Reforming dental workforce education and practice in the USA.

The USA dental education programmes are facing challenges similar to those confronting countries around the globe, particularly amongst the industrialised nations. The purpose of this study was to evaluate the educational programmes of 15 USA dental schools to determine their impact on improving workforce diversity and oral health care access. The study investigates the predictors of public service plans of dental school seniors in Pipeline and non-Pipeline Program dental schools. We analysed baseline and post-intervention data collected in the American Dental Education Association (ADEA) Annual Survey of Dental School Seniors and a set of contextual variables. Public service plans (dependent variable) was predicted by four types of independent variables: intervention, contextual, community-based dental education (CBDE), and student characteristics. Findings from the study show that access to a state or federally sponsored loan repayment program was the most significant predictor of public service plans and that increasing educational debt was the most significant barrier. In the short-term we may be able to sustain the USA loan repayment programs to motivate senior dental students to provide public service to address the oral health care access crisis. However, in the long-term, a new workforce development initiative will be required to transform dental education and practice, modelled after the well-respected licensure programmes for Physician Assistants and/or Advanced Practice Registered Nurses, to expand oral health care access, particularly amongst vulnerable population subgroups, such as low-income children and families.

D1 receptor alleles predict PET metabolic correlates of clinical response to clozapine.

A goal of pharmacogenetics is to clarify associations between allelic variation and risk factors in psychiatric illness. We report changes in regional brain metabolism based on dopamine alleles. Treatment-resistant schizophrenic subjects were positron emission tomography scanned with 18F-fluorodeoxyglucose after 5 weeks each of placebo and clozapine treatment. Significant regional brain metabolic effects were found for the D1 receptor genotypes (P < 0.05), adjusted for multiple comparisons. Metabolic decreases for the 2,2 genotype but not the 1,2 genotype were observed in all major sectors of the brain, with the exception of the ventral parts of the caudate and putamen. Frontal, temporal, parietal, and occipital neocortices showed decreased metabolism as did the cingulate juxta-allocortex and the parahippocampal allocortex. Decreases were also observed in the thalamus, amygdala, and cerebellum bilaterally. No significant metabolic differences by genotype were observed for D3, 5HT(2A), and 5HT(2C) polymorphisms. In terms of clinical response, the DRD1 2,2 genotype significantly improved with clozapine treatment, demonstrating a 30% decrease in the Brief Psychiatric Rating Scale positive symptoms in contrast to a 7% worsening for the 1,2 genotype (P < 0.05). In this preliminary study, brain metabolic and clinical response to clozapine are related to the D1 receptor genotype.

Brain metabolic and clinical effects of rivastigmine in Alzheimer's disease.

In-vivo metabolic measures with positron emission tomography using (18)F-fluorodeoxyglucose (FDG-PET) have demonstrated hypometabolism in temporal, frontal, and hippocampal areas during the early stages of Alzheimer's disease (AD). Progression of the dementia in AD involves compromised cholinergic functioning. Cholinesterase inhibitors have demonstrated efficacy in improving cognition and behaviour in AD. In this study, we demonstrate the usefulness of FDG-PET in measuring the progression of untreated AD and its modification by treatment with rivastigmine (Exelon, Novartis Pharmaceuticals, East Hanover, New Jersey, USA), a centrally selective cholinesterase inhibitor of the carbamate type. Patients with mild to moderate probable AD (Mini-Mental Status Exam scores of 10-26, inclusive) were enrolled in a double-blind, placebo controlled comparison of three fixed daily doses of rivastigmine (3, 6, or 9 mg/d) or placebo for 26 wk. FDG-PET scans were obtained on 27 patients at baseline and following 26 wk of treatment using the Snodgrass Picture Naming activation task. A total of 71.4% of the patients treated with placebo deteriorated clinically compared to only 25.0% of the patients treated with rivastigmine (chi2 = 4.8; p & 0.03). Rivastigmine-responders (i.e. those who clinically improved or remained clinically stable as measured by the Clinicianaposs Interview-Based Impression of Change-plus) showed a marked increase in brain metabolism (p <0.01) involving, but not limited to, structures comprising the memory-related cortices and the prefrontal system. These metabolic changes were not observed in the placebo-treated patients or the rivastigmine non-responders. Of note is that responders increased hippocampal metabolism by 32.5% (p < 0.03) compared to a non-significant decrease in the non-responders (6.4%) and placebo-treated patients (4.1%). These results are consistent with the literature suggesting that FDG-PET can sensitively measure the progression of AD and its improvement with cholinesterase inhibitors. Rivastigmine prevented the expected deterioration in clinical status and dramatically increased brain metabolic activity in a majority of patients.

The therapeutic design of environments for people with dementia: a review of the empirical research.

Design of the physical environment is increasingly recognized as an important aid in caring for people with dementia. This article reviews the empirical research on design and dementia, including research concerning facility planning (relocation, respite and day care, special care units, group size), research on environmental attributes (noninstitutional character, sensory stimulation, lighting, safety), studies concerning building organization (orientation, outdoor space), and research on specific rooms and activity spaces (bathrooms, toilet rooms, dining rooms, kitchens, and resident rooms). The analysis reveals major themes in research and characterizes strengths and shortcomings in methodology, theoretical conceptualization, and applicability of findings.

Plasma clozapine concentrations predict clinical response in treatment-resistant schizophrenia.

Steady-state blood clozapine concentrations in 58 schizophrenic patients varied more than 45-fold (40-1911 ng/mL) after fixed-dose treatment (400 mg/day). Discriminant function analysis determined that a blood clozapine concentration of 420 ng/mL optimally distinguished responders from nonresponders. After 4 weeks of treatment, only 8% of those patients with a blood clozapine concentration < 420 ng/mL responded compared with 60% of those who had a blood clozapine concentration > 420 ng/mL. When plasma concentrations were increased above 420 ng/mL (by a double-blind random assignment procedure), nonresponders increased their response rate to 73% if their plasma concentrations at Week 12 exceeded 420 ng/mL compared with a response rate of 29% if their Week 12 levels remained below 420 ng/mL (chi 2 = 4.2, p < .04).

S-adenosylmethionine blood levels in major depression: changes with drug treatment.

INTRODUCTION: The relationship between plasma levels of S-adenosylmethionine (SAMe), an endogenous methyl donor, and clinical response were studied in patients with a DSM-III-R diagnosis of major depression. MATERIAL AND METHODS: A double-blind randomized protocol comparing oral SAMe with oral desipramine, involving a total of 26 patients, was employed. RESULTS: At the end of the 4-week trial, 62% of the patients treated with SAMe and 50% of the patients treated with desipramine had significantly improved. Regardless of the type of treatment, patients with a 50% decrease in their Hamilton Depression Scale (HAM-D) score showed a significant increase in plasma SAMe concentration. CONCLUSION: The significant correlation between plasma SAMe levels and the degree of clinical improvement in depressed patients regardless of the type of treatment suggests that SAMe may play an important role in regulating mood.

Measuring the psychological construct of control. Discriminant, divergent, and incremental validity of the Shapiro Control Inventory and Rotter's and Wallstons' Locus of Control Scales.

The psychological construct of control is increasingly thought to be an important variable in psychosomatic medicine, but there are limitations with how it has been measured by previous instruments. The current study details four limitations of previous instruments as a rationale for developing a new multi-faceted, multi-dimensional instrument to measure control, the Shapiro Control Inventory (SCI). Discriminant, divergent, and incremental validity of the SCI is compared with the Rotter's Internal/External Locus of Control Scale and Wallstons' Multidimensional Health Locus of Control Scales on five groups, one normal and four clinical groups (depression, generalized anxiety disorder, borderline personality, and panic disorder). Analysis of variance showed significant differences among populations on each of the nine SCI scales. The majority of these results were highly significant, whereas for Rotter's scale the results were barely significant, and for Wallstons' three scales, not at all significant. Correlations of the SCI scales with Rotter's and Wallstons' scales were small to moderate, but in no case explained more than 15% of the variance. The SCI also provided incremental validity over Rotter's and Wallstons' scales both for sensitivity (clinical versus normal) and specificity (between clinical groups). The discussion section provides suggestions for future research.