Purpose: : This study aimed to investigate the impact of clinical reasoning competence, positive psychological capital, and nursing work environment on nursing performance of intensive care unit (ICU) nurses in tertiary general hospitals. Methods: : Data were collected from 169 ICU nurses in tertiary general hospitals in Busan, South Korea, from July 27 to August 15, 2023, using a self-report questionnaire. After excluding 12 questionnaires with insufficient responses, 157 responses were analyzed. Descriptive statistics, independent t-test, one-way ANOVA, Pearson’s correlation coefficient, and stepwise multiple regression analysis were employed. Results: : Factors influencing nursing performance included clinical reasoning competence (β=.51, p ＜.001), hope as a subfactor of positive psychological capital (β=.31, p ＜.001), and the nursing foundations for quality of care in the nursing work environment (β=.21, p ＜.001). The explanatory power of the regression model was 62% (F=87.41, p ＜ .001). Conclusion : The study underscores the importance of improving clinical reasoning competence among ICU nurses to enhance nursing performance and foster a hopeful attitude through reflective practices and personal growth. Organizational interventions, such as educational and psychological support programs, along with creating a supportive nursing environment, are crucial for improving nursing performance among intensive care unit nurses.

GV1001 is a peptide derived from the human telomerase reverse transcriptase (hTERT) sequence that is reported to have anti-cancer and anti-inflammatory effects. Enolase1 (ENO1) is a glycolytic enzyme, and stimulation of this enzyme induces high levels of pro-inflammatory cytokines from concanavalin A (Con A)-activated peripheral blood mononuclear cells (PBMCs) and ENO1-expressing monocytes in healthy subjects, as well as from macrophages in rheumatoid arthritis (RA) patients. Therefore, this study investigated whether GV1001 downregulates ENO1-induced pro-inflammatory cytokines as an anti-inflammatory peptide. The results showed that GV1001 does not affect the expression of ENO1 in either Con A-activated PBMCs or RA PBMCs. However, ENO1 stimulation increased the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6, and these cytokines were downregulated by pretreatment with GV1001. Moreover, p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB were activated when ENO1, on the surface of Con A-activated PBMCs and RA PBMCs, was stimulated, and they were successfully suppressed by pre-treatment with GV1001. These results suggest that GV1001 may be an effective anti-inflammatory peptide that downregulates the production of pro-inflammatory cytokines through the suppression of p38 MAPK and NF-kappaB activation following ENO1 stimulation.
Arthritis, Rheumatoid ; Concanavalin A ; Cytokines ; Down-Regulation* ; Humans ; Inflammation ; Interleukin-6 ; Interleukins ; Macrophages ; Monocytes ; NF-kappa B ; p38 Mitogen-Activated Protein Kinases ; Protein Kinases ; Telomerase ; Tumor Necrosis Factor-alpha

The L-gulono-gamma-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.
Animals ; Ascorbic Acid* ; Down-Regulation* ; Glucose ; Growth Plate ; L-Gulonolactone Oxidase ; Metabolism ; Mice ; Osteocalcin* ; Osteogenesis* ; Plasma ; Tibia ; Weight Loss