This study aimed to investigate the effects of virtual reality used in maternal-child nursing clinical practicums on nursing students’ competencies through a systematic review. Methods: The inclusion criteria were peer-reviewed papers in English or Korean presenting analytic studies of maternal-child nursing practicums using virtual reality. An electronic literature search of the Cochrane Library, CINAHL, EMBASE, ERIC, PubMed, and Research Information Sharing System databases was performed using combinations of the keywords “nursing student,” “virtual reality,” “augmented reality,” “mixed reality,” and “virtual simulation” from February 4 to 15, 2022. Quality appraisal was performed using the RoB 2 and ROBINS-I tools for randomized controlled trials (RCTs) and non-RCTs, respectively. Results: Of the seven articles identified, the RCT study (n=1) was deemed to have a high risk of bias, with some items indeterminable due to a lack of reported details. Most of the non-RCT studies (n=6) had a moderate or serious risk of bias related to selection and measurement issues. Clinical education using virtual reality had positive effects on knowledge, skills, satisfaction, self-efficacy, and needs improvement; however, it did not affect critical thinking or self-directed learning. Conclusion: This study demonstrated that using virtual reality for maternal-child nursing clinical practicums had educational effects on a variety of students’ competencies. Considering the challenges of providing direct care in clinical practicums, virtual reality can be a viable tool that supplements maternal-child nursing experience. Greater rigor and fuller reporting of study details are required for future research.

Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages (HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappaB signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-kappaB. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide (NO) production and expression of inducible NO synthase (iNOS) levels in HMDM. However, trichomonad-induced NF-kappaB activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA (NO synthase inhibitor). Moreover, pretreatment with NF-kappaB inhibitors (PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappaB, which might be closely involved in inflammation caused by T. vaginalis.
Animals ; Cells, Cultured ; Cytokines/*immunology ; Humans ; Macrophages/*immunology/parasitology ; Nitric Oxide/*immunology ; Trichomonas Infections/*immunology/parasitology ; Trichomonas vaginalis/*immunology

Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages (HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappaB signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-kappaB. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide (NO) production and expression of inducible NO synthase (iNOS) levels in HMDM. However, trichomonad-induced NF-kappaB activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA (NO synthase inhibitor). Moreover, pretreatment with NF-kappaB inhibitors (PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappaB, which might be closely involved in inflammation caused by T. vaginalis.
Animals ; Cells, Cultured ; Cytokines/*immunology ; Humans ; Macrophages/*immunology/parasitology ; Nitric Oxide/*immunology ; Trichomonas Infections/*immunology/parasitology ; Trichomonas vaginalis/*immunology

Elevated plasma concentration of native low-density lipoprotein (nLDL) is associated with vascular smooth muscle cell (VSMC) activation and cardiovascular disease. We investigated the mechanisms of superoxide generation and its contribution to pathophysiological cell proliferation in response to nLDL stimulation. Lucigenin-induced chemiluminescence was used to measure nLDL-induced superoxide production in human aortic smooth muscle cells (hAoSMCs). Superoxide production was increased by nicotinamide adenine dinucleotide phosphate (NADPH) and decreased by NADPH oxidase inhibitors in nLDL-stimulated hAoSMC and hAoSMC homogenates, as well as in prepared membrane fractions. Extracellular signal-regulated kinase 1/2 (Erk1/2), protein kinase C-theta (PKCtheta) and protein kinase C-beta (PKCbeta) were phosphorylated and maximally activated within 3 min of nLDL stimulation. Phosphorylated Erk1/2 mitogen-activated protein kinase, PKCtheta and PKCbeta stimulated interactions between p47phox and p22phox; these interactions were prevented by MEK and PKC inhibitors (PD98059 and calphostin C, respectively). These inhibitors decreased nLDL-dependent superoxide production and blocked translocation of p47phox to the membrane, as shown by epifluorescence imaging and cellular fractionation experiments. Proliferation assays showed that a small interfering RNA against p47phox, as well as superoxide scavenger and NADPH oxidase inhibitors, blocked nLDL-induced hAoSMC proliferation. The nLDL stimulation in deendothelialized aortic rings from C57BL/6J mice increased dihydroethidine fluorescence and induced p47phox translocation that was blocked by PD98059 or calphostin C. Isolated aortic SMCs from p47phox-/- mice (mAoSMCs) did not respond to nLDL stimulation. Furthermore, NADPH oxidase 1 (Nox1) was responsible for superoxide generation and cell proliferation in nLDL-stimulated hAoSMCs. These data demonstrated that NADPH oxidase activation contributed to cell proliferation in nLDL-stimulated hAoSMCs.
Animals ; Aorta/*cytology ; Cell Line ; Cell Proliferation ; Cells, Cultured ; Humans ; Lipoproteins, LDL/*metabolism ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/*cytology ; NADPH Oxidase/*metabolism ; Phosphorylation ; Protein Kinase C/metabolism ; Signal Transduction ; Superoxides/metabolism

PURPOSE: The present study developed formulas for estimation of standard liver volume (SLV) with high accuracy for the Korean population. MATERIALS AND METHODS: SLV estimation formulas were established using gender-balanced and gender-unbalanced measurements of anthropometric variables, body composition variables, and abdominal geometry of healthy Koreans (n=790). Total liver volume excluding blood volume, was measured based on CT volumetry. RESULTS: SLV estimation formulas as preferred in various conditions of data availability were suggested in the present study. The suggested SLV estimation formulas in the present study were found superior to existing formulas, with an increased accuracy of 4.0–217.5 mL for absolute error and 0.2–18.7% for percentage of absolute error. CONCLUSION: SLV estimation formulas using gender-balanced measurements showed better performance than those using gender-unbalanced measurements. Inclusion of body composition and abdominal geometry variables contributed to improved performance of SLV estimation.
Blood Volume ; Body Composition* ; Liver*

Background: Remimazolam is a novel ultra-short-acting benzodiazepine known for its hemodynamic stability over propofol. However, its hemodynamic effects compared to those of etomidate are not well established. This study aimed to determine whether the use of remimazolam is non-inferior to etomidate with regard to the occurrence of post-induction hypotension in patients undergoing coronary artery bypass grafting. Methods: Patients were randomly assigned to either the remimazolam group (6 mg/kg/h) or the etomidate group (0.3 mg/kg) for induction of anesthesia. Anesthetic depth was adjusted based on the bispectral index. Primary outcome was the incidence of post-induction hypotension, defined as a mean arterial pressure less than 65 mmHg within 15 min after endotracheal intubation, with a non-inferiority margin of 12%. Results: A total of 144 patients were finally analyzed. Incidence of post-induction hypotension was 36/71 (50.7%) in the remimazolam group and 25/73 (34.2%) in the etomidate group, with a rate difference of 16.5% (95% CI [3.0–32.6]) between the two groups that was beyond the prespecified non-inferiority margin of 12.0%. The number of patients who needed vasopressors was similar in the two groups. Conclusions In this non-inferiority trial, remimazolam failed to show non-inferiority to etomidate in terms of post-induction hypotension when used as an induction drug for general anesthesia in patients undergoing coronary artery bypass grafting. However, different doses or infusion techniques of remimazolam should be compared with etomidate in various patient groups to fully assess its hemodynamic non-inferiority during induction of anesthesia.

Background: Remimazolam is a novel ultra-short-acting benzodiazepine known for its hemodynamic stability over propofol. However, its hemodynamic effects compared to those of etomidate are not well established. This study aimed to determine whether the use of remimazolam is non-inferior to etomidate with regard to the occurrence of post-induction hypotension in patients undergoing coronary artery bypass grafting. Methods: Patients were randomly assigned to either the remimazolam group (6 mg/kg/h) or the etomidate group (0.3 mg/kg) for induction of anesthesia. Anesthetic depth was adjusted based on the bispectral index. Primary outcome was the incidence of post-induction hypotension, defined as a mean arterial pressure less than 65 mmHg within 15 min after endotracheal intubation, with a non-inferiority margin of 12%. Results: A total of 144 patients were finally analyzed. Incidence of post-induction hypotension was 36/71 (50.7%) in the remimazolam group and 25/73 (34.2%) in the etomidate group, with a rate difference of 16.5% (95% CI [3.0–32.6]) between the two groups that was beyond the prespecified non-inferiority margin of 12.0%. The number of patients who needed vasopressors was similar in the two groups. Conclusions In this non-inferiority trial, remimazolam failed to show non-inferiority to etomidate in terms of post-induction hypotension when used as an induction drug for general anesthesia in patients undergoing coronary artery bypass grafting. However, different doses or infusion techniques of remimazolam should be compared with etomidate in various patient groups to fully assess its hemodynamic non-inferiority during induction of anesthesia.

Background: Remimazolam is a novel ultra-short-acting benzodiazepine known for its hemodynamic stability over propofol. However, its hemodynamic effects compared to those of etomidate are not well established. This study aimed to determine whether the use of remimazolam is non-inferior to etomidate with regard to the occurrence of post-induction hypotension in patients undergoing coronary artery bypass grafting. Methods: Patients were randomly assigned to either the remimazolam group (6 mg/kg/h) or the etomidate group (0.3 mg/kg) for induction of anesthesia. Anesthetic depth was adjusted based on the bispectral index. Primary outcome was the incidence of post-induction hypotension, defined as a mean arterial pressure less than 65 mmHg within 15 min after endotracheal intubation, with a non-inferiority margin of 12%. Results: A total of 144 patients were finally analyzed. Incidence of post-induction hypotension was 36/71 (50.7%) in the remimazolam group and 25/73 (34.2%) in the etomidate group, with a rate difference of 16.5% (95% CI [3.0–32.6]) between the two groups that was beyond the prespecified non-inferiority margin of 12.0%. The number of patients who needed vasopressors was similar in the two groups. Conclusions In this non-inferiority trial, remimazolam failed to show non-inferiority to etomidate in terms of post-induction hypotension when used as an induction drug for general anesthesia in patients undergoing coronary artery bypass grafting. However, different doses or infusion techniques of remimazolam should be compared with etomidate in various patient groups to fully assess its hemodynamic non-inferiority during induction of anesthesia.