The "first-generation effect" on perceptions and academic performance of pharmacy students.

INTRODUCTION: The "first-generation effect" refers to familial educational attainment's role in first-generation student academic success. It often implies low academic achievements at associate and bachelor degree levels. Would this be true at the doctor of pharmacy (PharmD) level? This study assessed perceptions and first-professional (P1) year student academic performance of first-generation vs. non-first-generation PharmD cohorts at the Feik School of Pharmacy. METHODS: Perceptions (academic and personal support) were assessed via a 49-question survey at the start of the second- and third-professional years. Academic performance was assessed via measures of academic success (course grades, grade point average, supplemental instruction enrollments, and academic infractions) in P1 year. Statistical t-tests and F-tests were used to analyze differences in perceptions and academic performance for the two cohorts. RESULTS: From 132 eligible students, 128 completed the survey (97% response rate) and 58 (45%) were first-generation students. First-generation students had a lower perception of their academic success, and they perceived finances as one of their greatest barriers (86% vs. 64%). Fifteen P1 courses were reviewed for academic performance, and first generations had lower final course grades in only two courses (Anatomy and Physiology 1; Medical Microbiology and Immunology). For measures of academic success, no significant differences were noted. CONCLUSIONS: Overall, this study suggested that first-generation status may not be a hindrance to academic performance at the PharmD level, but that financial perceptions and a lower self-perception of academic success seem to be major barriers for first-generation PharmD students.

Synthesis and evaluation of ligands for D2-like receptors: the role of common pharmacophoric groups.

Arylcycloalkylamines, such as phenyl piperidines and piperazines and their arylalkyl substituents, constitute pharmacophoric groups exemplified in several antipsychotic agents. A review of previous reports indicates that arylalkyl substituents can improve the potency and selectivity of the binding affinity at D(2)-like receptors. In this paper, we explored the contributions of two key pharmacophoric groups, that is, 4'-fluorobutyrophenones and 3-methyl-7-azaindoles, to the potency and selectivity of synthesized agents at D(2)-like receptors. Preliminary observation of binding affinities indicates that there is little predictability of specific effects of the arylalkyl moieties but the composite structure is responsible for selectivity and potency at these receptors.

Haloperidol: towards further understanding of the structural contributions of its pharmacophoric elements at D2-like receptors.

An attempt to understand the pharmacophore-relevant position of the alcoholic moiety in haloperidol and the contributions of other pharmacophoric elements led to the re-synthesis of its tropane analogue (compound 2). An analysis of the binding data suggests that haloperidol binds to the DA receptors with the OH group in the axial position and the OH group, while not essential for binding, enhances binding especially at the D2 receptor. It also became clear that shortening the butyrophenone chain not only reduces binding affinity at the DA receptors but eliminates subtype selectivity.

The acute EPS of haloperidol may be unrelated to its metabolic transformation to BCPP+.

We have previously proposed that haloperidol's debilitating extrapyramidal symptoms (EPS) may be associated with its quaternary BCPP+ (an MPP+ like species) metabolite formed in vivo. However, recent work on D2 knock out mice suggests that haloperidol's EPS may be related to its potent D2 binding (K(i)=0.9 nM). In this study, we explore this question by synthesizing and testing an analogue (DS-27) that binds to D2 receptors with higher affinity than haloperidol, but cannot form quaternary metabolites. This study suggests that D2 affinity may be the primary underlying mechanism for acute catalepsy induction by haloperidol.