Theory analysis of the Dental Hygiene Human Needs Conceptual Model.

PURPOSE: Theories provide a structural knowing about concept relationships, practice intricacies, and intuitions and thus shape the distinct body of the profession. Capturing ways of knowing and being is essential to any professions' practice, education and research. This process defines the phenomenon of the profession - its existence or experience. Theory evaluation is a systematic criterion-based assessment of a specific theory. This study presents a theory analysis of the Dental Hygiene Human Needs Conceptual Model (DH HNCM). METHODS: Using the Walker and Avant Theory Analysis, a seven-step process, the DH HNCM, was analysed and evaluated for its meaningfulness and contribution to dental hygiene. The steps include the following: (i) investigate the origins; (ii) examine relationships of the theory's concepts; (iii) assess the logic of the theory's structure; (iv) consider the usefulness to practice; (v) judge the generalizability; (vi) evaluate the parsimony; and (vii) appraise the testability of the theory. FINDINGS: Human needs theory in nursing and Maslow's Hierarchy of Need Theory prompted this theory's development. The DH HNCM depicts four concepts based on the paradigm concepts of the profession: client, health/oral health, environment and dental hygiene actions, and includes validated eleven human needs that evolved overtime to eight. It is logical, simplistic, allows scientific predictions and testing, and provides a unique lens for the dental hygiene practitioner. With this model, dental hygienists have entered practice, knowing they enable clients to meet their human needs. CONCLUSION: For the DH HNCM, theory analysis affirmed that the model is reasonable and insightful and adds to the dental hygiene professions' epistemology and ontology.

Imbalance of a serotonergic system in frontotemporal dementia: implication for pharmacotherapy.

RATIONALE: Information is sparse on neurotransmitter deficiencies in frontotemporal dementia (FTD), in particular with reference to distinct histological subgroups and Alzheimer's disease (AD). OBJECTIVES: To evaluate in FTD with the major histologies, and compare with AD and controls, neurotransmission indices, as these may help in developing treatment. MATERIALS AND METHODS: Post-mortem grey matter from Brodmann Area 21, 9 and 7 of 51 brains was assayed for ten neurochemical parameters indexing neurotransmission. Repeated measures analyses of variance were carried out for each parameter comparing groups (FTD vs AD vs control) at each anatomical site. RESULTS: In FTD only the indices of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, serotonin (5-HT)(1A) and 5-HT(2A) receptors were significantly reduced from control values. Of the ten parameters only 5-HT(1A) receptors showed significant group x site interaction. This reflected disproportionate reduction in frontal and temporal compared to parietal cortex. In FTD three other receptors (muscarinic, M(1), N-methyl-D: -aspartate, NMDA, and kainate), choline acetyltransferase (ChAT) activity, 5-HT and 5-hydroxyindoleacetic acid content and 5-HT reuptake site values were not significantly reduced from control values. Only 5-HT, 5-HT reuptake site and ChAT values were significantly higher in FTD than AD. NMDA receptor and ChAT values were significantly reduced from control only in AD. CONCLUSIONS: Neurochemical results in FTD indicate degeneration and loss of pyramidal neurones in frontotemporal neocortex, yet 5-HT afferents and 5-HT concentration, which are inhibitory on pyramidal neurones, were relatively preserved. This could lead to an excess of extraneural 5-HT causing underactivity of surviving pyramidal neurones. Pharmacotherapy with a 5-HT(1A) receptor antagonist may be indicated.

The effects of perturbed energy metabolism on the processing of amyloid precursor protein in PC12 cells.

The mismetabolism of amyloid precursor protein (APP), favouring the production of A beta, is considered to be central to the pathogenesis of Alzheimer's disease (AD). However it remains to be established whether the causative factor is the reported toxicity of A beta or reduced production of secretory derivatives of APP which may have trophic or neuroprotective properties. One possible contributory factor to an imbalance in APP metabolism is the impaired cellular energy availability described in AD. The aim of this study was to investigate processing of APP-like proteins following inhibition of oxidative energy metabolism in PC12 cells. Under these conditions, intracellular and secreted APP-like proteins were significantly reduced. Treatment of energy perturbed cells with the lysosomotropic agent chloroquine restored intracellular concentrations of APP-like proteins to the control range, while the secretion was completely restored by activation of protein kinase C. These findings raise the possibility that energy related metabolic stress may lead to altered metabolism of APP-like proteins favouring a potentially amyloidogenic pathway. Furthermore, the observation that activation of PKC is able to overcome this potentially pathogenic process has important implications for treatment of AD with the current generation of cholinomimetic drugs, suggesting that such drugs may slow disease progression as well as improve cognitive dysfunction.

Neuronal degeneration by suicide transport following injection of volkensin into rat cerebral cortex.

We have examined the time course of neurodegeneration in subcortical nuclei and other cortical areas known to project to the rat parietal cortex, following unilateral injection of the suicide transport agent, volkensin, into the cortex of one side. Degenerating neurons, visualized by Gallyas silver staining were most prominent 21 days after injection. At this time darkly staining neurons were present in nuclei and areas known to project to the injected cortical area but not in other sites. Affected subcortical nuclei included the ipsilateral ventral thalamus and intralaminar nuclei, the basal nucleus of Meynert and claustrum of the same side, and the dorsal median raphé nucleus of both sides. Within the cortex degenerating pyramidal neurons were visible in the contralateral parietal cortex and in the frontal cortex of the same side. The distribution of degenerating cells is in agreement with the conclusion that only neurons projecting to the injection site were affected. The time course of the appearance of the degeneration and its distribution are in keeping with axonal transport rather than spread by diffusion of the toxin. Neuronal counts in Nissl-stained sections of the contralateral SMI confirmed significant neuronal loss 28 days after injection. In situ hybridization studies using an oligonucleotide probe directed against GAD mRNA and counts of GAD mRNA-positive neurons in the contralateral cortex confirmed that this population of cortical interneurons, which do not project to the injection site, were unaffected.

New approaches to imaging based on effects of neurotoxins.

Positron and single-photon emission tomography at present visualize only loss of overall brain substance, with a few exceptions. This has improved diagnostic accuracy in the clinic but further improvements could be made. By using toxins, such as volkensin, brain tissues can be produced that are deficient in various subpopulations of cortical pyramidal neurone. Experimental lesions in rats and quantitative autoradiography were used to investigate the cellular localization of receptors. Lesions were produced by intrastriatal or intracortical injections of volkensin to destroy corticofugal and corticortical pyramidal neurones respectively. Volkensin treatment caused significant loss of pyramidal neurones which was accompanied by reduced binding to certain receptors. Results are discussed in terms of the biology of cortical pyramidal neurones and in vivo imaging in Alzheimer's disease.

Factors influencing dental hygiene retention in private practice.

PURPOSE: The objective of this study was to identity specific factors that contribute to dental hygienists remaining in the same private practice employment setting for five or more years. Working conditions, the employer and the organizational structure of the employment setting, scope of practice, and personal factors were assessed. METHODS: In 1992, a self-designed questionnaire was sent to a sample of 1,200 licensed dental hygienists. One state was randomly chosen from each of the 12 American Dental Hygienists' Association (ADHA) regions of the United States, and 100 licensed dental hygienists were randomly selected from each of these twelve states. Data were analyzed using univariate analysis (frequency distribution) and multivariate analyses (factor analyses). RESULTS: A 62.9% (n = 755) response rate was obtained from the 1200 questionnaires mailed. Of those dental hygienists, 14.3% (n = 108) were not practicing, and 85.7% (n = 647) were currently practicing. Nearly two-thirds (63.3%; n = 480) of the total number of respondents had been practicing five or more years in the same practice setting. Six major factors were identified by dental hygienists as reasons for remaining in one private practice setting for at least five years (1) quality/safe work environment, (2) time management for high-quality dental hygiene services, (3) effective employer office policies/procedures and personnel management, (4) employer support of professional career, (5) supportive work environment, and (6) variety in scope of practice. CONCLUSIONS: Factors identified in this study as influential in dental hygienists' retention in private practice are similar to those identified as reasons for leaving the profession in previous attrition and reentry studies. To increase retention and job satisfaction of dental hygienists in the private practice setting, strategies for effectively working with employers should be emphasized in dental hygiene and dental curriculums and in continuing education programs.

Presynaptic serotonergic markers in community-acquired cases of Alzheimer's disease: correlations with depression and neuroleptic medication.

Presynaptic serotonergic markers, serotonin uptake sites, and concentrations of serotonin and 5-hydroxyindoleacetic acid were studied in the frontal and temporal cortex of 20 community-acquired cases of Alzheimer's disease and 16 controls matched for age, sex, postmortem delay, and storage. Clinical assessments, including behavioural symptoms, of the Alzheimer patients were made at 4-month intervals during life. There was significant reduction in the number of serotonin uptake sites in Alzheimer cases in temporal but not frontal cortex. There was no significant alteration in the concentrations of serotonin or 5-hydroxyindoleacetic acid in either region. Alzheimer patients who had persistent depressive symptoms during life had significantly fewer serotonin uptake sites in both cortical areas compared with Alzheimer patients without these symptoms. In addition, Alzheimer patients who were receiving chronic neuroleptic medication had significantly lower concentrations of serotonin in frontal cortex and 5-hydroxyindoleacetic acid in temporal cortex than those patients not receiving such treatment. These data suggest previous studies that reported uniform serotonergic dysfunction may have been subject to unintentional selection of behaviourally disturbed Alzheimer cases or those receiving chronic neuroleptic medication. This study also provides a basis for the treatment of behaviourally disturbed Alzheimer patients with serotonomimetics.

Changes in cortical nicotinic acetylcholine receptor numbers following unilateral destruction of pyramidal neurones by intrastriatal volkensin injection.

Experimental lesions using the retrogradely transported toxic lectin, volkensin, were used in conjunction with quantitative autoradiography to investigate the cellular localization of nicotinic and adenosine A1 receptors. Lesions were produced by unilateral intrastriatal injection of volkensin, ricin (another toxic lectin but not transported in the central nervous system), quinolinate, and unilateral intrathalamic injection of ibotenate. Volkensin injection significantly reduced the number and mean cell size of large, infragranular pyramidal neurones in cortical areas Fr1/Fr2 (close to the midline) and more laterally in Par1/Par2. Selective destruction of these cells was accompanied by significant increases in the binding of [3H] nicotine in cortical areas contralateral to the lesion. A small but significant reduction in the binding of [3H] 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) to adenosine A1 receptors was observed only in deep layers of Fr1/Fr2 on the side ipsilateral to the lesion. No other toxin consistently changed the binding of either ligand in control animal groups with the exception of [3H] nicotine where small reductions were observed in the middle layers of one thalamic injection group. These data indicate differential plasticity of nicotinic receptors compared with other receptors studied previously using this paradigm. In the light of these findings, nicotinic receptors are discussed as targets for pharmacological manipulation of the activity of pyramidal neurones.

Dental hygienists' information seeking and computer application behavior.

A questionnaire requesting information on information seeking, critical analysis, and computer applications was returned in 1992 by 136 of 197 (69 percent) currently licensed dental hygienists residing in Alaska, Delaware, and Idaho. The most common sources used for professional development and information retrieval were continuing education courses, discussions with colleagues, and journals. The respondents' own experience, credibility of the journal, and discussions with colleagues were the most frequent methods used to evaluate professional information. Many hygienists owned or had access to a computer, yet they rarely conducted online database searches to obtain professional information. The computer was primarily used to perform business functions rather than for clinical applications in these dental hygienists' employment settings. The majority of these hygienists were interested in attending related continuing education courses and indicated that computer skills should be part of dental hygiene curricula.

Cholinomimetics increase glutamate outflow via an action on the corticostriatal pathway: implications for Alzheimer's disease.

Physostigmine, the acetylcholinesterase inhibitor (0.3 mg/kg, i.m.), increased extracellular glutamate but not aspartate concentrations in the striatum of anaesthetised rats, determined using microdialysis and HPLC. The rise was both tetrodotoxin and calcium dependent. In contrast, neither physostigmine (10 microM) added to the perfusion fluid nor vehicle (injected intramuscularly) affected amino acid concentrations. To obtain evidence that the action of acetylcholine was to modulate positively cortical pyramidal neurone activity via the M1 receptor, the selective M1 agonist PD 142505-0028 (10 microM) was topically applied to the frontal cortex. Like physostigmine, PD 142505-0028 rapidly increased glutamate but not aspartate concentrations in the striatum. Moreover, the effect of intramuscular physostigmine was blocked by a topically applied M1 antagonist. These new data add to our hypothesis that cholinomimetics increase pyramidal neurone function.

Information-seeking practices of dental hygienists.

This paper reports on a survey of the information-seeking, critical-analysis, and computer-application practices of dental hygienists. Questionnaires were mailed to a convenience sample of seventy-one dental hygiene practitioners. A 62% response rate was achieved. Results indicated that discussions with colleagues, continuing education courses, journals, and newsletters were the sources used most frequently for professional development and information retrieval. To evaluate professional information, these hygienists tended to rely on personal experience, credibility of the journal, and discussions with colleagues. Word processing was the most frequently used computer application; online database searching was rare in this group. Computer used within the employment setting was primarily for business rather than clinical applications. Many hygienists were interested in attending continuing education courses on use of computers to acquire professional information.

NMDA-induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5-HT1A antagonist.

1. We have investigated an aspect of the regulation of cortical pyramidal neurone activity. Microdialysis was used to assess whether topical application of drugs (in 10 microliter) to fill a burr hole over the frontal cortex, where part of the corticostriatal pathway originates, would change concentrations of the excitatory amino acids glutamate and aspartate in the striatum of the anaesthetized rat. 2. Topical application of N-methyl-D-aspartate (NMDA, 2 and 20 mM) dose-dependently increased glutamate and aspartate concentrations in the striatum. Coapplication of tetrodotoxin (10 microM) blocked the NMDA-evoked rise in these amino acids. A calcium-free medium, perfused through the probe also blocked the rise, indicating that it was due to an exocytotic mechanism in the striatum. 3. It was hypothesized that the rise observed was due to an increase in the activity of the corticostriatal pathway. As 5-hydroxytryptamine1A (5-HT1A) receptors are enriched on cell bodies of corticostriatal neurones, a selective 5-HT1A-antagonist (WAY 100135) was coapplied with the lower dose of NMDA. Compared to NMDA alone, coapplication of 50 microM WAY 100135 significantly increased glutamate release. This effect was sensitive to tetrodotoxin and calcium-dependent. Application of 50 microM WAY 100135 alone significantly enhanced glutamate release above baseline; this was also tested at 100 microM (not significant). 4. Compared to NMDA alone, coapplication of WAY 100135 (20 microM) significantly enhanced aspartate release; the mean value was also increased (not significantly) with 50 microM. This rise was calcium-dependent, but not tetrodotoxin-sensitive. WAY 100135 (100 microM) reduced NMDA-induced aspartate release. WAY 100135 (100 microM) reduced NMDA-induced aspartate release. Application of the drug alone had no effect on basal aspartate release.5. Coapplication of the 5-HT1A agonist, 8-OHDPAT (5 sanM) with NMDA did not affect the NMDA evoked increase in glutamate and aspartate.6. Topical application of high potassium (100 sanM) to the surface of the cortex did not result in a detectable rise in striatal glutamate or aspartate.7. Perfusion of WAY 100135 (tested at 50 microM) through the dialysis probe did not affect glutamate oraspartate concentrations.8. It was concluded that a selective 5-HT1A-antagonist can increase the activity of corticostriatal pyramidal neurones. As in Alzheimer's disease hypoactivity of pyramidal neurones almost certainly exists, a selective 5-HT1A-antagonist may be potentially useful in the treatment of the cognitive symptoms of this disease.

A novel protein, amyloid precursor-like protein 2, is present in human brain, cerebrospinal fluid and conditioned media.

A monoclonal antibody, 3B11, was raised to a novel protein, amyloid precursor-like protein 2, which did not recognize amyloid precursor protein. Multiple bands were detected in human brain fractions and cell lysate by Western blotting, indicating the presence of isoforms, 3B11 immunoreactivity was also detected in cerebrospinal fluid and conditioned medium, indicating that the protein is secreted. Immunocytochemistry revealed 3B11 immunoreactivity in sections of human brain.

A neurochemical approach for studying response to acetylcholine in Alzheimer's disease.

The proposal of cholinomimetic treatment as a rational basis for the therapy of Alzheimer's disease has been prematurely dismissed by some workers on the hypothesis of impaired coupling/signal transduction of postsynaptic cholinergic receptors. Disparity of reports studying such impairment may be due to inappropriate extrapolation of experimental systems to the physiological situation, as well as inadequate consideration of disease epiphenoma. In the present study we have used samples with short duration of terminal coma, collected using techniques to minimise postmortem autolysis, and samples obtained during neurosurgery to examine carbachol stimulated hydrolysis of [3H]phosphatidylinositol (PI) as a marker for receptor/signal transduction integrity. The influence of postmortem delay was also studied using another series of samples and a rat model. While a significant correlation of postmortem delay and carbachol stimulated [3H]PI hydrolysis was found, comparison of pooled neurosurgical and postmortem controls with AD samples revealed no significant reduction. Thus this study concurs with a similar one previously reported here, using [3H]phosphatidylinositol 4,5-bisphosphate (1). They provide evidence for competent receptor-signal transduction events in AD, supporting the use of cholinomimetic therapy for disease treatment.

Increased transmitter amino acid concentration in human ventricular CSF after brain trauma.

The concentrations of L-aspartate, L-glutamate, L-serine, glycine and gamma-aminobutyric acid (GABA) were determined in repeated samples of ventricular CSF from five patients with severe closed head injury. The values were compared with those obtained from five subjects undergoing surgical treatment for intractable depression. In the head-injured patients, the concentrations of aspartate, glutamate and glycine were 2- to 8-fold higher and the concentration of GABA 56- to 317-fold higher than control values; the concentration of serine was unaffected. Spearman correlation analysis indicated that the concentration of glutamate significantly increased after injury (Rs = 0.60, p < 0.0001, n = 42), reaching an average concentration of about 7 microM 3 days after the injury. This is probably sufficient to cause further excitotoxicity, which suggests the use of excitatory amino acid receptor antagonists as a treatment following severe head injury may require prolonged administration for maximum therapeutic benefit.

Postmortem brains reveal similar but not identical amyloid precursor protein-like immunoreactivity in Alzheimer compared with other dementias.

Concentrations of amyloid precursor protein (APP)-like immunoreactivity (APPLIR) have been determined by Western blotting in a soluble fraction and two membrane fractions of two areas of brain cortex from patients with Alzheimer's disease (AD) and other dementias. There were no significant differences between AD and other cases in species with the Kunitz protease inhibitor domain. However, the total soluble APPLIR was higher in AD and it was hypothesized that this relates to cholinergic hypoactivity.