no reliable evidence to determine which is the most effective way to treat perimplantitis. This is not to say that currently used interventions are not effective. The majority of trials testing more complex and expensive therapies did not show any statistically or clinically significant advantages over the deep mechanical cleaning around the affected implants.     

Loss of inhibition in the CA1 region of the kainic acid lesioned hippocampus is not associated with changes in postsynaptic responses to GABA

Somatic and dendritic responses to gamma-aminobutyric acid (GABA) were recorded intracellularly from CA1 pyramidal cells in slices of the hippocampus ipsilateral and contralateral to a unilateral kainic acid lesion of the CA3 region. Ipsilateral CA1 cells show a loss of GABA-mediated synaptic inhibition. However, somatic GABA responses and the sensitivity of cells to GABA were very similar in ipsilateral and contralateral cells. This was also true for dendritic applications of GABA.     

Molecular mechanisms that underlie structural and functional changes atthe postsynaptic membrane duringsynaptic plasticity

The synaptic plasticity that is addressed in this review follows neurodegeneration in the brain and thus has both structural as well as functional components. The model of neurodegeneration that has been selected is the kainic acid lesioned hippocampus. Degeneration of the CA3 pyramidal cells results in a loss of the Schaffer collateral afferents innervating the CA1 pyramidal cells. This is followed by a period of structural plasticity where new synapses are formed. These are associated with changes in the numbers and shapes of spines as well as changes in the morphometry of the dendrites. It is suggested that this synaptogenesis is responsible for an increase in the ratio of NMDA to AMPA receptors mediating excitatory synaptic transmission at these synapses. Changes in the temporal and spatial properties of these synapses resulted in an altered balance between LTP and LTD. These properties together with a reduction in the inhibitory drive increased the excitability of the surviving CA1 pyramidal cells which in turn triggered epileptiform bursting activity. In this review we discuss the insights that may be gained from studies of the underlying molecular machinery.

Developments in one of the collections of the cogs in this machinery has been summarized through recent studies characterizing the roles of neural recognition molecules in synaptic plasticity in the adult nervous systems of vertebrates and invertebrates. Such investigations of neural cell adhesion molecules, cadherins and amyloid precursor protein have shown the involvement of these molecules on the morphogenetic level of synaptic changes, on the one hand, and signal transduction effects, on the other. Further complex cogs are found in the forms of the low-density lipoprotein receptor (LDL-R) family of genes and their ligands play pivotal roles in the brain development and in regulating the growth and remodelling of neurones. Evidence is discussed for their role in the maintenance of cognitive function as well as Alzheimer's. The molecular mechanisms responsible for the clustering and maintenance of transmitter receptors at postsynaptic sites are the final cogs in the machinery that we have reviewed.

Postsynaptic densities (PSD) from excitatory synapses have yielded many cytoskeletal proteins including actin, spectrin, tubulin, microtubule-associated proteins and calcium/calmodulin-dependent protein kinase II. Isolated PSDs have also been shown to be enriched in AMPA, kainate and NMDA receptors. However, recently, a new family of proteins, the MAGUKs (for membrane-associated guanylate kinase) has emerged. The role of these proteins in clustering different NMDA receptor subunits is discussed. The MAGUK proteins are also thought to play a role in synaptic plasticity mediated by nitric oxide (NO). Both NMDA and non-NMDA receptors are highly clustered at excitatory postsynaptic sites in cortical and hippocampal neurones but have revealed differences in their choice of molecular components. Both GABA_A and glycine (Gly) receptors mediate synaptic inhibition in the brain and spinal cord. Whilst little is known about how GABA_A receptors are localized in the postsynaptic membrane, considerable progress has been made towards the elucidation of the molecular mechanisms underlying the formation of Gly receptors. It has been shown that the peripheral membrane protein gephyrin plays a pivotal role in the formation of Gly receptor clusters most likely by anchoring the receptor to the subsynaptic cytoskeleton. Evidence for the distribution as well as function of gephyrin and Gly receptors is discussed. Postsynaptic membrane specializations are complex molecular machinery subserving a multitude of functions in the proper communication between neurones. Despite the fact that only a few key players have been identified it will be a fascinating to watch the story as to how they contribute to structural and functional plasticity unfold.