Evaluating the Impact of Interventions and Improvements in Outpatient Intravenous Infusion Therapy at a Hospital in China: A Comprehensive Analysis of Prescription Patterns and Safety Measures.

Background: The excessive use of intravenous infusion in China was once a serious problem, but in recent years, attention has been paid to the phenomenon, and the government has implemented several policies to solve the problem, which has been gradually improved. Aim: This study focuses on evaluating the impact of ongoing interventions and improvements in outpatient intravenous infusion therapy. Methods: From January 2016 to December 2022, we conducted a study to gather annual data on intravenous infusion prescriptions. A data questionnaire, encompassing information on departments, clinical diagnosis, and infusion drugs, was developed for this purpose. We analyzed the changing trends of Top 10 clinical departments with higher intravenous infusion usage rates and Top 10 drugs used. We also evaluated the compliance of intravenous infusion prescriptions with management regulations and drug instructions, for further intervention in the future. Results: The analysis of intravenous infusion prescription rates revealed a gradual decrease from 10.89% to 5.63%. This reduction was statistically significant (P < 0.05). High levels of intravenous infusion use were consistently observed in emergency surgery and emergency medicine. Commonly administered drugs via infusion included antibacterial drugs, tumor medications, proton pump inhibitors, and injections of traditional Chinese medicine. Inappropriate prescriptions are often characterized by issues related to drug dosage, usage, indication, and selection. Trend analysis of unreasonable types revealed significant improvements in "Diagnosis incomplete/unwritten", "Solvent selection", "Dosing frequency", and "Treatment without indication" (P < 0.05). Conclusion: The findings of this study indicate a gradual improvement in the situation regarding intravenous infusion. However, there are still prevalent instances of unreasonable practices that need to be addressed.

Piceatannol protects against myocardial ischemia/reperfusion injury by inhibiting ferroptosis via Nrf-2 signaling-mediated iron metabolism.

Myocardial tissue ischemia damages myocardial cells. Although reperfusion is an effective technique to rescue myocardial cell damage, it may also exacerbate myocardial cell damage. Ferroptosis, an iron-dependent cell death, occurs following myocardial ischemia-reperfusion (I/R). Piceatannol (PCT) is a natural stilbene compound with excellent antioxidant properties that protect against I/R injury and exerts protective effects against ferroptosis-induced cardiomyocytes following I/R injury; however, the exact mechanism remains to be elucidated. PURPOSE: This study aims to investigate the protective effect and mechanism of PCT on myocardial ischemia-reperfusion injury. METHODS: An ischemia-reperfusion model was established via ligation of the left anterior descending branch of mice's hearts and hypoxia-reoxygenation (H/R) of cardiomyocytes. RESULTS: During ischemia-reperfusion, Nuclear factor E2-related factor 2 (Nrf-2) expression was downregulated, the left ventricular function was impaired, intracellular iron and lipid peroxidation product levels were elevated, and cardiomyocytes underwent ferroptosis. Furthermore, ferroptosis was enhanced following treatment with an Nrf-2 inhibitor. After PCT treatment, Nrf-2 expression significantly increased, intracellular ferrous ions and lipid peroxidation products significantly reduced, Ferroportin1 (FPN1) expression increased, and transferrin receptor-1 (TfR-1) expression was inhibited. CONCLUSIONS: PCT regulates iron metabolism through Nrf-2 to protect against myocardial cell ferroptosis induced by myocardial I/R injury.

Development and validation of a nomogram to predict recurrence in children with Henoch-Schönlein purpura.

BACKGROUND: To screen risk factors for the recurrence in children with Henoch-Schönlein Purpura (HSP) and to develop and validate a nomogram for recurrence in children with HSP. METHODS: During September 2019 and September 2021, 212 children with HSP were selected in this study. The children were divided into two sets in a proportion of 7:3 using R language, with the first group as the training sets and the second as the internal validation sets. The related variables were analyzed by univariate and multivariate logistic regression analyses, and a nomogram for predicting the recurrence in HSP children was established. The nomogram was evaluated by ROC curve, calibration curve and decision curve, and 1000 times bootstrap resampling method was used to verify the model internally. RESULTS: Univariate and multivariate regression analyses identified respiratory infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine as risk factors for the recurrence in children with HSP. Those risk factors were used to construct a predictive nomogram. The calibration curves revealed excellent accuracy of the predictive nomogram model, internally and externally. CONCLUSIONS: We constructed and validated a clinical nomogram to predict the recurrence in children with HSP. We confirmed that respiratory tract infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine were independent recurrence risk factors. This nomogram had a good performance in clinical decision-making.

lncRNA-NEAT1 Sponges miR-128 to Promote Inflammatory Reaction and Phenotypic Transformation of Airway Smooth Muscle Cells.

OBJECTIVE: Pediatric asthma is still a health threat to the children. Long noncoding RNA-NEAT1 (lncRNA-NEAT1) was reported to be positively correlated with the severity of asthma. We aimed to study the effects and mechanism of lncRNA-NEAT1on inflammatory reaction and phenotypic transformation of airway smooth muscle cells (ASMCs) in the bronchial asthma. METHOD: The degree of lncRNA-NEAT1 and miR-128 mRNA in children with bronchial asthma and healthy individuals was tested by qRT-PCR. After the inflammatory reaction and phenotypic transformation of PDGF-BB-induced ASMCs, the expression of lncRNA-NEAT1 or miR-128 in the AMSC was disturbed in the AMSC. Subsequently, the expression of lncRNA-NEAT1 and miR-128 was detected by the way of qRT-PCR, and western blot was applied to measure the expression of MMP-2, MMP-9, α-SMA, calponin, NF-κB, and so on in the cells. The content of TNF-α, IL-1ß, IL-6, and IL-8 in the cell culture supernatant was checked by ELISA. MTT, Transwell, and flow cytometry were used to detect cell proliferation, migration, and apoptosis. Further, the targeting relations between lncRNA-NEAT1 and miR-128 were evaluated by the dual-luciferase reporter assay. RESULT: In the sputum of children with bronchial asthma, lncRNA-NEAT1 was significantly upregulated while miR-128 was rapidly downregulated. Besides, lncRNA-NEAT1 and miR-128 were competitively combined and, for their expression, negatively correlated. CONCLUSION: lncRNA-NEAT1 sponges miR-128 to boost PDGF-BB-induced inflammatory reaction and phenotypic transformation of ASMCs to aggravate the occurrence and development of childhood bronchial asthma.

TCF7L2 activated HOXA-AS2 decreased the glucocorticoid sensitivity in acute lymphoblastic leukemia through regulating HOXA3/EGFR/Ras/Raf/MEK/ERK pathway.

Acute lymphoblastic leukemia (ALL) is characterized by abnormal lymphoblasts accumulation in the bone marrow and blood. Despite great efforts have been made in exploring novel therapeutic method, the prognosis of children with ALL is still unsatisfied. Glucocorticoid (GC) resistance is a great obstacle for the clinical treatment of ALL. Therefore, it is essential to investigate the molecular mechanism underlying the GC resistance. According to previous reports, long noncoding RNAs (lncRNAs) are involved in drug resistance of various human cancers. LncRNA HOXA cluster antisense RNA2 (HOXA-AS2) has been reported in several human malignancies due to its oncogenic property. However, the molecular mechanism of HOXA-AS2 involved in the GC resistance of ALL still needs to be further clarified. At first, we found that lncRNA HOXA-AS2 was highly expressed both in prednisone insensitive ALL cell lines and patient samples. Gain or loss-of-function assays revealed that HOXA-AS2 enhanced GC resistance via promoting cell proliferation and inhibiting cell apoptosis. Furthermore, we validated that HOXA-AS2 upregulated HOXA3, thereby activating EGFR/Ras/Raf/MEK/ERK signaling pathway. Our findings showed that HOXA-AS2 may be a potential therapeutic target for ALL patients with poor GC resistance.