Tonometric Vascular Function Assessment

Non

Significance of EpCAM and TROP2 expression in non-small cell lung cancer

<p>Abstract</p> <p>Background</p> <p>The tumor-associated calcium signal transducer (<it>TACSTD</it>) genes, originally designated epithelial cell adhesion molecule (EpCAM) and TROP2, represent true oncogenes. Little is known about EpCAM and TROP2 gene expression in non-small cell lung carcinoma (NSCLC). This study evaluated EpCAM and TROP2 protein expression and clinicopathologic significance in cases of NSCLC.</p> <p>Methods</p> <p>Tissue microarray blocks acquired from 164 cases of NSCLC, including 100 cases of adenocarcinoma (AdC) and 64 of squamous cell carcinoma (SCC), were examined by immunohistochemical staining for EpCAM, and TROP2. The results were correlated with clinicopathologic data.</p> <p>Results</p> <p>EpCAM and TROP2 were significantly overexpressed in SCC than in AdC (<it>P </it>< 0.01). In AdC, EpCAM overexpression was closely related to sex, histologic grade, pathologic T stage, pathologic N stage, and TNM stage, and TROP2 overexpression was only related to histologic grade (<it>P </it>< 0.05, respectively). In SCC, correlations were evident between EpCAM overexpression and TNM stage (<it>P </it>= 0.01), and between TROP2 overexpression and pathologic T stage (<it>P </it>= 0.02). EpCAM overexpression showed no significance with overall survival in AdC and SCC patients. However, TROP2 overexpression in AdC had a positive influence on overall survival (<it>P </it>= 0.02) and disease-free survival (<it>P </it>= 0.03). In particular, AdC patients with stage II or III showed better overall survival (<it>P </it>= 0.05) and disease-free survival (<it>P </it>= 0.04).</p> <p>Conclusions</p> <p>While EpCAM and TROP2 show weak and non-complete membranous staining in normal bronchial epithelium and pneumocyte, their complete membranous expression in carcinoma suggests their role in carcinogenesis. EpCAM and TROP2 were more frequently overexpressed in SCC. EpCAM overexpression had no prognostic value in this study, but TROP2 overexpression showed better survival in AdC patients and might be a better prognostic marker in advanced stage AdC.</p

Learner Involvement in Self- and Peerassessment of Task-based Oral Performance

The new understanding of learner role as active participants in learning has accompanied a paradigm shift in assessment practices. Learners are perceived to be responsible not only for their own learning but also for the assessment of their performances in terms of its procedures and rationales (Cheng & Warren, 2005; Fa1chikov, 1986; Luoma & Tarnanen, 2003; Orsmond & Merry, 1996). This study explores the plausibility of employing self- and peer-assessment as alternative approaches to assessment of seven Korean learners' oral presentation task performance. In order to cope with the subjectivity aspect of evaluating behavior, the study encouraged learner involvement in task assessment, which was operationalized as students' participation in the development of assessment sub-criteria and learner training as well as discussion regarding the criteria. The results from three periods of students' self- and peer-assessment on their presentation performance revealed that learner involvement in assessment can lead to a high comparability among three different assessment types; self-, peer-, and teacher-assessment. The students also reported that they had positive attitudes toward the alternative assessment

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12