Evaluation of student achievement and educational outcomes.

Development of problem-solving skills is vital to professional education as is factual recall. Student mastery must be measured to document student achievement requiredfor completion of educational requirements and professional certification. These measurements also help determine if the educational process is meeting its goal of helping students develop critical cognitive skills for therapeutic problem solving. Testing student growth in the ability to solve problems is less understood. Stressing integration of information across disciplines to derive answers is also important. Test items should resemble the real-world task that students are expected to master. Thatisreallythe essence of content validity, which means faculty should be biased toward presenting information that way. This article is based on a symposium presented at the annual meeting of the American College of Clinical Pharmacology in September 1996. Symposium goals were to define purposes and uses of student evaluations by type and format, including application of techniques that improve evaluation, precision, and validity. Technical applications of computer-based learning and evaluation of problem-solving skills are described. Actual experience with evaluation of problem solving in the curriculum is discussed. The process by which a medical school developed and implemented an evaluation system for a new problem-based curriculum is presented, followed by a critique of the successes and problems encountered during the first year of implementation. Criteria that a well-constructed evaluation program must meet are explored. The approach and philosophy of national standardized testing centers are explained.

Performance on the National Board of Medical Examiners. Part I Examination by men and women of different race and ethnicity.

OBJECTIVE: To investigate the performance of men and women from various racial and ethnic backgrounds on the National Board of Medical Examiners Part I examination, controlling for any differences in measures of educational background and academic performance before entering medical school. DESIGN: A retrospective analysis of existing records from the National Board of Medical Examiners and the Association of American Medical Colleges. SETTING: National Board of Medical Examiners. PARTICIPANTS: All students taking the June administration of Part I for the first time in 1986, 1987, or 1988 and who were 2 years from graduation from an accredited medical school. METHODS: Multiple regression methods were used to estimate Part I examination group differences in performance that would be expected if all students entered medical school with similar Medical College Admission Test scores, undergraduate grade point averages, and other prematriculation measures. MAIN OUTCOME MEASURE: Performance on the Part I examination. RESULTS: There were substantial differences in performance, with white students scoring highest, followed by Asian/Pacific Islanders, Hispanics, and blacks; within all racial and ethnic categories, women scored lower than men. Controlling for dissimilarities in academic background greatly reduced Part I differences among most racial and ethnic groups, except Asian/Pacific Islander men; unexplained differences remained between men and women. Results were consistent for the 3 years examined. CONCLUSIONS: The results of this study do not imply that physician performance varies among racial and ethnic groups or between men and women; no written examination can measure all the abilities that may be desirable to assess. Validity research investigating reasons for the reported gender and racial and ethnic differences in performance on the National Board examinations should be continued.

Impact of the USMLE step 1 on teaching and learning of the basic biomedical sciences. United States Medical Licensing Examination.

Medical licensure in the United States is in transition. In June 1991, the National Board of Medical Examiners (NBME) made major modifications in the content, format, pass/fail standards, and score reports of the NBME Part I examination. This year, Part I became Step 1, the first of three components of the United States Medical Licensing Examination (USMLE), which will shortly be the sole examination pathway to initial licensure for allopathic physicians. This essay describes Step 1, reviews the phase-in plans for the USMLE, and discusses the potential impact of both on medical schools' teaching and students' learning of the basic biomedical sciences. The authors recommend that medical schools (1) abandon the use of Step 1 as a sole criterion for student promotion to the third year and (2) carefully review other examination-related requirements for promotion and graduation.

Score reporting on NBME examinations.

Because the National Board of Medical Examiners (NBME) will introduce new comprehensive Part I and Part II examinations in 1991, a review has been made of score reporting methods to be used in the new examinations. The review was conducted also because of concern expressed by some that NBME examination scores are misused in medical schools and in resident selection. In this paper, selected aspects of score reporting are defined, the uses of score reports outlined, and the potential for misuse described. It should be noted that the NBME is obliged to make available numerical scores to state medical boards and to examinees. Individual scores are reported to others only with the permission of the examinee. The results of an opinion poll conducted by the NBME of medical educators and medical students are presented. The range of opinion is broad but favors numerical score reporting and a designated pass/fail score.

Standardized testing of patient management skills. A computer-based method.

Clinical cases can be simulated by using computers with programs designed to provide all of the information required to make a diagnosis and initiate a treatment plan. The cases are uncued, simulate time, and require sound clinical judgment for management. All transactions between the physician and case are recorded so that each action can be evaluated from the standpoint of timeliness, sequence, appropriateness, risk, and cost. Results from field studies indicate that the performance by residents in the management of clinical case simulations measures more than knowledge.

The National Boards of the future.

The National Board of Medical Examiners has decided to implement computer-based testing as the standard examination methodology for all students in the near future. The author describes how computer-based testing will eventually be used and the direction that the National Board Examinations will take in the future.

Muscarinic receptors and [3H]inositol incorporation in a rat sympathetic ganglion.

[3H]Inositol incorporation into phosphatidylinositol was accelerated in rat superior cervical ganglia treated with 4-aminopyridine or Bethanechol. The inositol response to these drugs occurred in intact and denervated ganglia and was prevented by atropine. The possibility that muscarinic receptor subtypes are present in the ganglia is considered because bethanechol, but not 4-aminopyridine, is known to increase cGMP in rat superior cervical ganglia by an atropine-sensitive process.

cAMP in guinea-pig superior cervical ganglia during preganglionic nerve stimulation.

Preganglionic nerve stimulation or elevated [K+]o increase cAMP levels in isolated guinea-pig superior cervical ganglia, a ganglion lacking adrenergic inhibitory synaptic potentials. The cAMP response to K+ and nerve stimulation is not prevented by atropine or phentolamine. The regulation of cAMP content does not involve cholinergic or adrenergic mechanism. Of polypeptides tested, only VIP (5 X 10(-6) M) increases cAMP content to the extent observed with preganglionic nerve stimulation.

Regulation of cyclic GMP levels in nerve tissue.

In rat superior cervical ganglia the regulation of cyclic GMP (cGMP) formation does not involve muscarinic or adrenergic transmitters or receptors. Marked increases in cGMP content during preganglionic axonal stimulation by electric currents, elevated K+, or drugs that cause transmitter release are unaffected by muscarinic and adrenergic receptor blockade. However, the cGMP response does require Ca2+ and intact preganglionic axonal terminals. Two possibilities exist: either cGMP accumulates in the preganglionic nerves or a noncholinergic, nonadrenergic transmitter activates guanylate cyclase in postsynaptic structures. Sodium azide and nitroprusside cause cGMP accumulation in denervated ganglia, which indicates that postsynaptic structures are capable of forming cGMP. In pineal glands elevated [K+]o releases [3H]norepinephrine and causes cGMP accumulation, which suggests a relationship between the two responses and the possibility that cGMP accumulation is involved in autoinhibition of transmitter release. The finding that phentolamine, alpha-adrenergic receptor antagonists, prevent the cGMP response to K+ is compatible with this review. However, clonidine, an alpha-receptor agonist, depresses norepinephrine release but has no effect on pineal gland cGMP. Conversely, large increases in pineal gland cGMP produced by nitroprusside do not affect K+-evoked norepinephrine release. For these reasons it is not possible to relate cGMP to the auto-inhibition of [3H]norepinephrine release that is mediated by prejunctional alpha-adrenergic receptors.

Regulation of cyclic AMP accumulation in a rat sympathetic ganglion: effects of vasoactive intestinal polypeptide.

Cyclic AMP accumulation in rat superior cervical ganglia during synaptic activity occurs by a noncholinergic, nonadrenergic process. Both preganglionic nerve stimulation and 4-aminopyridine increase ganglion cyclic AMP levels in the presence of atropine or phentolamine. Of the polypeptides tested as putative transmitters, vasoactive intestinal polypeptide (10(-6) M) causes ganglion cyclic AMP accumulation comparable to that produced by preganglionic nerve stimulation.

The regulation of cyclic nucleotides in a sympathetic ganglion.

Preganglionic nerve terminal stimulation in rat superior cervical ganglia causes marked increases in the levels of cyclic nucleotides. Results are similar when preganglionic nerve stimulation is compared with elevated [K+]0 or 4-aminopyridine. Although intact nerve terminals and Ca2+ are required for the response to occur, pharmacological studies indicate that acetylcholine and adrenergic transmitters are not involved in the cyclic nucleotide response. It is suggested that cyclic nucleotide accumulation occurs in the nerve terminals or an unknown transmitter or substance participates in the postsynaptic accumulation of the cyclic nucleotides. Polypeptides tested thus far do not seem to be implicated. Interrelationships among phospholipid turnover, Ca2+-exchange and cyclic nucleotide accumulation in rat sympathetic ganglia are considered, but are difficult to establish.

Ketamine and ditran block end-plate ion conductance and [3H]phencyclidine binding to electric organ membrane.

Alterations by ketamine (10-100 microM) and ditran (50-100 microM) of end-plate currents were studied using transected cutaneous pectoris muscles. Both drugs reduced peak current and shortened the time constant for end-plate current decay (tau). Ketamine was more effective at pH 5.3 than at 7.4 or 9.1. Recovery from blockade was asymmetrical in that tau recovered more quickly than did peak current when the drugs were removed from the bath. By contrast, 4-aminopyridine antagonized the depression of peak current by ketamine, but not the reduction of tau. Both ketamine and ditran disrupted the voltage dependence of tau. The binding to microsacs prepared from electric organs of [3H]phencyclidine ([3H]PCP) was blocked by ketamine and ditran. In microsacs treated with carbachol, the IC50 for ketamine block of [3H]PCP binding was 6.6 X 10(-6) M. For ditran, the IC50 for block of [3H]PCP binding in the presence of carbachol was 1.7 X 10(-6) M. The binding of [alpha-125I]bungarotoxin to the microsacs or to the cultured chick myotubes was reduced only slightly by ketamine. Because ketamine has no effect on transmitter release and little effect on [alpha-125I]bungarotoxin binding, it is concluded that, like PCP, ketamine and ditran block open channels in the end-plate. In addition, the asymmetrical recovery of end-plate current parameters suggests that ketamine may block closed channels. The recovery from block of closed channels (caused by either a direct action on closed channels or a very slow channel unblocking rate) proceeds more slowly than does the block of open channels.

Cyclic guanosine 3':5'-monophosphate accumulation and 45Ca-uptake by rat superior cervical ganglia during preganglionic stimulation.

Repetitive preganglionic nerve stimulation increases cyclic guanosine 3':5'-monophosphate (cGMP) content in rat superior cervical ganglia by a mechanism requiring Ca++ but resistant to blockade by cholinergic receptor antagonists. Similarly, 45Ca-uptake during prolonged preganglionic nerve stimulation is unaffected by hexamethonium or atropine. These findings indicate that nerve stimulation increases cGMP accumulation and 45Ca-uptake by a noncholinergic mechanism Substance P, met-enkephalin and luteinizing hormone-releasing factor have little or no effect on cGMP content. By contrast, bethanechol causes a 3-fold increase in cGMP content and postganglionic cell firing. Thus, as reported by others, muscarinic receptor activation increases ganglionic cGMP[. 4-Aminopyridine causes an increase in cGMP of resting ganglia that requires Ca++ and the nerve terminal is blocked by tetrodotoxin but unaffected by atropine or hexamethonium. Ouabain also increases ganglionic cGMP content by a process that requires Ca++ and the nerve terminals. Like preganglionic nerve stimulation, 4-aminopyridine and ouabain cause cGMP accumulation in the nerve terminals or in the ganglion cells as a consequence of releasing a noncholinergic transmitter. The uptake of Ca++ by ganglion cells is not an adequate stimulus for cGMP accumulation because the nicotinic receptor agonist dimethylphenylpiperazinium increases 45Ca-uptake but has no effect on cGMP formation in ganglia.

Multiple actions of beta-bungarotoxin on acetylcholine release at amphibian motor nerve terminals.

The action of beta-bungarotoxin (beta-BuTX) on spontaneous transmitter release, as monitored by miniature endplate potential (MEPP) frequency, and nerve-stimulated release, which relates directly to endplate potential (EPP) amplitude, was studied at frog sciatic nerve-sartorius muscle junctions. Three phases were found for both spontaneous and evoked release: a transient decrease followed by an increase and a later decrease leading to complete failure. The initial inhibitory phase for both spontaneous and neurally-evoked release occurred at the same time and was independent of stimulation frequency. Both the excitatory and late inhibitory phases for both types of release had a more rapid onset when stimulation frequency was increased, with the effects on evoked release occurring more rapidly than the effects on spontaneous release. Even though EPP amplitude decreased to low levels while MEPP frequency was still high, EPPs did not completely fail until the MEPPs had also declined to very low levels. In elevated K+ solutions, the number of quanta released after toxin application was only about half that released during the control experiment. During the terminal part of the late inhibitory phase of beta-BuTX action on MEPP frequency, no effect or only small transient increases were observed after La3+ administration, elevated [K+]0, or increased osmotic pressure. The present study suggests that depolarization of nerve terminals by the toxin is responsible for initiation of the excitatory phases of both types of release followed by inhibition of nerve-evoked release, and then depletion of vesicular transmitter accounts for the eventual disappearance of both MEPPs and EPPs.