Predicting performance in health professions education programs from admissions information - Comparisons of other health professions with pharmacy.

BACKGROUND: The goal of the present review was to assess the state of performance prediction in healthcare programs generally, versus performance prediction in pharmacy schools, using didactic and non-didactic admissions measures. This is important because clinical success represents a combination of skills that are not fully predicted by either type of measure alone. METHODS: PubMed searches were conducted focusing on work published from 2000 onwards, since it is during this period that non-didactic admissions measures have come to be incorporated into the applicant evaluation process. Relevant free full text papers available were used. When these papers were not available by direct import into EndNote, we went directly to the journal to try to retrieve the paper. RESULTS: We acknowledge that health professions programs have been successful in recruiting excellent candidates into their schools. However, based on the modest amount of healthcare program performance accounted for by didactic measures, admissions committees should consider expanding their holistic evaluation of applicants. Schools would benefit from using two-step screening phases in the application process - perhaps evaluating didactic potential in phase 1 and experiential in phase 2. Using combination measures throughout the admission process should help ensure admission of students more likely to be successful throughout their healthcare practice. IMPLICATIONS: Future investigations of the prediction of healthcare program performance by formal combinations of didactic and non-didactic admissions measures are imperative. In addition, it is likely that combination admission measures will incorporate more metrics of critical thinking than do simpler approaches. Furthermore, systematic evaluation of the usefulness of the two-step screening approaches to admissions used by most competitive health professions programs also needs to be done.

Prevention of relapse to addiction: information for the practitioner.

The purposes of this review are to convey the current distinction between pathological drug dependence and voluntary drug abuse; to provide an overview of the anatomy and biochemistry of dependence; to discuss the rationale for attempting to prevent relapse by using therapeutic agents; and to describe effective agents that reduce relapse in alcohol- and opioid-dependent people. Drug dependence (formerly called "addiction") has as its essential characteristic "impaired control over use of the drug." Impaired control occurs when pathways are sensitized within the emotional brain, (usually) in genetically predisposed individuals. At the nerve cell level, impaired control occurs because of a type of neural adaptation (change in synaptic plasticity) within the pathway's nerve cells that alters their chemistry. Relapse in alcohol-dependent patients can be prevented by any of several agents that reduce craving for alcohol: naltrexone (ReVia), ondansetron (Zofran), and acamprosate (Campral, not yet available in the United States). Relapse in opioid-dependent patients can be prevented by the full agonists methadone and L-alpha-acetyl-methadol (LAAM) and the partial opioid agonist buprenorphine (Subutex and Suboxone). No other universally effective anti-relapse medications exist for other chemical dependencies.

Theories and treatment of drug dependency: a neurochemical perspective.

Treatment of chemical dependence ("addiction") requires an understanding of its effects on the brain. To guide research in the area of chemical dependence, several foundational theories have been developed. These include the incentive salience, receptor down-regulation, opponent process, and psychomotor stimulant theories. These have been important both in summarizing and in guiding investigations. However, the extant theories do not provide a single unified framework nor have they yielded all of the guidance necessary for effective chemical dependence treatment. The present paper summarizes and then integrates these theories and suggests some implications for the treatment followed by this integration.

Comparative molecular field analysis (CoMFA) for sulfoxidation reactions in Mortierella isabellina ATCC 42613 and Helminthosporium sp. NRRL 4671.

Previous models for mechanisms of enzymatic sulfoxidation have been somewhat limited by a lack of knowledge of the essential features of substrate-enzyme versus product-enzyme relationships. Computerized methods for modeling ligand-protein (substrate-enzyme) interactions can overcome some of these limitations. Specifically, CoMFA (comparative molecular field analysis) provided a useful general approach in which to evaluate substrate-enzyme and product-enzyme relationships. The present investigation examined the relationship between substrate and product structure in predicting enantioselective sulfoxidation reactions using CoMFA for two species of microorganisms that have been used as models for mammalian metabolism, Mortierella isabellina and Helminthosporium sp. The overall enantioselectivity observed was based on the composite stereoselectivity of sulfoxide formation, sulfone formation (from the sulfoxide), and sulfoxide reduction back to the achiral substrate (sulfide).

Educating treatment professionals about addiction science research: demographics of knowledge and belief changes.

Communication of accurate, objective, and timely scientific information to treatment professionals is important--especially in the "drug abuse" and addiction field where misinformation and a lack of exposure to new information are common. The purpose of this study was to assess knowledge and belief changes that accompanied educational workshops (3 or 6 hr-long) on addiction science targeted to treatment professionals (N=1403) given in the United States and Puerto Rico between July 2000 and August 2001. Each workshop covered three main concepts: (1) terms and definitions; (2) basic neurochemistry of addiction; and (3) how new neurobiological knowledge will affect the treatment of addictions in the future. Analysis of variance was used to compare mean pretest to posttest change scores among levels of four independent variables: gender, age, occupation/position, and race/ethnicity. Workshop participants achieved a significant improvement in knowledge about addiction with younger groups achieving greater gains. Participants' beliefs shifted in the desired direction. Significant differences in belief shifts occurred among occupational and gender groups, but not among race/ethnicity or age groups. There was also a consistent change in the policy belief subscale that related to how strongly the audience members believed research on addiction was important. We conclude that addiction science education provided to treatment professionals can increase their knowledge and change their beliefs about the causes of addictions. In addition, the workshop participants form a base of constituents who are likely to support greater addiction research funding.

Effectiveness of addiction science presentations to treatment professionals, using a modified Solomon study design.

OBJECTIVES: Knowledge of addiction research findings is critical for healthcare professionals who treat addicted patients. However, there is little information available about the instructional effectiveness of lecture-slide presentations in changing knowledge vs. beliefs of such professionals. DESIGN: A modified Solomon four-group experimental design was used to assess the instructional effectiveness (knowledge gain vs. belief changes) of three-hour addiction science workshops presented to health-care professionals by neurobiologically-trained academic researchers. Effectiveness of the workshops was assessed by a 28-item questionnaire on participant versus control group knowledge/beliefs on addiction. Six-month follow-up questionnaires measured "retention" of knowledge and belief changes. RESULTS: The workshop participants showed significant knowledge gain and belief changes, whereas the two control groups showed no change in knowledge or beliefs. After six months, knowledge gains decreased, but were still higher than pre-test scores. In contrast, belief changes on three subscales persisted over six months in 40 to 52 percent of the subjects. CONCLUSIONS: These results illustrate a successful continuing education model by which academic researchers who are skilled teachers present a three-hour lecture-slide workshop with extensive question-and-answer sessions on addictions. We conclude that motivated health-care professionals can experience important knowledge gains and belief changes by participating in such workshops. In contrast to the transient retention of knowledge, belief changes persisted surprisingly well for at least six months in about half the subjects. These results suggest that long-term changes in the professional orientation of these health-care workers are possible.

Antagonistic effects of dopaminergic signaling and ethanol on protein kinase A-mediated phosphorylation of DARPP-32 and the NR1 subunit of the NMDA receptor.

BACKGROUND: This article extends our initial investigation of the interactions between dopamine and glutamate receptor systems after acute exposure to ethanol. DARPP-32 (dopamine and cyclic adenosine monophosphate-regulated phosphoprotein of approximate molecular weight 32 kDa) is an important regulator of protein phosphatase-1 that in turn regulates a large number of effectors, including the NMDA receptor. METHODS: We measured the protein kinase A (PKA)-mediated phosphorylation of DARPP-32 and the NR1 subunit of the NMDA receptor. Initially, corpus striatum was assayed after intraperitoneal treatment of mice with the D1 agonist SKF82958, the D2 agonist and anticraving drug bromocriptine, or ethanol. In other experiments we blocked D1 receptors with the selective D1 antagonist SCH23390 or blocked D2 receptors with the selective D2 antagonist eticlopride. Finally, we examined combinations of some dopaminergic drugs with and without ethanol. RESULTS: SKF82958 alone significantly increased PKA-mediated phosphorylation of both DARPP-32 and NR1. Bromocriptine alone had no effect on pDARPP-32 or on pNR1. However, when D1 receptors were blocked, bromocriptine reduced the PKA-mediated phosphorylation of both DARPP-32 and NR1. Coincident treatment with bromocriptine and ethanol reversed both of these effects with D1 receptors blocked. The combination of eticlopride (D2 blocker) and SF82958 (D1 agonist) did not significantly alter either pDARPP-32 or pNR1. CONCLUSIONS: These data demonstrate antagonistic effects of acute ethanol exposure on D1 signaling in vivo and the potential of acute in vivo challenge protocols to help fill gaps in the understanding of ethanol's effects on protein phosphorylation.