Associations between formative practice quizzes and summative examination outcomes in a medical anatomy course.

Formative practice quizzes have become common resources for self-evaluation and focused reviews of course content in the medical curriculum. We conducted two separate studies to (1) compare the effects of a single or multiple voluntary practice quizzes on subsequent summative examinations and (2) examine when students are most likely to use practice quizzes relative to the summative examinations. In the first study, providing a single on-line practice quiz followed by instructor feedback had no effect on examination average grades compared to the previous year or student performances on similar questions. However, there were significant correlations between student performance on each practice quiz and each summative examination (r = 0.42 and r = 0.24). When students were provided multiple practice quizzes with feedback (second study), there were weak correlations between the frequency of use and performance on each summative examination (r = 0.17 and r = 0.07). The frequency with which students accessed the practice quizzes was greatest the day before each examination. In both studies, there was a decline in the level of student utilization of practice quizzes over time. We conclude that practice quizzes provide some predictive value for performances on summative examinations. Second, making practice quizzes available for longer periods prior to summative examinations does not promote the use of the quizzes as a study strategy because students appear to use them mostly to assess knowledge one to two days prior to examinations.

Medial prefrontal cortex inactivation attenuates the diurnal rhythm in amphetamine reward.

Psychostimulant reward, as assessed via the conditioned place preference (CPP) paradigm, exhibits a daily rhythm with peaks in the late dark and early light periods, and a nadir near the light-to-dark transition. While this diurnal rhythm is correlated with neural activity in several corticolimbic structures, the brain regions mediating this behavioral rhythm remain unknown. Here, we examine the role of the ventral medial prefrontal cortex (mPFC). The effects of excitotoxic mPFC lesions on daily rhythms in amphetamine CPP were examined at previously observed peak (zeitgeber time [ZT] 23) and nadir times (ZT11). mPFC lesions encompassing the prelimbic and infralimbic subregions increased the CPP for amphetamine at the nadir time, thereby eliminating the daily rhythm in amphetamine reward. To examine the effects of transient mPFC inactivation, rats received intra-mPFC infusions of GABA receptor agonists during the acquisition or expression phases of CPP testing. Inactivation of the ventral mPFC at either of these phases also eliminated the daily rhythm in amphetamine-induced CPP via an increase in drug-paired chamber dwell time at the baseline nadir. Together, these results indicate that the ventral mPFC plays a critical role in mediating the diurnal rhythm in amphetamine CPP during both the acquisition and expression of learned reward-context associations. Moreover, as the loss of rhythmicity occurs via an increase at the nadir point, these results suggest that excitatory output from the ventral mPFC normally inhibits context-elicited reward seeking prior to the light-to-dark transition.

A comprehensive linkage analysis of chromosome 21q22 supports prior evidence for a putative bipolar affective disorder locus.

Previously, we demonstrated evidence of linkage to bipolar affective disorder (BP) in a single large, multigenerational family with a LOD score of 3.41 at the PFKL locus on chromosome 21q22.3. Additional families showed little support for linkage to PFKL under homogeneity or heterogeneity, in that study. We have expanded on that analysis, with 31 microsatellite markers at an average marker spacing of

Characterization of the human glutamate receptor subunit 3 gene (GRIA3), a candidate for bipolar disorder and nonspecific X-linked mental retardation.

The X-chromosome breakpoint in a female patient with a balanced translocation t(X;12)(q24;q15), bipolar affective disorder and mental retardation was mapped within the glutamate receptor 3 (GRIA3) gene by fluorescence in situ hybridization. The GRIA3 cDNA of 5894 bp was cloned, and the gene structure and pattern of expression were determined. The most abundant GRIA3 transcript is composed of 17 exons. An additional 5 exons (2a, 2b, 5a, 5b, and 5c) from the 5' end of the GRIA3 open reading frame were identified by EST analysis (ESTs AI379066 and AA947914). Two new polymorphic microsatellite repeats, (TC)(n=12-26) and (AC)(n=15-19), were identified within GRIA3 5' and 3'UTRs. No mutations were detected in families segregating disorders mapping across GRIA3, one with X-linked bipolar affective disorder (BP) and one with a nonspecific X-linked mental retardation (MRX27). To assess the possibility of the involvement of the GRIA3 gene in familial cases of complex BP, a large set of 373 individuals from 40 pedigrees segregating BP were genotyped using closely linked (DXS1001) and intragenic (DXS1212 and GRIA3 3' UTR (AC)(n))) GRIA3 STR markers. No evidence of linkage was found by parametric Lod score analysis (the highest Lod score was 0. 3 at DXS1212, using the dominant transmission model) or by affected sib-pair analysis.

American families with Crohn's disease have strong evidence for linkage to chromosome 16 but not chromosome 12.

BACKGROUND & AIMS: Two European genome-wide screens for inflammatory bowel disease have identified two significant regions of linkage on chromosomes 16 (IBD1) and 12 (IBD2) and two regions with suggestive levels of significance (chromosomes 3p and 7q). The aim of this study was to determine if there was evidence for linkage to these regions in non-Jewish and Ashkenazi Jewish families multiplex for Crohn's disease from the United States. METHODS: One hundred forty-eight affected relative pairs, 34% Ashkenazim, were genotyped with 10-14 highly polymorphic markers overlying each candidate region. Nonparametric multipoint and two-point linkage analyses were performed. RESULTS: Significant evidence for replication of linkage was found only for the chromosome 16 locus, IBD1, maximal at D16S769 (nonparametric linkage score [NPL], 2.49; P = 0.007). Analysis by ethnicity showed stronger evidence for Ashkenazim (D16S769; NPL = 2. 52; P = 0.007) than for non-Jewish white populations (D16S401; NPL = 1.40; P = 0.082). There was no significant evidence for replication on chromosome 12 (IBD2). Minimal evidence for extension of linkage evidence was observed for the chromosomes 3p and 7q regions. CONCLUSIONS: American families, particularly Ashkenazim, have significant evidence for the Crohn's disease susceptibility locus, IBD1, on chromosome 16, but not for IBD2 on chromosome 12.

[Knowledge about AIDS prevention among professionals and students in health care]. / Conhecimentos sobre prevenção da SIDA entre profissionais e acadêmicos da área de saúde.

This work is a exploratory research based on the analysis of the answers to the questionnaires of 52 students and health care professionals knowledge about AIDS sexual prevention, biosecurity, diagnosis tests, patients and workers rights and the modifications of nursing and medical care to this kind of disease.

[Efficacy of the administration of serum amd vaccine for the antirabies treatment of experimentally-infected sheep]. / Eficacia de la administración de suero y vacuna en el tratamiento antirrábico de ovinos infectados experimentalmente.

The objectives of this study were to examine the humoral immune response of sheep to experimental infection with an isolate of rabies virus from a fox, to analyse the efficacy of vaccination as a method of post-infection treatment, and to find a suitable animal model to evaluate new procedures for human vaccination following infection. A total of 47 sheep were used. Initially, 26 sheep received an intramuscular injection of a suspension of virus (titre: 10(6.8) 50% lethal dose for mice by the intracerebral route). Half of the sheep were subsequently treated using a vaccine on the day of infection and at 3, 7, 14 and 30 days post-infection. The remaining half comprised the unvaccinated controls. This vaccination protected seven of thirteen sheep, while nine of the thirteen controls died. Subsequently, 21 sheep were inoculated under the same conditions as in the previous trial. The animals were divided into three groups of seven animals each. The first group was vaccinated in the same way as described above. The second group received an injection of anti-rabies immunoglobulin of human origin (26.3 IU/kg of body weight), followed by the course of vaccine treatment 24 hours later. The remaining group acted as unvaccinated controls. Of the seven sheep given vaccine alone, four were protected, while all seven animals given immunoglobulin and vaccine were protected. Six of the seven untreated controls died. In this study, no apparently-healthy carriers of rabies virus were created by any of the treatments used, nor was there any shortening of the incubation periods. Additional observations were made concerning incubation periods and the course of the disease, as well as symptoms, lesions and the presence of rabies virus in various nerve centres and salivary glands of the experimental sheep.

Is thrombolytic therapy safe during active menstruation?

A 39-year-old female presented to the Emergency Department during the fourth day of menstruation and within 2 hours of the onset of chest pain associated with dyspnea, diaphoresis, and emesis. An electrocardiogram showed acute inferior myocardial infarction and serial CPK enzyme levels peaked at 958 IU/L with 9% MB fraction. Along with aspirin and intravenous nitroglycerin, the patient was given thrombolytic therapy consisting of tPA with an initial bolus of 35 units, followed by 65 units infused within 60 minutes together with heparin 5000 units intravenous bolus, and 1000 units/hour maintenance infusion for 5 days. The menses were prolonged 1 day longer than her usual 5 days; however, there was no increase in the amount of bleeding during any day. The hemoglobin dropped from 12.5 G/dl to 11.3 G/dl in the first 6 hours, but remained stable thereafter. This initial drop in hemoglobin was considered a dilutional effect of 1.5 L of normal saline the patient received intravenously during that period. Although no available guidelines exist regarding the safety of thrombolytic agents during active menstruation, this case report and a few others reported in the literature suggest that normal menstruation is not a contraindication to thrombolytic therapy during acute myocardial infarction.

Dipyridamole-thallium stress testing: a local community hospital experience.

Clinical data on the first 100 patients who underwent dipyridamole-thallium stress testing in our hospital were reviewed in order to re-evaluate safety guidelines and diagnostic utility in patients with coronary artery disease. Forty patients developed symptoms, including three major ones. One patient had significant bronchospasm, and two others developed significant hypotension with near syncope. The rest had nonspecific chest, shoulder, arm or throat pain, dyspnea, nausea, vomiting, and paresthesia. Most symptoms occurred within the first 10 minutes of dipyridamole infusion. Twenty-eight patients required treatment with intravenous (IV) aminophylline. Of the remaining 60 patients, 30 became hypotensive but remained asymptomatic. Fourteen of 20 patients who underwent coronary angiography had coronary disease. Thirteen were correctly identified by thallium imaging, and only one was identified by electrocardiogram (EKG). Six patients' angiographies showed no evidence of coronary disease. Five of these patients developed perfusion abnormalities during thallium scintigraphy. These results suggest that dipyridamole is a relatively safe drug for pharmacologic stress testing even though the incidence of side effects is relatively high. The high incidence of thallium perfusion abnormalities in patients without coronary disease probably reflects bias in patient selection for coronary angiography, resulting in a relatively small sample of catheterized patients. However, this requires further investigation.

[Experimental infection of sheep with a rabies virus of canine origin: study of the pathogenicity for that species]. / Infección experimental de ovinos por un virus de la rabia de origen canino: estudio del poder patógeno para esta especie.

The effects of the inoculation of a canine strain of rabies virus in sheep were studied using ten animals which received different amounts of this virus. Two subjects, inoculated with 10(5.4) mouse intracerebral lethal doses 50% (MICLD50), died from rabies after 19 and 40 days of incubation. Clinical signs were anorexia, emaciation, nervous reactions and prostration before death. The virus was recovered from different parts of the central nervous system and salivary glands with high titres. Only three animals showed an antibody response, at very low levels.

Case report: myocardial ischemia: an overlooked substrate in syncope of aortic stenosis.

The cause of the syncope in aortic stenosis has been the subject of controversy partly because only a few patients have been monitored during their syncopal episodes. Among the mechanisms proposed are hypersensitive carotid sinus, complete A-V block, ventricular arrhythmias, and ischemic myocardial depression. It is now accepted that the syncope is caused by a vasodepressor response from stimulation of left ventricular baroceptors, resulting in reflex hypotension and bradycardia. This case report describes a patient who developed a syncopal episode during stress testing. Although the mechanism for the syncope is consistent with the vasodepressor response, ischemic changes were observed in the electrocardiogram before the development of syncope. Review of literature shows that, although different mechanisms for syncope have been described, all reported patients manifested myocardial ischemia before the development of their syncopal episodes even when the syncope was nonexertional and clearly caused by a vasodepressor response. The authors conclude that, independent of the mechanism proposed, myocardial ischemia is overlooked as an important substrate in which the syncopes are precipitated in aortic stenosis.

Effective postexposure treatment of rabies-infected sheep with rabies immune globulin and vaccine.

An experiment to assess the efficiency of the treatment recommended for humans after exposure to rabies was conducted in 68 sheep experimentally infected with a fox rabies virus. The infected sheep were divided into three groups and were given either a cell-culture vaccine (on the day of infection, then at day 3, 7, 14), human rabies immunoglobulin (26 IU kg-1 on the day of infection) or a combination of the vaccine immunoglobulin. The latter combination was the only treatment found to be effective in 100% of the animals, as 71% of the controls died. This model appears to be useful in assessing new regimens of postexposure treatment for humans as well as in the reconsideration of its feasibility, or validity, in animals.

Sudden cardiac death from acute fluoride intoxication: the role of potassium.

The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.

Echocardiogram of pulmonary embolism in evolution.

Echocardiography during active pulmonary embolism can reveal the embolic mass in transit through the chambers of the right side of the heart. The pattern produced is that of multiple masses of varying sizes, shapes, and densities moving from the right atrium to the right ventricle. It was not present on repeated echocardiogram performed several weeks later, after anticoagulation treatment. Proper recognition of this pattern can lead to prompt medical treatment with anticoagulants, which, in this case, led to a quite satisfactory clinical outcome.

Spontaneous contrast visualization on the right side of the heart during echocardiography.

Microbubble contrast visualization within the right heart is almost always due to intravenous injections containing microbubbles. In the absence of immediate administration of agitated solutions, several other mechanisms for the occurrence of echo contrast spontaneously in the cardiovascular system have been postulated. Often overlooked as a source of contrast are microbubbles from remotely injected solutions that persist in the circulation because of markedly delayed clearance. Two patients were observed with apparently spontaneous contrast detected in the right heart chambers, both of whom had congestive heart failure, tricuspid regurgitation, and pulmonary hypertension. Regardless of the exact mechanism involved, the finding of this phenomenon reflects the presence of right heart failure and a low flow state.

The manipulation of potassium efflux during fluoride intoxication: implications for therapy.

Based on findings in 2 fluoride-toxic patients, it was suspected that hyperkalemia played a clinically important role in the etiology of sudden death from fluoride poisoning. Using fluoridated human erythrocytes as an in vitro model, it was confirmed that fluoride produced a marked potassium efflux from intact cells. Further, neither glucose and insulin in pharmacologic doses, nor various buffers could halt the efflux by shifting the potassium intracellularly. If these results can be extrapolated to the clinical situation, removal of potassium and fluoride via exchange resins or dialysis remains the only reasonable approach to this life threatening problem. Aside from sudden hyperkalemia and hypocalcemia, no serologic marker for fluoride toxicity has been identified. A high degree of clinical suspicion is therefore essential to the diagnosis.