Failure to fail - Factors affecting faculty decisions to pass underperforming nursing students in the clinical setting: A quantitative study.

AIM: The purpose of the study was to explore the relationship between face-implicating factors and faculty's likelihood of failing students in the clinical setting who do not meet passing criteria. BACKGROUND: Clinical nursing faculty members struggle to assign failing grades to underperforming students in the clinical setting; this is known as failure to fail. Qualitative literature has revealed common factors for failure to fail; however, quantitative studies are required to determine the extent to which those factors affect faculty's decision-making process. DESIGN: A quantitative, descriptive design was used. METHODS: Snowball sampling was used to recruit participants from CCNE- and ACEN-accredited nursing programs to complete an online survey. There were 353 responses to the survey (a 30% return rate) and 327 usable responses. Eligibility criteria included pre-licensure nursing faculty members who had taught in the clinical setting within the past three years. The tool used for the study was adapted from Dibble's (2014) tool, which explored face-implicating factors' impact on the transmission of bad news. RESULTS: Respondents who did not commit failure to fail (F2FN) disagreed more strongly with every survey item than those who committed failure to fail (F2FY). The differences in mean scores were compared and 64% of those differences were statistically significant (p < 0.05). Respondents who did not commit failure to fail were less affected by the face-implicating factors than those who committed failure to fail. CONCLUSIONS: the null hypothesis was rejected; a direct connection was found between face-implicating factors and faculty's likelihood of passing students in the clinical setting who do not meet passing criteria.

Locus of the interaction among 5-fluorouracil, leucovorin, and interferon-alpha 2a in colon carcinoma cells.

Prior studies from these laboratories demonstrated 3.2-fold potentiation of 5-fluorouracil (FUra) cytotoxicity by recombinant human interferon-alpha 2a (rIFN-alpha 2a) in GC3/cl colon adenocarcinoma cells that was significantly enhanced to 14-fold when FUra was combined with rIFN-alpha 2a + a mixture of the diasteroisomers of the biologically active (6S) and inactive (6R) leucovorin or 5-formyl-H4PteGlu (LV), events that were reversible by thymidine (dThd). In GC3/clTS-c3/c3 cells, deficient in thymidylate synthase, rIFN-alpha 2a cytotoxicity was not influenced by the concentration of dThd, indicating no direct effect at the level of dThd-less stress. Direct assays of thymidylate synthase indicated no significant difference between FUra-induced accumulation of total thymidylate synthase or free or unbound thymidylate synthase in cells receiving FUra + modulators. In addition, the cytotoxic activity of CB3717, a specific quinazoline-based inhibitor of thymidylate synthase, was not potentiated by rIFN-alpha 2a. These studies suggested that thymidylate synthase was not the primary target site for rIFN-alpha 2a activity. Since data indicated that a 5-fluoropyrimidine was required in the interaction among FUra, LV, and rIFN-alpha 2a, attention was focused at the level of DNA. Both DNA single-strand breaks (SSBs) and DNA double-strand breaks (DSBs) induced by FUra were significantly elevated by rIFN-alpha 2a and LV administered as single modulators and were influenced by the concentrations of both FUra and rIFN-alpha 2a. However; when FUra was combined with LV, rIFN-alpha 2a further potentiated the frequency of DNA SSBs, and data correlated with the relative cytotoxic activity of FUra-LV-rIFN-alpha 2a combinations. No effect on CB3717-induced DNA SSBs or DSBs by rIFN-alpha 2a was demonstrated. Drug exposure for 48 h was required to detect measurable differences in DNA SSB frequency among FUra-LV-rIFN-alpha 2a treatment groups and correlated with decreased clonogenic survival under these conditions. Continuous exposure to FUra (72 h) allowed shorter exposures to LV and/or rIFN-alpha 2a (48 h) to maintain maximal cytotoxicity. Shorter exposure times for FUra during continuous exposure to the modulators were less cytotoxic. Data suggest that the primary locus of the interaction among FUra, LV, and rIFN-alpha 2a lies at the level of DNA. rIFN-alpha 2a may exert its effects via enhancement of FUra base excision or incorporation into DNA, events that subsequently become influenced by thymidylate synthase inhibition and dThd-less stress and are further potentiated by LV.(ABSTRACT TRUNCATED AT 400 WORDS)

Interaction between 5-fluorouracil, [6RS]leucovorin, and recombinant human interferon-alpha 2a in cultured colon adenocarcinoma cells.

Recombinant human interferon-alpha 2a (rIFN-alpha 2a; 500 or 5,000 IU/mL) or [6RS] leucovorin ([6RS]LV; 1 microM) each potentiated the cytotoxic activity of 5-fluorouracil (FUra) by 2.6- to 3.2-fold during 72 hr exposures in two human colon adenocarcinoma cell lines (GC3/c1; VRC5/c1). When all three agents were combined, FUra cytotoxicity was further potentiated by 3.2- to 4.3-fold (total 10- to 14-fold). Potentiation of FUra cytotoxicity occurred at clinically achieveable concentrations of rIFN-alpha 2a and [6RS]LV. Effects were reversed by dThd (20 microM), although the activity of CB3717, a quinazoline-based, specific inhibitor of thymidylate synthase, was not potentiated by rIFN-alpha 2a. Data suggest the requirement of a 5-fluoropyrimidine for biochemical modulation and interaction at the level of thymidylate synthase or DNA.

Management of infantile-onset esotropia.

Background information on the prevalence, clinical characteristics, and differential diagnosis of infantile-onset esotropia is presented. A brief overview of early development of binocularity is also presented to set the stage for management, as well as a sequential treatment plan for two age groups of infantile esotropes: 1) infants and toddlers, and 2) preschool and "older" patients. Flowcharts and case examples are included to highlight the management principles for attaining maximum binocular function.