0.05), while significant difference was found in group A before and after intravenous ferrotherapy (P

with hyperbilirubinemia admitted to the Neonatology Department of the First Affiliated Hospital of Zhengzhou University from January 2016 to October 2018 were divided into the control group (n=51) and the observation group (n=51) by random number table method. Both groups underwent auditory brainstem response hearing screening. The control group was given routine nursing intervention, the observation group was given non-drug sedation nursing intervention. The sedative effects of the two groups were compared. The Score of Newborn Facial Coding System (NFCS) and effective rates of examination between the two groups were compared. Results? After intervention, mean heart rate and mean respiratory rate in the observation group were statistically lower than those in the control group (P＜0.05), and average sleep latency was significantly shorter than that in the control group with statistical difference(P＜0.05). After intervention, only NFCS score in the control group significantly increased compared with that before intervention, and the NFCS score of the observation group was significantly lower than that of the control group during and after screening with statistical difference (P＜0.05). The effective rate of examination in the observation group was 98.04%, significantly higher than that of the control group (86.27%) with statistical difference(χ2=4.883,P＜0.05). Conclusions? The application of non-drug sedative nursing intervention in auditory brainstem response in hyperbilirubinemia neonatal hearing screening has good sedative effect, can significantly reduce the stress response of children to the outside world, and improve the efficiency of examination. It has certain application value in neonatal medical examination.

Nonalcoholic fatty liver disease (NAFLD) occurrence and progression are associated with lipid accumulation, insulin resistance, inflammation, liver damage, fibrosis, and other factors. AMP-dependent protein kinase (AMPK) is a key molecule that regulates bioenergy metabolism and participates in multiple biological processes, including lipid metabolism, autophagy, inflammation, and cell apoptosis. Promoting AMPK activation can reduce hepatic lipid accumulation and insulin resistance, alleviate the development of NAFLD, reduce liver inflammation and fibrosis, and inhibit the progression of NAFLD to nonalcoholic steatohepatitis.

‍ ObjectiveTo investigate the protective effect of safranal against sepsis-related liver injury （SRLI） induced by lipopolysaccharide （LPS） in mice and its mechanism. MethodsA total of 32 experimental male C57BL/6 mice were divided into control group， single drug group， model group， and treatment group using the simple random method， with 8 mice in each group. The mice in the single drug group and the treatment group were intraperitoneally injected with safranal （60 mg/kg） for 7 days of pretreatment， and the mice in the model group and the treatment group were intraperitoneally injected with LPS （10 mg/kg） to induce acute liver injury. The activities of serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were measured； HE staining was used to observe liver tissue sections； immunohistochemistry was used to analyze the expression of the downstream protein heme oxygenase-1 （HO-1） in the signal pathway； TUNEL was used to analyze the apoptosis of hepatocytes； Western blot was used to measure the expression of total proteins （nuclear factor erythroid 2-related factor 2 ［Nrf-2］ and HO-1） in liver tissue. The human liver cell line L02 was pretreated with safranal （100 μmol/L）， followed by induction of acute hepatocellular injury with LPS （100 ng/mL）， and DCFH-DA fluorescent labeling was used to detect reactive oxygen species （ROS）. ResultsAfter safranal pretreatment， the treatment group had significantly lower levels of ALT and AST than the model group （both P<0.001）， with a relatively intact pseudolobular structure and a smaller necrotic area in the liver. Compared with the model group， the treatment group had significant increases in the expression levels of Nrf2 and HO-1 in liver tissue after safranal+LPS treatment （both P<0.001）， and immunohistochemistry showed that safranal pretreatment increased the number of HO-1-positive cells. In the cell model of LPS-induced acute liver injury， the treatment group had a significant reduction in the production of ROS compared with the model group. ConclusionSafranal can exert a protective effect against SRLI induced by LPS in mice through the Nrf2/HO-1 pathway.