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In 2010, second-year physiology (n = 165) had a traditional single 3-h end-of-semester exam. To provide diagnostic feedback earlier, for students enrolled in 2011 (n = 128), we incorporated an in-class exam at 3 wk in addition to the final exam. Based on initial analysis and positive student comments, for the 2012 cohort (n = 148), we expanded this to incorporate four 1-h in-class exams every 3 wk plus a short final integrative exam. Average scores from exams and questionnaires (student evaluations of learning and teaching, 10 questions) were compared among 2010, 2011, and 2012 cohorts. We also compared scores in the practical component of the course, which had a constant format for all cohorts. Data are given as means ± SD; statistical analyses were done with unpaired two-way Students t-tests. From 2010 to 2012, there was a significant improvement in total exam scores (59.7 ± 15.8 vs. 68.6 ± 14.2, P < 0.001) but no significant change in total practical scores (72.3 ± 9.0 vs. 74.4 ± 10.2, P = 0.05), indicating that the rise in exam score was not due to higher academic abilities of the 2012 cohort. Overall mean student evaluation of learning and teaching responses (4.9 ± 0.4 vs. 5.3 ± 0.3, P = 0.015) and overall percent broad agreement (66.0 ± 8.0 vs. 79.2 ± 7.5, P = 0.003) indicated a significant improvement in student satisfaction. In conclusion, both learning outcome and perceived course quality were enhanced by the increased frequency of examinations, possibly by promoting consistent student study habits.

Background/objectives Amitriptyline (AMY) is a tricyclic anti-depressant that has recently been shown to have anti-inflammatory properties. We investigated whether AMY is cardioprotective against reperfusion injury in ex-vivo rat hearts. Methods Thirty adult Sprague-Dawley rat hearts were perfused ex-vivo in a Langendorff apparatus. All hearts except SHAM (n = 6, perfused for 110 min.) received 30 min no-flow ischemia followed by 40 min reperfusion (I-R). One group (n = 6) was untreated before I-R (non-preconditioned; NPC), another non-preconditioned group was perfused with 10 μM amitriptyline for 30 min before I-R (NPC-AMY, n = 6). One group was preconditioned with 3 x 5-minute periods of ischemia before I-R (PC, n = 6) and a fifth group was preconditioned in the presence of 10 μM amitriptyline (PC-AMY, n = 6). p38 phosphorylation and HMGB1 levels were quantified using Western blots. Data was analysed using multiway ANOVAs with Tukey HSD and linear regression models with Sobel mediator tests. Results NPC hearts recovered poorly (LVDP recovered to 26.5 ± 10.5% of pre-ischemic values, compared to PC hearts (82.8 ± 14.9%: P < 0.05)). PC-AMY (69.9 ± 6.16%) and NPC-AMY (90.3 ± 10.0%) groups both recovered well (P < 0.05). The Sobel mediator test suggested that p38 activity may be indirectly involved in the amitriptyline induced cardioprotection (P < 0.05). HMGB1 was lower in amitriptyline treated hearts compared to the non-preconditioned hearts (P < 0.05) but the multiway ANOVA test suggests that HMGB1 was not involved in amitriptyline induced protection. Conclusions Amitriptyline at 10 μM protects hearts against ischemic-reperfusion injury which may be partially mediated through p38 phosphorylation. [ABSTRACT FROM AUTHOR]

Abstract: There is a direct relationship between elevated blood pressure and cardiovascular disease, so screening for elevated blood pressure is an essential nursing activity. This quality improvement project involving faith community nurses (FCNs) in 24 congregations and other sites tracked readings of blood pressures taken, referrals made, and education sessions provided during a 21-month period. Surveys revealed the project increased participants' awareness about screenings, FCN services, and evidence-based protocols, in addition to identifying high-risk congregants for care and treatment., (Copyright © 2022 InterVarsity Christian Fellowship.)

Decades of focus on selective ion channel blockade has been dismissed as an effective approach to antiarrhythmic drug development. In that context many older antiarrhythmic drugs lacking ion channel selectivity may serve as tools to explore mixed ion channel blockade producing antiarrhythmic activity. This study investigated the non-clinical electrophysiological and antiarrhythmic actions of bisaramil and penticainide using in vitro and in vivo methods. In isolated cardiac myocytes both drugs directly block sodium currents with IC 50 values of 13μM (bisaramil) and 60μM (penticainide). Both drugs reduced heart rate but prolonged the P-R, QRS and Q-T intervals of the ECG (due to sodium and potassium channel blockade) in intact rats. They reduced cardiac conduction velocity in isolated rat hearts, increased the threshold currents for capture and fibrillation (indices of sodium channel blockade) and reduced the maximum following frequency as well as prolonged the effective refractory period (indices of potassium channel blockade) of electrically stimulated rat hearts. Both drugs reduced ventricular arrhythmias and eliminated mortality due to VF in ischemic rat hearts. The index of cardiac electrophysiological balance (iCEB) did not change significantly over the dose range evaluated; however, different drug effects resulted when changes in BP and HR were considered. While bisaramil is a more potent sodium channel blocker compared to penticainide, both produce a spectrum of activity against ventricular arrhythmias due to mixed cardiac ion channel blockade. Antiarrhythmic drugs exhibiting mixed ion channel blockade may serve as tools for development of safer mixed ion channel blocking antiarrhythmic drugs., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Background: RSD921, the R,R enantiomer of the kappa (k) agonist PD117,302, lacks significant activity on opioid receptors., Methods: The pharmacological and toxicological actions were studied with reference to cardiovascular, cardiac, antiarrhythmic, toxic and local anaesthetic activity., Results: In rats, dogs and baboons, RSD921 dose-dependently reduced blood pressure and heart rate. In a manner consistent with sodium channel blockade it prolonged the PR and QRS intervals of the ECG. Furthermore, in rats and NHP, RSD921 increased the threshold currents for induction of extra-systoles and ventricular fibrillation (VF t ), and prolonged effective refractory period (ERP). In rats, RSD921 was protective against arrhythmias induced by electrical stimulation and coronary artery occlusion. Application of RSD921 to voltage-clamped rat cardiac myocytes blocked sodium currents. RSD921 also blocked transient (i to ) and sustained (I Ksus ) outward potassium currents, albeit with reduced potency relative to sodium current blockade. Sodium channel blockade due to RSD921 in myocytes and isolated hearts was enhanced under ischaemic conditions (low pH and high extracellular potassium concentration). When tested on the cardiac, neuronal and skeletal muscle forms of sodium channels expressed in Xenopus laevis oocytes, RSD921 produced equipotent tonic block of sodium currents, enhanced channel block at reduced pH (6.4) and marked use-dependent block of the cardiac isoform. RSD921 had limited but quantifiable effects in subacute toxicology studies in rats and dogs. Pharmacokinetic analyses were performed in baboons. Plasma concentrations producing cardiac actions in vivo after intravenous administration of RSD921 were similar to the concentrations effective in the in vitro assays utilized., Conclusions: RSD921 primarily blocks sodium currents, and possesses antiarrhythmic and local anaesthetic activity., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)