The ASK-SEAT: a competency-based assessment scale for students majoring in clinical medicine.

BACKGROUND: To validate a competency-based assessment scale for students majoring in clinical medicine, ASK-SEAT. Students' competency growth across grade years was also examined for trends and gaps. METHODS: Questionnaires were distributed online from May through August in 2018 to Year-2 to Year-6 students who majored in clinical medicine at the Shantou University Medical College (China). Cronbach alpha values were calculated for reliability of the scale, and exploratory factor analysis employed for structural validity. Predictive validity was explored by correlating Year-4 students' self-assessed competency ratings with their licensing examination scores (based on Kendall's tau-b values). All students' competency development over time was examined using the Mann-Whitney U test. RESULTS: A total of 760 questionnaires meeting the inclusion criteria were analyzed. The overall Cronbach's alpha value was 0.964, and the item-total correlations were all greater than 0.520. The overall KMO measure was 0.966 and the KMO measure for each item was greater than 0.930 (P < 0.001). The eigenvalues of the top 3 components extracted were all greater than 1, explaining 55.351, 7.382, and 5.316% of data variance respectively, and 68.048% cumulatively. These components were aligned with the competency dimensions of skills (S), knowledge (K), and attitude (A). Significant and positive correlations (0.135 < Kendall's tau-b < 0.276, p < 0.05) were found between Year-4 students' self-rated competency levels and their scores for the licensing examination. Steady competency growth was associated with almost all indicators, with the most pronounced growth in the domain of skills. A lack of steady growth was seen in the indicators of "applying the English language" and "conducting scientific research & innovating". CONCLUSIONS: The ASK-SEAT, a competency-based assessment scale developed to measure medical students' competency development shows good reliability and structural validity. For predictive validity, weak-to-moderate correlations are found between Year-4 students' self-assessment and their performance at the national licensing examination (Year-4 students start their clinical clerkship during the 2nd semester of their 4th year of study). Year-2 to Year-6 students demonstrate steady improvement in the great majority of clinical competency indicators, except in the indicators of "applying the English language" and "conducting scientific research & innovating".

Role of Small GTPase RhoA in DNA Damage Response.

Accumulating evidence has suggested a role of the small GTPase Ras homolog gene family member A (RhoA) in DNA damage response (DDR) in addition to its traditional function of regulating cell morphology. In DDR, 2 key components of DNA repair, ataxia telangiectasia-mutated (ATM) and flap structure-specific endonuclease 1 (FEN1), along with intracellular reactive oxygen species (ROS) have been shown to regulate RhoA activation. In addition, Rho-specific guanine exchange factors (GEFs), neuroepithelial transforming gene 1 (Net1) and epithelial cell transforming sequence 2 (Ect2), have specific functions in DDR, and they also participate in Ras-related C3 botulinum toxin substrate 1 (Rac1)/RhoA interaction, a process which is largely unappreciated yet possibly of significance in DDR. Downstream of RhoA, current evidence has highlighted its role in mediating cell cycle arrest, which is an important step in DNA repair. Unraveling the mechanism by which RhoA modulates DDR may provide more insight into DDR itself and may aid in the future development of cancer therapies.

Role of Rho guanine nucleotide exchange factors in non-small cell lung cancer.

Conventionally, Rho guanine nucleotide exchange factors (GEFs) are known activators of Rho guanosine triphosphatases (GTPases) that promote tumorigenesis. However, the role of Rho GEFs in non-small cell lung cancer (NSCLC) remains largely unknown. Through the screening of 81 Rho GEFs for their expression profiles and correlations with survival, four of them were identified with strong significance for predicting the prognosis of NSCLC patients. The four Rho GEFs, namely ABR, PREX1, DOCK2 and DOCK4, were downregulated in NSCLC tissues compared to normal tissues. The downregulation of ABR, PREX1, DOCK2 and DOCK4, which can be attributfed to promoter methylation, is correlated with poor prognosis. The underexpression of the four key Rho GEFs might be related to the upregulation of MYC signaling and DNA repair pathways, leading to carcinogenesis and poor prognosis. Moreover, overexpression of ABR was shown to have a tumor-suppressive effect in PC9 and H1703 cells. In conclusion, the data reveal the unprecedented role of ABR as tumor suppressor in NSCLC. The previously unnoticed functions of Rho GEFs in NSCLC will inspire researchers to investigate the distinct roles of Rho GEFs in cancers, in order to provide critical strategies in clinical practice.