Performance and retention of basic life support skills improve with a peer-led training program.

BACKGROUND AND PURPOSE: Pharmacy students' performance and retention of Basic Life Support (BLS) skills were evaluated 120 days after completion of a peer-led BLS training program. EDUCATIONAL ACTIVITY AND SETTING: This was a single-center, parallel group, observational study. Doctor of pharmacy (PharmD) students in their third professional year completed a peer-led BLS training program (n = 148) and participated in a high-fidelity mannequin simulation activity 120 days later. Students were randomly assigned to rapid response teams (n = 24) of five to six members and the American Heart Association's standardized form for BLS assessment was used to assess BLS skills performance. The performance of skills was compared to that of students two years prior to the implementation of the peer-led BLS program. FINDINGS AND DISCUSSION: Students who received peer-led BLS training demonstrated retention of BLS skills 120 days after the BLS training program. The teams also displayed significant improvement of the skills evaluated when compared to student teams prior to implementation of the peer-led training (n = 22). Improvement was demonstrated for assessment of responsiveness (96% vs. 41%, p < 0.001), assessment for breathing (100% vs. 32%, p < 0.001), assessment for pulse (96% vs. 36%, p < 0.001), and administration of appropriate ventilation (100% vs. 32%, p < 0.001). Numerical superiority was exhibited for high-quality cardiopulmonary resuscitation (CPR) initiation by teams who received peer-led training (100% vs. 86%, p = 0.101). SUMMARY: Students who received peer-led BLS training demonstrated significant improvement in BLS skills performance and retention 120 days after the training program. Data suggests that peer-led BLS training can improve student BLS skills performance and retention.

A selective Akt inhibitor produces hypotension and bradycardia in conscious rats due to inhibition of the autonomic nervous system.

Akt is a serine-threonine kinase that is amplified in a variety of human cancers, and as with other anticancer agents, some Akt inhibitors have produced functional cardiovascular effects such as marked hypotension that may limit their clinical benefit. Although identified in preclinical studies, the mechanism(s) responsible for these effects are often not fully characterized; potential targets include Akt signaling disruption in cardiac tissue, vascular smooth muscle, and/or autonomic system signaling. A selective Akt inhibitor was found to produce a rapid and marked hypotension and bradycardia in conscious rats. Isolated right atrial tissue and isolated thoracic aortic rings were used to examine direct effects of Akt inhibition on cardiac and vascular tissues, respectively. In addition, rats surgically prepared with telemetry units for monitoring blood pressure and heart rate were used to investigate potential effects on the autonomic nervous system (ANS). Whereas this Akt inhibitor did not produce any significant effect on atrial tissue, it did cause vasorelaxation of aortic rings. More significantly, in conscious rats, the Akt inhibitor inhibited the neural pressor response to the known nicotinic acetylcholine receptor (nAchR) agonist dimethylphenylpiperazinium (DMPP). In fact, the response observed was comparable to the response observed with the known ganglionic blocker hexamethonium. Thus, the hypotension and bradycardia produced by the Akt inhibitor is primarily due to blockade of nAchRs in autonomic ganglia. This finding highlights the importance of evaluating the ANS for cardiovascular effects associated with new chemical entities as well as suggesting a novel direct effect of an Akt inhibitor on nAchRs.

Carotenoids normally present in serum inhibit proliferation and induce differentiation of a human monocyte/macrophage cell line (U937).

Carotenoids, plant pigments with potent antioxidant activity, are implicated in chronic disease protection. They are absorbed from the diet and transported by plasma lipoproteins. Monocytes, as circulating blood cells, are exposed to carotenoid-rich lipoproteins. Such exposure may lead to enrichment with carotenoids and may affect the functions of monocyte-derived macrophages. This study explored the effect of cellular enrichment in vitro with beta-carotene, lycopene, or lutein on monocyte/macrophage function, using U937 cells as a model. Cell proliferation, production of reactive oxygen species, and cell-substrate adhesion were examined. Maximal carotenoid levels in medium supplemented with preenriched human serum were 2-8 mumol/L; incubation for 1-6 d resulted in 0.2-1.1 nmol carotenoid/mg cell protein (0.25-1 nmol/10(6) cells), approximately 10-fold more than that reported in normal tissue in vivo but within the range that might be anticipated with dietary supplementation. beta-Carotene, lycopene, and lutein markedly inhibited the proliferation of U937 cells, to an extent similar to or greater than that due to phorbol myristic acetate, a known differentiation/activation agent. Lycopene, but not beta-carotene or lutein, caused a significant increase in reactive oxygen species, indicating the induction of cell differentiation. Adhesion and LDL oxidation were unaffected. Thus, cellular carotenoids inhibit proliferation, and for lycopene at least, this may involve cell differentiation. The effectiveness of lycopene, a nonprovitamin A carotenoid, is consistent with a vitamin A-independent pathway modulating cell function.

Carotenoid uptake and secretion by CaCo-2 cells: beta-carotene isomer selectivity and carotenoid interactions.

In presence of oleate and taurocholate, differentiated CaCo-2 cell monolayers on membranes were able to assemble and secrete chylomicrons. Under these conditions, both cellular uptake and secretion into chylomicrons of beta-carotene (beta-C) were curvilinear, time-dependent (2-16 h), saturable, and concentration-dependent (apparent K(m) of 7-10 microM) processes. Under linear concentration conditions at 16 h incubation, the extent of absorption of all-trans beta-C was 11% (80% in chylomicrons), while those of 9-cis- and 13-cis-beta-C were significantly lower (2-3%). The preferential uptake of the all-trans isomer was also shown in hepatic stellate HSC-T6 cells and in a cell-free system from rat liver (microsomes), but not in endothelial EAHY cells or U937 monocyte-macrophages. Moreover, extents of absorption of alpha-carotene (alpha-C), lutein (LUT), and lycopene (LYC) in CaCo-2 cells were 10%, 7%, and 2.5%, respectively. Marked carotenoid interactions were observed between LYC/beta-C and beta-C/alpha-C. The present results indicate that beta-C conformation plays a major role in its intestinal absorption and that cis isomer discrimination is at the levels of cellular uptake and incorporation into chylomicrons. Moreover, the kinetics of cellular uptake and secretion of beta-C, the inhibition of the intestinal absorption of one carotenoid by another, and the cellular specificity of isomer discrimination all suggest that carotenoid uptake by intestinal cells is a facilitated process.