Development and effectiveness of online teaching on practical skills among nursing students: A systematic review and meta-analysis.

OBJECTIVE: The purpose of this meta-analysis was to assess the effects of online education for practical skills among nursing students. METHODS: This research was done by searching PubMed, Embase, CINAHL, and Web of Science electronic databases from inception to August 18, 2023, to identify English-language articles. Data extraction, quality assessment, and literature screening were carried out independently by two researchers. The Cochrane risk of bias tool and the Methodological Items for Nonrandomized Studies (MINORS) tool were used to assess the risk of bias of the included studies. Meta-analysis was carried out using Review Manager (RevMan) version 5.3 software. RESULTS: Eighteen studies involving 2274 nursing students met the inclusion criteria. Nursing students' skills (SMD = 0.43, 95 % CI [0.33, 0.54], P<0.00001), knowledge (SMD = 0.16, 95 % CI (0.02, 0.30], P = 0.02), satisfaction (SMD = 0.29, 95 % CI (0.10, 0.47], P < 0.01), and confidence (SMD = 0.56, 95 % CI [0.29, 0.83], P < 0.0001) were all significantly improved by the online teaching intervention compared with traditional face-to-face instruction. Self-efficacy (SMD = 0.1, 95 % CI [-0.13, 0.33], P = 0.41) was also improved, but the difference was not statistically significant. CONCLUSION: Online learning is a novel and efficient approach to teaching practical skills to nursing students. Online education can enhance students' knowledge, skills, confidence, and learning satisfaction, and it is superior to traditional classroom instruction. The findings of this study can serve as a basis for the development of standardized online teaching techniques and assessment metrics.

Comparison of bioimpedance equations and dual-energy X-ray for assessment of fat free mass in a Chinese dialysis population.

PURPOSE: Bioelectrical impedance analysis (BIA) is simple, noninvasive, inexpensive and frequently used for estimating fat free mass (FFM). The aims of this study were to evaluate the applicability of different BIA equations on FFM in Chinese subjects, and to compare the difference in hemodialysis and peritoneal dialysis patients with healthy controls respectively. METHODS: Dialysis patients and healthy adults were enrolled in this study, and the subjects were matched by age, gender, and the minimum sample size in each group was calculated using PASS. FFM estimated by BIA was calculated using equations of Kyle, Sun SS and Segal, and TBW/0.73. Dual-energy X-ray absorptiometry (DXA) method was set as reference method. Pearson's correlation and Bland-Altman analysis were used to test the validity of the BIA equations. RESULTS: 50 hemodialysis (HD) patients, 52 peritoneal dialysis (PD) patients and 30 healthy adults aged 22-67 y were included in this study. Age, height, weight, BMI and gender did not differ significantly among HD, PD patients, and healthy controls (p > 0.05), but BIA parameters were quite different (p＜0.01). Bland-Altman analysis showed that in healthy volunteers, all equations showed good agreement with DXA measured. For dialysis patients, the FFM predictions of different equations showed differences between HD and PD patients, and the equations seemed more applicable for HD patients. CONCLUSION: The equations developed by healthy subjects might be not appropriate for dialysis patients, especially peritoneal dialysis patients. It is recommended to develop a specific BIA equation from dialysis population.

Roxadustat improves renal osteodystrophy by dual regulation of bone remodeling.

PURPOSE: Renal osteodystrophy (ROD), a component of chronic kidney disease-mineral and bone disorder (CKD-MBD) can lead to bone loss increasing fracture risks in CKD patients. Therefore, it is important to prevent and treat ROD. Activation of hypoxia-inducible factor-1α (HIF-1α) signaling was reported to prevent osteoporotic bone loss. Roxadustat, which is used to treat renal anemia in the clinic, is a novel HIF stabilizer. In our study, we aimed to investigate the effects of roxadustat on ROD. METHODS: We established an adenine-induced CKD rat model. Roxadustat was administered intragastrically to normal and CKD rats for 4 weeks. Hemoglobin concentrations and serum biochemical parameters were tested, and bone histomorphometric analysis was performed. RESULTS: CKD rats exhibited impaired renal function with anemia, secondary hyperparathyroidism and high-turnover ROD-induced significant bone loss. Roxadustat ameliorated renal anemia and attenuated the extreme increase in intact parathyroid hormone (iPTH) and fibroblast growth factor 23 (FGF23) in CKD rats. Bone histomorphometric analysis showed that roxadustat significantly alleviated bone loss and bone microarchitecture deterioration in CKD rats by increasing osteoblast activity and inhibiting osteoclast activity. We did not find that roxadustat had significant effects on bone metabolism in normal rats. CONCLUSION: Roxadustat can improve ROD via dual regulation of bone remodeling. The use of roxadustat may be a promising strategy to treat osteoporotic bone disorders, such as ROD.

A comparison of fluid status determination using bioelectric impedance and the isotope dilution method in hemodialysis and peritoneal dialysis patients.

We aimed to compare fluid status as determined by multifrequency bioimpedance spectroscopy (MF-BIS, Xitron 4200, USA) with that determined by the isotope dilution method among a contemporary Chinese cohort. Healthy Chinese subjects (HS, n = 30) were recruited in Zhengzhou. Hemodialysis (HD, n = 49) and peritoneal dialysis (PD, n = 48) patients were screened at the First Affiliated Hospital of Zhengzhou University. Total body water (TBW) and extracellular water (ECW) were measured by deuterium (TBWD) and bromide (ECWBr) dilution, respectively, and by MF-BIS using the Moissl equation (ME). The results of MF-BIS were compared to the reference method by Pearson analysis and Bland-Altman analysis in the three groups. The accuracy of overhydration as determined by MF-BIS was analyzed by receiver operating characteristic (ROC) curves. The TBWD and TBWME values were 34.67 ± 7.31 and 35.41 ± 5.76 L, 37.30 ± 8.58 and 37.02 ± 8.10 L, and 38.61 ± 10.02 and 38.44 ± 7.59 L in the HS, HD and PD groups, respectively. The ECWBr and ECWME values were 14.88 ± 3.33 and 15.53 ± 2.39 L, 16.24 ± 5.08 and 16.90 ± 3.93 L, and 19.08 ± 6.41 and 18.23 ± 3.61 L in the HS, HD and PD groups, respectively. The mean bias between TBWD and TBWME was -0.74 L, 0.28 L, and 0.17 L in the HS, HD and PD groups, respectively. The mean bias between ECWBr and ECWME was -0.65 L, -0.66 L, and 0.85 L in the HS, HD and PD groups, respectively. Compared to the ECWBr/TBWD ratio, the area under the ROC curve (AUC) of the ECWME/TBWME ratio for the diagnosis of overhydration was 0.76 and 0.68 in the HD and PD groups, respectively. In summary, MF-BIS with ME could be used in Chinese HD and PD patients.

Roxadustat promotes osteoblast differentiation and prevents estrogen deficiency-induced bone loss by stabilizing HIF-1α and activating the Wnt/ß-catenin signaling pathway.

BACKGROUND: Osteoporosis is a very common skeletal disorder that increases the risk of fractures. However, the treatment of osteoporosis is challenging. Hypoxia-inducible factor-1α (HIF-1α) plays an important role in bone metabolism. Roxadustat is a novel HIF stabilizer, and its effects on bone metabolism remain unknown. This study aimed to investigate the effects of roxadustat on osteoblast differentiation and bone remodeling in an ovariectomized (OVX) rat model. METHODS: In vitro, primary mouse calvarial osteoblasts were treated with roxadustat. Alkaline phosphatase (ALP) activity and extracellular matrix mineralization were assessed. The mRNA and protein expression levels of osteogenic markers were detected. The effects of roxadustat on the HIF-1α and Wnt/ß-catenin pathways were evaluated. Furthermore, osteoblast differentiation was assessed again after HIF-1α expression knockdown or inhibition of the Wnt/ß-catenin pathway. In vivo, roxadustat was administered orally to OVX rats for 12 weeks. Then, bone histomorphometric analysis was performed. The protein expression levels of the osteogenic markers HIF-1α and ß-catenin in bone tissue were detected. RESULTS: In vitro, roxadustat significantly increased ALP staining intensity, enhanced matrix mineralization and upregulated the expression of osteogenic markers at the mRNA and protein levels in osteoblasts compared with the control group. Roxadustat activated the HIF-1α and Wnt/ß-catenin pathways. HIF-1α knockdown or Wnt/ß-catenin pathway inhibition significantly attenuated roxadustat-promoted osteoblast differentiation. In vivo, roxadustat administration improved bone microarchitecture deterioration and alleviated bone loss in OVX rats by promoting bone formation and inhibiting bone resorption. Roxadustat upregulated the protein expression levels of the osteogenic markers, HIF-1α and ß-catenin in the bone tissue of OVX rats. CONCLUSION: Roxadustat promoted osteoblast differentiation and prevented bone loss in OVX rats. The use of roxadustat may be a new promising strategy to treat osteoporosis.

Low shear stress-induced endothelial mesenchymal transformation via the down-regulation of TET2.

Atherosclerotic cardiovascular disease is the major cause of death worldwide. Low shear stress plays key roles on the initiation and progression of atherosclerosis (As). However, its underlying mechanism remains unclear. In this study, the effect of low shear stress on endothelial mesenchymal transformation (EndMT) and its underlying mechanism were explored. Results showed that in cultured human umbilical vein endothelial cells, low shear stress down-regulated the expression of TET2 and promoted EndMT. Loss of TET2 promoted EndMT with the Wnt/ß-catenin signaling pathway. The enhancement in EndMT induced by low shear stress was attenuated by TET2 overexpression. In apoE-/- mice subjected to carotid artery local ligation, the EndMT and atherosclerotic lesions induced by low shear stress was attenuated by TET2 overexpression. Taken together, low shear stress promoted EndMT through the down-regulation of TET2, indicating that intervention with EndMT or the up-regulation of TET2 might be an alternative strategy for preventing As.

Direct analysis of bromine and iodine in dried serum spots by laser ablation inductively coupled plasma mass spectrometry.

RATIONALE: Accurate quantitative analysis of bromine and iodine in serum is an important aspect of monitoring body condition, but the volatile loss of halogen in sample pretreatment is a troublesome problem. We present a validated and flexible high-throughput method for quantification of bromine and iodine in dried serum spots (DSS) using laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) and an external aqueous standard calibration curve. The influence of serum matrix and laser ablation (LA) conditions on the analysis of bromine and iodine in DSS was researched systematically. METHODS: Aqueous standards without matrix matching were used for calibration to analyze bromine and iodine in serum by LA-ICP-MS. 5-µL volumes of the aqueous standard solution and serum samples in 10 times diluted concentration were deposited on the PTFE paper to form dried standard calibration spots (DSCS) and DSS, of less than 2 mm in diameter. LA was performed using a focused Nd:YAG laser beam in raster lineal scan mode. RESULTS: The limits of detection (LODs) for bromine and iodine in DSS were 0.23 and 0.03 mg L-1 , respectively. The relative standard deviation (RSD) for this method was less than 10%. The samples were also detected with matrix matching calibration by ICP-MS. The accuracy of the method was verified by statistical analysis of these results from ICP-MS and LA-ICP-MS. The accuracy is satisfactory with recoveries ranging from 81.5% to 118%. CONCLUSIONS: A novel and simple approach for high-throughput screening of bromine and iodine in DSS has been established by LA-ICP-MS. Calibration could be achieved using an aqueous standard solution instead of a matrix-matching solution. The method allowed analysis of low-volume biological samples without derivatization and decreased the risk of contamination or loss.

A novel synthetic curcumin derivative MHMM-41 induces ROS-mediated apoptosis and migration blocking of human lung cancer cells A549.

Many curcumin derivatives were produced and characterized to improve the physiochemical instability and low solubility of curcumin. Here, MHMM-41 (a novel curcumin derivative) was used to treat non-small lung cancer cells of human (known as A549) and to identify its anti-proliferative activities. Our results suggested that MHMM-41 display no significant cytotoxicity toward normal human lung fibroblast 2BS cells and mouse embryonal fibroblast 3T3 cells. It also had better anti-proliferative activity than curcumin in A549 cells. Further study showed a significant increase of apoptotic A549 cells in time and dose dependent manners. The activation of caspase-3, 8, 9, 12, Bax and PARP proteins were detected. Consequently, MHMM-41 treatment led to the reduction of mitochondrial membrane potential by JC-1 staining and characteristic nuclei fragmentation by Hoechst 33,342 staining, respectively, which showed that A549 apoptosis could be triggered by the extrinsic and intrinsic mitochondrial pathways. The release of ROS was also measured by flow cytometry. Further, wound healing assay and transwell experiments confirmed the anti-migration ability of MHMM-41 in A549 cells. Our current study suggested the potentials of MHMM-41 to inhibit the A549 cell proliferation. However, the intensive mechanical research on the anti-proliferation of A549 cells needs to be performed in the future.

Oxymatrine induces A549 human non­small lung cancer cell apoptosis via extrinsic and intrinsic pathways.

Oxymatrine is one of the primary natural compounds extracted from the Sophora flavescens, and has been reported to exhibit numerous pharmacological properties including cancer­preventive and anti­cancer effects, however the mechanisms as to how oxymatrine exhibits anti­proliferative activity in non­small cell lung carcinoma cells remains uncertain. The present study aimed to explore the mechanism of its anti­cancer effect, and whether it is due to apoptosis induction and anti­migration in the A549 lung cancer cell line. Detection of morphological alterations, MTT analysis, Hoechst/propidium iodide dual staining and terminal deoxynucleotidyl transferase dUTP nick end labeling assays verified that oxymatrine induced A549 cell apoptosis. The caspase pan­inhibitor z­VAD­FMK resulted in disappearance of oxymatrine­elicited nuclei fragmentation via Hoechst 33342 staining. JC­1 staining demonstrated a decrease in mitochondrial membrane potential which further verified the induction of apoptosis by oxymatrine. The caspase­3, 8 and 9 activities of oxymatrine­treated cells were activated, which suggested that extrinsic and intrinsic apoptotic pathways were involved in the anti­proliferative effects of oxymatrine in A549 cells. Furthermore, the wound healing assay verified the anti­migratory effects of oxymatrine in A549 cells.

Endothelial-to-Mesenchymal Transition: A Potential Mechanism for Atherosclerosis Plaque Progression and Destabilization.

Endothelial-to-mesenchymal transition (EndMT) is a cellular reprogramming mechanism by which endothelial cells acquire a mesenchymal phenotype. EndMT is associated with fibroproliferative diseases, such as cancer progression and metastasis and cardiac and kidney fibrosis, and this condition has been extensively investigated over the past decade. Recently, studies showed that EndMT contributes to the initiation and progression of atherosclerotic lesion and plaque destabilization. Unstable atherosclerotic plaque rupture and subsequent thrombosis are the main pathological causes of acute cardiovascular events. EndMT is plastic and reversible. Therefore, our enhanced understanding on the mechanisms controlling EndMT and its roles in the atherosclerosis plaque progression and instability may provide a basis for the development of novel therapeutic strategies to stabilize and reverse atherosclerotic plaques.

Tet methylcytosine dioxygenase 2 inhibits atherosclerosis via upregulation of autophagy in ApoE-/- mice.

Tet methylcytosine dioxygenase 2 (TET2) mediates the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). The loss of TET2 is associated with advanced atherosclerotic lesions. Our previous study showed that TET2 improves endothelial cell function by enhancing endothelial cell autophagy. Accordingly, this study determined the role of TET2 in atherosclerosis and potential mechanisms. In ApoE-/- mice fed high-fat diet, TET2 overexpression markedly decreased atherosclerotic lesions with uniformly increased level of 5hmC and decreased level of 5mC in genomic DNA. TET2 overexpression also promoted autophagy and downregulated inflammation factors, such as vascular cell adhesion molecule 1, intercellular adhesion molecule 1, monocyte chemotactic protein 1, and interleukin-1. Consistently, TET2 knockdown with small hairpin RNA (shRNA) in ApoE-/- mice decreased 5hmC and increased 5mC levels in atherosclerotic lesions. Meanwhile, autophagy was inhibited and atherosclerotic lesions progressed with an unstable lesion phenotype characterized by large lipid core, macrophage accumulation, and upregulated inflammation factor expression. Experiments with the cultured endothelial cells revealed that oxidized low-density lipoprotein (ox-LDL) inhibited endothelial cell autophagy. TET2 shRNA strengthened impaired autophagy and autophagic flux in the ox-LDL-treated endothelial cells. TET2 overexpression reversed these effects by decreasing the methylation level of the Beclin 1 promoter, which contributed to the downregulation of inflammation factors. Overall, we identified that TET2 was downregulated during the pathogenesis of atherosclerosis. The downregulation of TET2 promotes the methylation of the Beclin 1 promoter, leading to endothelial cell autophagy, impaired autophagic flux, and inflammatory factor upregulation. Upregulation of TET2 may be a novel therapeutic strategy for treating atherosclerosis.