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Background: Medication counseling is a critical component of pharmaceutical care to promote the safe and effective use of medications and to maximize therapeutic outcomes. The assessment of patients' and pharmacists' satisfaction with medication counseling services could be one of the vital parameters for predicting the quality of pharmacy services. No study has measured and compared both patients' and pharmacists' satisfaction with medication counseling. The objectives of this study were to describe and compare patients' and pharmacists' levels of satisfaction with medication counseling services offered by community pharmacists in South Korea.Methods: This was a descriptive, cross-sectional survey. The online survey was distributed to patients and community pharmacists using a structured questionnaire. The questionnaires consisted of 4 main areas: (1) responders' characteristics (2) current state of medication counseling methods provided by community pharmacies (3) overall satisfaction with medication counseling (4) demand for the development of medication counseling standards. A comparison between patients and pharmacists was made using either a chi-square test or a Fisher's exact test.Results: Between June 13, 2014 and July 15, 2014, a total of 252 patients and 620 pharmacists completed the survey. It was found that 47.3% of pharmacists and 34.0% of patients were satisfied with the current medication counseling service. Pharmacists showed a higher degree of satisfaction with the medication counseling service compared to patients (p <0.05). A major reason for patients not being satisfied with the medication counseling from community pharmacists was the insufficient time spent on counseling (51.2%). The pharmacists' perception of a major barrier to providing appropriate medication counseling for patients was the lack of time (24.3%). Moreover, a substantial number of patients (88%) and pharmacists (73%) supported the development of medication counseling standards to improve community pharmacist counseling services (p < 0.001).Conclusions: This study showed that both patients and pharmacists have low levels of satisfaction with the current medication counseling service offered by community pharmacists. This study provides baseline data for the development of national guidelines for medication counseling by pharmacists. [ABSTRACT FROM AUTHOR]

2-Methoxyestradiol is an endogenous nonpolar metabolite of 17β-estradiol with a strong antitubulin activity. Earlier we showed that 2-methoxyestradiol increases the level and activity of cyclin B1/CDK1, which subsequently induces mitotic prometaphase arrest. In the present study, we demonstrate that upregulation of cyclin B1/CDK1 is responsible for the increased phosphorylation of the anti-apoptotic proteins Bcl-2 and Bcl-X L in 2-methoxyestradiol-induced, mitotically-arrested cancer cells. Additional analysis shows that only the increase in phosphorylation of Bcl-X L , but not Bcl-2, is associated with activation of the mitochondrial cell death pathway. We find that MAD2 is an important upstream mediator of the antitubulin function of 2-methoxyestradiol, resulting in activation of the MKK4-JNK1 pathway. JNK1 activation then leads to cyclin B1/CDK1 upregulation, which further increases Bcl-2 and Bcl-X L phosphorylation. Together, these results indicate that cyclin B1/CDK1 upregulation in cancer cells undergoing 2-methoxyestradiol-induced mitotic catastrophe causes apoptosis via Bcl-X L phosphorylation., (Copyright © 2019 Elsevier Inc. All rights reserved.)

The present study investigates the anticancer effect of ascorbate in MIA-PaCa-2 human pancreatic cancer cells using both in vitro and in vivo models, with a focus on assessing the role of oxidative stress and autophagy as important mechanistic elements in its anticancer actions. We showed that ascorbate suppresses the growth of human pancreatic cancer cells via the induction of oxidative stress and caspase-independent cell death. Ascorbate induces the formation of autophagosomes and the presence of autophagy inhibitors suppresses ascorbate-induced cell death. These data suggest that the induction of autophagosome formation contributes to ascorbate-induced pancreatic cancer cell death., (Georg Thieme Verlag KG Stuttgart · New York.)

Dideoxypetrosynol A, a polyacetylene from the sponge Petrosia sp., is known to exhibit significant selective cytotoxicity against several human tumor cell lines. In the present study, we investigated the possible mechanisms by which dideoxypetrosynol A exerts its anti-proliferative action in cultured human SK-MEL-2 skin melanoma cells. Exposure of SK-MEL-2 cells to dideoxypetrosynol A resulted in growth inhibition and induction of apoptosis in a dose-dependent manner as measured by MTT assay, fluorescent microscopy and flow cytometry analysis. The increase in apoptosis was associated with a dose-dependent up-regulation in proapoptotic Bax expression and down-regulation of anti-apoptotic Bcl-2. Apoptosis-inducing concentrations of dideoxypetrosynol A induced caspase-3 and caspase-9 activation accompanied by proteolytic degradation of poly(ADP-ribose)-polymerase and selective down-regulation of cIAP-1. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of dideoxypetrosynol A.

As previously demonstrated, the synthetic bile acid derivatives mediate anti-proliferative properties in a variety of human cancer cells. In the present study, the effects of the synthetic derivatives of ursodeoxycholic acid (UDCA), HS-1030 and HS-1183, and chenodeoxycholic acid (CDCA), HS-1199 and HS-1200, on the proliferation of HT-29 human colon cancer cells were investigated. Whereas UDCA and CDCA had no effect on the growth of cells in the concentration ranges we have tested, HS-1199 and HS-1200 completely inhibited cell proliferation, while HS-1030 and HS-1183 showed weak inhibitory activities. Simultaneous estimation of cell cycle parameters and apoptosis by flow cytometry showed that the synthetic bile acid derivatives produced the arrest of cell cycle progression at the G1 phase and ensuing increase of sub-G1 fraction, which resulted in the induction of apoptosis. The induction of apoptosis was confirmed by observation of cleavages of poly(ADP-ribose) polymerase and DNA fragmentation. Furthermore, Western blot analysis showed decreased expression levels of cyclin D1, cyclin E, cyclin A, Cdk2, Cdk4, and Cdk6 proteins. In addition, the synthetic bile acid derivatives markedly induced the level of Cdk inhibitor, p21WAF1/CIP1, in a p53-independent manner. Furthermore, the exposure of cells to the synthetic bile acid derivatives resulted in a decrease in the level of pRb and enhanced binding between pRb and E2F-1. Based on these data, these synthetic bile acid derivatives may serve as potential lead compounds in the treatment of colon cancer.