Objective:To explore the causes of high noise exposure in PICU, and to provide reference for formulating effective intervention measures to improve the status of noise exposure.Methods:With phenomenological method, eleven nurses of Xinhua Hospital, Shanghai Jiaotong University School of Medicine from August to September 2020 were enrolled by purposive sampling method, and joined face-to-face and semi-structured interviews with researchers. Interview data were analyzed by Colaizzi 7-step analysis method.Results:Four themes were extracted, including the characteristics of PICU, difficulty in equipment alarm management, the crying of children which was difficult to appease, and the low level of knowledge, attitude and practice of noise management of medical staff.Conclusions:High noise exposure of PICU is caused by many reasons. Researchers and managers can optimize the equipment alarm management, implement ideal analgesia and sedation and humanistic care, and carry out noise management training to improve the noise exposure in PICU and the quality of clinical nursing.

The IKAROS family zinc finger 1 (IKZF1) gene encodes the Ikaros protein, which regulates the development and differentiation of hematopoietic cells, and is essential for autoimmune and tumor suppression.With the development of genomics, IKZF1 has become an important prognostic biomarker for the occurrence and progression of acute lymphoblastic leukemia.Mutations in the IKZF1 gene appears in about 15% of childhood acute B-lymphoblastic leukemia.The mutation impairs the tumor-suppressor function of the IKZF1 gene, enhances the proliferation and anti-apoptotic ability of leukemia cells, and develops resistance to key chemotherapy drugs.IKZF1 mutations are more common in patients with other adverse prognostic factors and face difficulties in the course of treament with high recurrence rate, short remission period and high mortality.Intensive therapy, hematopoietic stem cell transplantation and immunotherapy for childhood acute B-lymphoblastic leukemia with IKZF1 mutation can reduce the recurrence rate and improve the remission rate and survival rate.Targeted therapy is promising to improve the prognosis of children with IKZF1 mutation.

BACKGROUND:In order to solve the problems of poly-l-lactic acid (PLLA) stents, such as poor support, acidic metabolites, we researched a novel biogradable stent-PLLA/amorphous calcium plosphate (ACP).
OBJECTIVE: To discuss the safety and histocompatibility of the novel biogradable stent-PLLA/ACP stent implanted in the coronary artery in a porcine model.
METHODS:Sixteen novel biogradable stents were randomly implanted into the coronary arteries, left anterior descending branch, left circumflex artery or right coronary artery of sixteen healthy Tibet miniature pigs. The blood routine and blood biochemistry were measured pre-operation and at 1 month after operation. The coronary blood vessels where the stent was implanted were examined by hematoxylin-eosin staining at 1 and 6 months after operation.
RESULTS AND CONCLUSION: Compared with pre-operation, the post-operation indicators of the blood routine and blood biochemistry were of no significant difference. Coronary angiography revealed coronary artery patency and no thrombosis, the vascular stent segments exhibited clear boundaries with the surrounding tissue, with no tissue adhesion, necrosis, and adherence abnormalities. The results of hematoxylin-eosin staining showed that there was no significant difference in vascular injury integral between 1 month after operation and 6 months after operation. However, 6 months after operation, the scores of the inflammation were lower (P < 0.05), and the scores of the endothelialization were increased (P < 0.05). There was no myocardial infarction and inflammatory cellinfiltration around the stent. These results suggest that the novel biodegradable stent has good safety and histocompatibility.

Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease (IBD) that has become a major gastroenterologic problem during recent decades. Numerous complicating factors are involved in UC development such as oxidative stress, inflammation, and microbiota disorder. These factors exacerbate damage to the intestinal mucosal barrier. Spirulina platensis is a commercial alga with various biological activity that is widely used as a functional ingredient in food and beverage products. However, there have been few studies on the treatment of UC using S. platensis aqueous extracts (SP), and the underlying mechanism of action of SP against UC has not yet been elucidated. Herein, we aimed to investigate the modulatory effect of SP on microbiota disorders in UC mice and clarify the underlying mechanisms by which SP alleviates damage to the intestinal mucosal barrier. Dextran sulfate sodium (DSS) was used to establish a normal human colonic epithelial cell (NCM460) injury model and UC animal model. The mitochondrial membrane potential assay 3-‍‍(4,5-dimethylthiazol-2-yl)-2,‍5-diphenyltetrazolium bromide (MTT) and staining with Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) and Hoechst 33258 were carried out to determine the effects of SP on the NCM460 cell injury model. Moreover, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qPCR), western blot, and 16S ribosomal DNA (rDNA) sequencing were used to explore the effects and underlying mechanisms of action of SP on UC in C57BL/6 mice. In vitro studies showed that SP alleviated DSS-induced NCM460 cell injury. SP also significantly reduced the excessive generation of intracellular reactive oxygen species (ROS) and prevented mitochondrial membrane potential reduction after DSS challenge. In vivo studies indicated that SP administration could alleviate the severity of DSS-induced colonic mucosal damage compared with the control group. Inhibition of inflammation and oxidative stress was associated with increases in the activity of antioxidant enzymes and the expression of tight junction proteins (TJs) post-SP treatment. SP improved gut microbiota disorder mainly by increasing antioxidant enzyme activity and the expression of TJs in the colon. Our findings demonstrate that the protective effect of SP against UC is based on its inhibition of pro-inflammatory cytokine overproduction, inhibition of DSS-induced ROS production, and enhanced expression of antioxidant enzymes and TJs in the colonic mucosal barrier.
Animals ; Antioxidants/pharmacology* ; Colitis/prevention & control* ; Colitis, Ulcerative/metabolism* ; Colon/metabolism* ; Dextran Sulfate/toxicity* ; Disease Models, Animal ; Gastrointestinal Microbiome ; Inflammation/metabolism* ; Mice ; Mice, Inbred C57BL ; Oxidative Stress ; Reactive Oxygen Species/metabolism* ; Spirulina