Objective. To incorporate Bloom's taxonomy into multiple-choice examination questions in a pharmacotherapeutics course and assess its effectiveness in detecting areas of improvement in learning. Design. Bloom's taxonomy was incorporated into examination questions through a multi-step process: Sample questions representing each learning domain within Bloom's taxonomy (knowledge, comprehension, application, analysis, synthesis, and evaluation) were introduced to students during lecture presentations and discussions. Quiz and examination containing questions categorized according to Bloom's taxonomy were administered to students. During review sessions following each quiz or examination, the categorization of each question was provided to students and feedback from students was gathered. Assessment. The effect of the 5 types of test questions on the correct response fraction and discrimination index was determined after combining synthesis and evaluation. Correct response fractions for knowledge, comprehension, and application questions were significantly higher than those for analysis and synthesis/evaluation questions (p,0.05). However, discrimination index for application and synthesis/ evaluation questions were significantly higher than those for knowledge and comprehension questions (p,0.05). In interviews with students who had requested learning assistance, the majority realized the importance of critical-thinking skills in the learning process. Conclusion. Well-designed multiple-choice questions incorporating different learning domains of Bloom's taxonomy may be a potential method of assessing critical-thinking skills in large classes of students.
Drug resistance is a fundamental problem in cancer chemotherapy. Intracellular calcium concentration ([Ca2+]i) may play a role in the development of chemoresistance. We investigated the regulatory role of [Ca2+]i in Taxol resistance in the non‐small‐cell lung cancer cell line A549 and its chemoresistant subclone A549‐T24. Measurement of cytosolic calcium ([Ca2+]c) in single cells and cell populations revealed similar levels of basal calcium in the two cell lines. However, a reduced response to thapsigargin (a sarcoplasmic/endoplasmic reticulum Ca2+‐ATPase (SERCA) inhibitor) in A549‐T24 cells compared to the parent cell line suggested a lower ER Ca2+ content in these cells. mRNA expression of SERCA2b and SERCA3, major Ca2+ pumps involved in ER Ca2+ homeostasis, did not significantly differ between the two cell lines, as revealed by RT–PCR. An altered calcium influx pathway in the Taxol‐resistant cell line was observed. Modulation of the ER calcium pools using CMC (4‐chloro‐m‐cresol) and ATP revealed lower ryanodine receptor (RyR) and IP3 receptor (IP3R)‐sensitive Ca2+ stores in the chemoresistant cell line. Western blot and RT–PCR studies suggested that A549‐T24 cells expressed higher levels of the antiapoptotic protein Bcl‐2 and the calcium‐binding protein sorcin, respectively, in comparison to the parent cell line. Both of these proteins have been previously implicated in chemoresistance, in part, due to their ability to modulate [Ca2+]i. These results suggest that altered intracellular calcium homeostasis may contribute to the Taxol‐resistant phenotype. British Journal of Pharmacology (2004) 142, 305–316. doi:
The aryl hydrocarbon receptor (AhR) is a ligand-sensitive transcription factor which is responsible for most 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicities. Without ligand, the AhR complex is cytoplasmic and contains p23. Our objective was to investigate whether the wild type p23 levels are important for the AhR function. We generated eight p23-specific knockdown stable cell lines via either electroporation or lentiviral infection. Five of these stable cell lines were generated from a mouse hepatoma cell line (Hepa1c1c7) and three were from human hepatoma and cervical cell lines (Hep3B and HeLa). All of them expressed lower AhR protein levels, leading to reduced ligand-induced, DRE-driven downstream activity. The AhR protein levels in p23-specific knockdown stable cells were reversed back to wild type levels after exogenous p23 was introduced. Reduction of the AhR protein levels in these stable cells was caused by a decrease in the AhR message levels and an increase of the AhR protein degradation in the absence of ligand. This ligand-independent degradation of AhR was insensitive to MG132, suggesting that the 26S proteasome was not responsible for the degradation. In addition, MG132 could not protect AhR from the ligand-induced degradation in both mouse and human p23-knockdown stable cells.
At 6 months after discontinuation of the pharmacist-managed anticoagulation service, the frequency of adverse events increased significantly, resulting in both an increased number of hospitalizations and an increased number of hospital days accrued. This coordinated anticoagulation program using a pharmacist reduced warfarin-related complications.
In this study, we isolated scopoletin from Cirsium setidens Nakai (Compositae) and tested its effects on melanogenesis. Scopoletin was not toxic to cells at concentrations less than 50 µM and increased melanin synthesis in a dose-dependent manner. As melanin synthesis increased, scopoletin stimulated the total tyrosinase activity, the rate-limiting enzyme of melanogenesis. In a cell-free system, however, scopoletin did not increase tyrosinase activity, indicating that scopoletin is not a direct activator of tyrosinase. Furthermore, Western blot analysis showed that scopoletin stimulated the production of microphthalmia-associated transcription factor (MITF) and tyrosinase expression via cAMP response element-binding protein (CREB) phosphorylation in a dose-dependent manner. Based on these results, preclinical and clinical studies are needed to assess the use of scopoletin for the treatment of vitiligo.
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