An evaluation of nursing students' learning self-efficacy: A multi-dimensional instrument development and structural validation.

BACKGROUND: Nursing learning self-efficacy (NLSE) is essential in nursing students' learning, and since it is a task-dependent construct, accurate measurements require a multidimensional instrument. OBJECTIVE: This research aimed to develop and validate a multidimensional NLSE instrument to measure Taiwanese nursing students' views of nursing learning self-efficacy. DESIGN: The cross-sectional study design was used for this investigation. PARTICIPANTS: The study included 1143 nursing students from a nursing junior college. METHODS: To assess the validity and reliability of the instrument's factors, exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) were utilized. Conceptual understanding, higher-order cognitive skills, practical work, everyday application, and nursing communication were identified as five factors. A comparison of five proposed models was also conducted. RESULTS: The study found that the correlated and one-factor second-order models were acceptable and provided a simple structure for evaluating nursing students' perceptions of NLSE. Furthermore, a specific model with two second-order scales (Cognition and Application) and one first-order scale (nursing communication) was identified, highlighting the crucial role of nursing communication in nursing students' self-efficacy. CONCLUSIONS: Evaluating nursing students' learning self-efficacy using a valid and reliable instrument is crucial for understanding their learning confidence. The creation of such a scale constitutes the primary contribution of this study.

The effects of an active learning mechanism on cognitive load and learning achievement: A new approach for pharmacology teaching to Taiwanese nursing students.

BACKGROUND: Nursing students require learning strategies when studying pharmacology. The COVID-19 pandemic has increased the prevalence of online self-study. The design of effective online learning materials has therefore become vital to nursing education. OBJECTIVES: The objective of this study was to describe the active learning mechanism that helped nursing students learn pharmacology through interactive learning materials and to demonstrate that no increased cognitive load in nursing students when studying pharmacology using interactive learning materials. METHOD: We designed an active learning mechanism to help nursing students study pharmacology by using interactive learning materials. An experimental pre- and post-test design was conducted. The participants were second-year nursing students (age 16-17) in a junior college of nursing. Students were randomly assigned to an experimental group (n = 98) and a control group (n = 90). RESULTS: We developed multi-media interactive learning materials and an active learning mechanism to enable nursing students to learn pharmacology. The proposed approach not only improved learning achievements but also reduced the cognitive load of nursing students. CONCLUSION: The major contribution of this study exhibits a new approach to practice wherein active learning is incorporated into interactive pharmacology materials for nursing students. This can be attributed to the design features of "explanation," "quiz and feedback," and "encouragement." Our results aid the development of effective interactive learning materials for pharmacology for Taiwanese nursing students.

Anti-Cancerous Effect of Inonotus taiwanensis Polysaccharide Extract on Human Acute Monocytic Leukemia Cells through ROS-Independent Intrinsic Mitochondrial Pathway.

Acute leukemia is one of the commonly diagnosed neoplasms and causes human death. However, the treatment for acute leukemia is not yet satisfactory. Studies have shown that mushroom-derived polysaccharides display low toxicity and have been used clinically for cancer therapy. Therefore, we set out to evaluate the anti-cancerous efficacy of a water-soluble polysaccharide extract from Inonotus taiwanensis (WSPIS) on human acute monocytic leukemia THP-1 and U937 cell lines in vitro. Under our experimental conditions, WSPIS elicited dose-dependent growth retardation and induced apoptotic cell death. Further analysis showed that WSPIS-induced apoptosis was associated with a mitochondrial apoptotic pathway, such as the disruption of mitochondrial membrane potential (MMP), followed by the activation of caspase-9, caspase-3, and PARP (poly(ADP-ribose) polymerase) cleavage. However, a broad caspase inhibitor, Z-VAD.fmk, could not prevent WSPIS-induced apoptosis. These data imply that mechanism(s) other than caspase might be involved. Thus, the involvement of endonuclease G (endoG), a mediator arbitrating caspase-independent oligonucleosomal DNA fragmentation, was examined. Western blotting demonstrated that WSPIS could elicit nuclear translocation of endoG. MMP disruption after WSPIS treatment was accompanied by intracellular reactive oxygen species (ROS) generation. However, pretreatment with N-acetyl-l-cysteine (NAC) could not attenuate WSPIS-induced apoptosis. In addition, our data also show that WSPIS could inhibit autophagy. Activation of autophagy by rapamycin decreased WSPIS-induced apoptosis and cell death. Taken together, our findings suggest that cell cycle arrest, endonuclease G-mediated apoptosis, and autophagy inhibition contribute to the anti-cancerous effect of WSPIS on human acute monocytic leukemia cells.

Developing a medical picture book for reducing venipuncture distress in preschool-aged children.

AIM: Distress associated with needle-related procedures is a major concern in preschool-aged children nursing. This study developed a medical picture book for supporting preschool-aged children facing a venipuncture and determined the effectiveness of such a book intervention in decreasing behavioural distress. METHODS: The picture book was designed in 3 stages: developing stories on medical situations, penning the text, and drafting the book. We conducted a quasiexperimental study to examine the effectiveness of the book. The behavioural distress of the control and picture book groups were assessed before, during, and after the intervention by using the Observational Scale of Behavioral Distress-Revised (OSBD-R). RESULTS: We created a 12-page picture book, Sick Rui-Rui Bear, in which cartoon characters were depicted undergoing venipunctures, as a guide for vein injection and for facilitating positive venipuncture outcomes in preschool-aged children. Over time, the OSBD-R scores of the picture book group were significantly lower than those of the control group (P < .001). CONCLUSION: We recommend the picture book be routinely read and used during venipunctures to decrease procedural distress in preschool-aged children.

Isoobtusilactone A sensitizes human hepatoma Hep G2 cells to TRAIL-induced apoptosis via ROS and CHOP-mediated up-regulation of DR5.

Hepatoma cells are relatively resistant to TRAIL. We have previously shown that isoobtusilactone A (IOA), a potent anticancer agent isolated from Cinnamomum kotoense, induced mitochondria-mediated apoptosis in hepatoma cells. Here, we report that IOA could potentiate TRAIL-induced apoptosis in Hep G2 cells. The combined treatment with IOA and TRAIL significantly induced caspase-dependent apoptosis. This correlated with the up-regulation of C/EBP homologous protein (CHOP) and death receptor 5 (DR5) protein levels. Gene silencing of the DR5 by small interfering RNA abrogated the apoptosis induced by the combined regimen of IOA and TRAIL, suggesting that the sensitization to TRAIL was mediated through DR5. By analyzing the DR5 promoter, we found that IOA induced a CHOP-dependent DR5 transactivation. DR5 expression after IOA treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation. Pretreatment with N-acetyl-L-cysteine (NAC) attenuated IOA-induced CHOP and DR5 expression and inhibited TRAIL-induced apoptosis. Taken together, our data suggested that ROS-dependent and CHOP-regulated DR5 expression played a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by IOA in Hep G2 cells.

6-dehydrogingerdione sensitizes human hepatoblastoma Hep G2 cells to TRAIL-induced apoptosis via reactive oxygen species-mediated increase of DR5.

The anticancer effects of 6-dehydrogingerdione (6-DG), a compound isolated from the rhizomes of Zingiber officinale , and its mechanisms of sensitization to TRAIL-induced apoptosis were studied using human hepatoblastoma Hep G2 cells. This study demonstrates for the first time that 6-DG-induced apoptosis might be executed via mitochondrial- and Fas receptor-mediated pathways. Further studies also demonstrated that 6-DG could sensitize Hep G2 cells to TRAIL-induced apoptosis. 6-DG also up-regulated Ser-15 phosphorylation and evoked p53 nuclear translocation. Abrogation of p53 expression by p53 small interfering RNA significantly attenuated 6-DG-induced DR5 expression, thus rendering these cells resistant to TRAIL-induced apoptosis. DR5 expression after 6-DG treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation. Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis. In contrast to Hep G2 cells, DR5 up-regulation and sensitization to TRAIL-induced apoptosis instigated by 6-DG were not observed in normal MDCK cells. Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells.

Isoobtusilactone A induces both caspase-dependent and -independent apoptosis in Hep G2 cells.

Isoobtusilactone A, a constituent isolated from the leaves of Cinnamomum kotoense, has been demonstrated by us earlier to be an agent capable of inducing apoptotic cell death of Hep G2 cells. In order to clarify if caspases alone were the sole mediator for eliciting this apoptotic process, a broad caspases inhibitor, Z-VAD.fmk, was utilized to explore this possibility. Interestingly, although Z-VAD.fmk was demonstrated to be capable of completely inhibiting isoobtusilactone A-induced oligonucleosomal DNA fragmentation, yet it could only prevent limited amount of cells from becoming apoptosis-prone. These data implied that some other mechanism(s) might be involved. Thus, the involvement of apoptosis-inducing factor (AIF), a mediator arbitrating caspase-independent apoptosis, in isoobtusilactone A-induced apoptotic process was examined. These findings indicated that isoobtusilactone A could elicit the nuclear translocation of AIF that accompanied the occurrence of large-scale DNA fragmentation. Reduction of AIF expression by AIF-siRNA transfection suppressed large-scale DNA fragmentation. Interestingly, inhibition of AIF expression by AIF-siRNA could not prevent isoobtusilactone A-induced oligonucleosomal DNA fragmentation. In the same vein, when the cells were simultaneously combined pretreatment with AIF-siRNA and Z-VAD.fmk, both large-scale DNA and oligonucleosomal DNA fragmentations could nearly be prevented. Taken together, these findings suggested that isoobtusilactone A-induced apoptotic cell death was mediated via both caspase-dependent and -independent pathways.

Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms.

Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Under our experimental conditions, isoobtusilactone A was found to elicit a concentration-dependent growth impediment (IC(50)=37.5 microM). The demise of these cells induced by isoobtusilactone A was apoptotic in nature, exhibiting a concentration-dependent increase in sub-G(1) fraction and DNA fragmentation. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome c, followed by activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (DeltaPsi(m)). The presence of a ROS scavenger (N-acetyl-L-cysteine) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride) blocked ROS production and the subsequent apoptotic cell death. In addition, in order to investigate the acute toxicity of isoobtusilactone A, groups of 5-6-week old Sprague-Dawley rats were subjected to oral administration of 350, or 700 mg/kg bw isoobtusilactone A four times each week for two weeks. There was no significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A, and the dosages of isoobtusilactone A tested in this study did not cause animal toxicity.

Lipid peroxidation in workers exposed to aluminium, gallium, indium, arsenic, and antimony in the optoelectronic industry.

OBJECTIVE: The objective of this study was to investigate whether exposure to aluminum, gallium, indium, arsenic, and antimony induces lipid peroxidation in humans. METHODS: Whole blood and urine levels of 103 exposed electronic industry workers and 67 referents were analyzed by use of inductively coupled plasma mass spectrometry. Malondialdehyde (MDA), the product of lipid peroxidation, was determined by high-performance liquid chromatography. RESULTS: The mean plasma MDA level in the 103 workers was significantly higher than that in 67 referents. The levels of MDA in the exposed workers were correlated significantly with the levels of urinary gallium and arsenic. CONCLUSIONS: Malondialdehyde as an index of lipid peroxidation can be induced by gallium and arsenic exposure. By reducing exposure to these metals, biologic effects such as lipid peroxidation may also be diminished.

Molecular mechanism of cell cycle blockage of hepatoma SK-Hep-1 cells by Epimedin C through suppression of mitogen-activated protein kinase activation and increased expression of CDK inhibitors p21(Cip1) and p27(Kip1).

Reports elsewhere demonstrated that Epimedin C, a constituent isolated from the leaves of Epimedium sagittatum, possessed anti-tumor activity. However, its mechanism of action remains unresolved. Using SK-Hep-1 cells, a poorly-differentiated hepatoma subline, as an experimental model, we present evidence here that the anti-tumor activity of Epimedin C may involve cell cycle blockage. Immunoblotting analyses demonstrated that Epimedin C caused a decreased expression of hyperphosphorylated retinoblastoma (Rb) protein, cyclin D1, c-Myc, and c-Fos. In parallel, we measured the kinase activities and found that CDK2 and CDK4 were suppressed with commensurate increased levels of CDK inhibitors, p21(Cip1) and p27(Kip1). These data suggested that Epimedin C arrested the proliferation of these cells at G0/G1 phase through inhibition of CDK2 and CDK4 activities via an increased induction of p21(Cip1) and p27(Kip1). Alternatively, we investigated whether the anti-proliferative effect of Epimedin C on these cells might involve MAP kinase cascade. Using western blotting technique, we demonstrated that Epimedin C also selectively decreased ERK1/2 phosphorylation. Among the downstream effectors of ERK examined, we found that Epimedin C selectively decreased the expression of c-Fos, but not c-Jun. By EMSA assay, we further demonstrated that decreased c-Fos resulted in the downregulation of AP-1/DNA binding activity. Taken together, the molecular mechanisms of anti-tumor activity of Epimedin C may be proceeded by the combined effects of the cell cycle blockage via either the inhibition of CDK2 and CDK4 activities, with commensurate increase in their inhibitors, p21(Cip1) and p27(Kip1) or negatively modulates the ERK/c-Fos/AP-1 signaling pathway.

Oxidative stress and heat shock protein response in human paraspinal muscles during retraction.

OBJECT: The need for wide dissection and forceful retraction of paraspinal muscles often required for posterolateral lumbar fusion and fixation may severely jeopardize the muscles, structurally and functionally. The underlying pathophysiology of muscle damage may involve both mechanical and ischemic mechanisms. On the other hand, the surgery-related stress may trigger certain protective responses within the insulted paraspinal muscles. This study was conducted to assess the relationship between the oxidative stress and the stress response mediated by heat shock protein 70 (HSP70) induction within paraspinal muscles being retracted. METHODS: Multifidus muscle specimens were surgically obtained before, during, and after retraction in patients with lumbar spondylolisthesis undergoing posterolateral lumbar fusion, pedicle fixation, and laminectomy. Muscle samples were analyzed to determine HSP70 and malondialdehyde (MDA) levels. Both HSP70 expression and MDA production within multifidus muscle cells were increased significantly by retraction. Expression of HSP70 then decreased after a peak at 1.5 hours of retraction, whereas MDA levels remained elevated even after release of retractors for reperfusion of the muscles. Analysis of histopathological and immunohistochemical evidence indicated that the decline of HSP70 synthesis within muscle cells after prolonged retraction was the result of severe muscle damage. CONCLUSIONS: Results of this study highlight the deleterious effect of intraoperative retraction on human paraspinal muscles at the cellular and molecular levels. The authors also found that intraoperative maneuvers aimed at reducing the oxidative stress within the paraspinal muscles may help to attenuate surgery-related paraspinal muscle damage.

Brain lipid peroxidation and changes of trace metals in rats following chronic manganese chloride exposure.

The aim of this study was to investigate the effects of chronic, daily, 30-d administration of manganese chloride (MnCl2) to male Sprague-Dawley rats on lipid peroxidation and changes of trace elements (manganese, iron, copper, zinc) in various brain regions. Rats were intraperitoneally injected with MnCl2 (20 mg/kg) once daily for 30 consecutive days. The Mn accumulated in frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus, medulla, cerebellum, and spinal cord. Malondialdehyde, an end product of lipid peroxidation, was markedly decreased in frontal cortex and cerebellum. An increased level of Cu was observed in frontal cortex, medulla, and a cerebellum. A decreased Fe level was found only in cerebellum, and a decreased Zn level was observed in hippocampus and striatum. In a second group of animals, Mn (20 mg/kg/d) and glutathione (GSH, 15 mg/kg/d) were administered ip for 30 d. In CSH-Mn-treated rats, compared to Mn-treated rats, MDA concentrations were significantly reduced in frontal cortex, medulla and cerebellum. The changes of trace elements in rat brain were similar to the Mn-treated group. We suggest that Mn is an atypical antioxidant, as well as not involved in oxidative damage in rat brain. Fe and Cu may play roles in the protective effect of Mn against lipid peroxidation in rat brain.