Nursing Progress of Hypertonic Saline Inhalation in the Treatment of Infantile Bronchitis Based on Image Enhancement.

The onset of bronchiolitis is closely related to the anatomical characteristics of the bronchi in children of this age. This kind of injury is caused by epithelial necrosis, nasal mucosa, and mucosal edema caused by narrowing and blockage of the trachea. Children with this serious phenomenon will have respiratory and heart failure, which threatens the life of children to a large extent. In this paper, based on image enhancement technology, hypertonic saline aerosol inhalation treatment of pediatric bronchiolitis nursing care, through related cases, the application of image enhancement technology in hypertonic saline aerosol inhalation therapy and pediatric bronchiolitis is analyzed, and the tone mapping function is used. Tone mapping functions, hereditary arithmetics, and slope regimes for experimental field capture and detection were used for the objective of therapeutic approaches for the treatment of pediatric capillary pneumonia by hypertonic inhalation. Experimental results show that imaging technology hypertonic inhalation can control the main symptoms of bronchiolitis in infants and young children. Inhalation of 3% saline can shorten the course of moderately chronic children to half a year and can reduce the length of hospital stay by a quarter of the original requires hospitalization time, and the cure rate of pediatric bronchiolitis is increased to 93.7%.

Circ_0085296 suppresses trophoblast cell proliferation, invasion, and migration via modulating miR-144/E-cadherin axis.

BACKGROUND: Circular RNAs (circRNAs) have been revealed to be important regulators in the biological behavior of cells, and aberrant circRNAs may be associated with the etiology of pre-eclampsia (PE). However, the role and underlying molecular mechanisms of circ_0085296 in PE remain unclear. METHODS: The expression of circ_0085296, microRNA (miR)-144, and E-cadherin was detected using quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation, migration, and invasion were analyzed by cell counting kit-8, colony formation and transwell assay. The interaction between miR-144 and circ_0085296 or E-cadherin was analyzed by the dual-luciferase reporter assay and pull-down assay. RESULTS: Circ_0085296 was elevated in PE placental tissues, knockdown of circ_0085296 promoted trophoblast cell proliferation, invasion, and migration, while circ_0085296 up-regulation showed opposite effects. MiR-144 was down-regulated in PE placental tissues, and restoration of miR-144 induced proliferation, invasion, and migration in trophoblast cells. Further mechanistic analysis found miR-144 directly bound to circ_0085296 and E-cadherin, and circ_0085296 functioned as a sponge of miR-144 to regulate E-cadherin expression. Furthermore, miR-144 inhibition or E-cadherin overexpression attenuated the effectsof circ_0085296 on cell processes in trophoblast cells. CONCLUSION: Circ_0085296 inhibited trophoblast cell proliferation, invasion, and migration via regulating miR-144/E-cadherin axis, providing a novel insight into the pathogenesis of PE and a new prospective therapeutic target for PE patients.